PASC co, which encompasses Long COVID or post-COVID syndrome, is a condition marked by the continuation of COVID-19 symptoms—or the emergence of new ones—4 or more weeks after infection with SARS-CoV-2 (http://www.CDC.gov), or those persistently symptomatic for >30 days from onset of infection (http://www.NIH.gov). Alternatively, the World Health Organization describes PASC (or Post COVID-19 condition) as occurring in individuals with a history of probable or confirmed SARS-CoV-2 infection, usually 3 months from the onset of COVID-19 with symptoms that last for at least 2 months and cannot be explained by an alternative diagnosis (http://www.WHO.int). The current PASC definition in the NIH RECOVER (REsearching COVID to Enhance Recovery) Initiative program is: ‘ongoing, relapsing, or new symptoms, or other health effects occurring after the acute phase of SARS-CoV-2 infection (i.e., present four or more weeks after the acute infection)’. The RECOVER Initiative is an NIH-funded project whose goal is to rapidly improve our understanding of and ability to predict, treat, and prevent PASC (post-acute sequelae of SARS-CoV-2), including Long COVID.

The symptoms of PASC whether in hospitalized or non-hospitalized patients are numerous and diverse and include shortness of breath, chest pain, cognitive impairment, and fever, among others (Michelen et al., 2021). Reports also reveal that there are wide and country-specific variations in the prevalence of PASC ranging from 3.3% in the UK, 13.9% in the USA, to 39% in Denmark and the Faroe Islands (Mantovani et al., 2022; Perlis et al., 2022; Petersen et al., 2022; Subramanian et al., 2022). The pathophysiologic mechanisms underlying PASC remain to be determined. However, the clinical features and epidemiology may provide insights into possible mechanisms. Although PASC may be a consequence of long-term organ damage attributable to acute-phase infection, it is postulated that specific mechanistic pathways exacerbate the initial illness adversely affecting many organs and resulting in the development of later symptoms. As such, this multifactorial condition displays over 200 symptoms and affects multiple tissues, organs, and biological systems (i.e., ears, eyes, head, nose, throat, kidney, brain, cardiopulmonary, endocrine, gastrointestinal (GI), musculoskeletal, neuropsychiatric, and systemic) to varying degrees. So far, immune dysregulation, autoimmunity, dysautonomia, endothelial dysfunction (ED), occult viral persistence, reactivation of pre-existing chronic viral infections as well as coagulopathies are some of the main underlying pathophysiological mechanisms described (Ahamed and Laurence, 2022; Al-Ramadan et al., 2021; Amenta et al., 2020; Camargo-Martínez et al., 2021; Carod-Artal, 2021; Choutka et al., 2022; Cortés-Telles et al., 2021; Doykov et al., 2020; Fernández-de-Las-Peñas et al., 2021; Gottschalk et al., 2023; Lee et al., 2021; Mantovani et al., 2022; McFarland et al., 2021; Oronsky et al., 2023; Silva Andrade et al., 2021; Song et al., 2021; Toniolo et al., 2021; Touyz et al., 2021; Townsend et al., 2021; Wirth and Scheibenbogen, 2021; Wong et al., 2021). Although PASC has been described as ‘a mysterious mix of symptoms with no clear pattern’, it bears similarities to other post-viral syndromes, and to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), certain phenotypic clusters are emerging in the literature.

This review will delineate the current knowledge about the underlying mechanisms and/or biological pathways responsible for tissue damage including pulmonary, cardiac, GI, neuronal, vascular, etc. associated with COVID-19 and the subsequent generation of symptoms. It will highlight the underlying causes of PASC and suggest ways to understand the clinical symptomatology for improved diagnostic and therapeutic procedures for the condition. We will also postulate on the pathophysiology and pathobiology of PASC by providing working hypotheses that could aid in further exploration of this multifaceted syndrome. This review will attempt to decipher the possible underlying tissue injury mechanisms for long-term residual illness post-SARS-CoV-2 infection.

Epidemiological studies in the UK and USA have found similar symptoms, but differing rates and durations of Long COVID (Groff et al., 2021). A UK study discovered that SARS-CoV-2 infection was linked to 62 symptoms lasting beyond 12 weeks, including anosmia, hair loss, sneezing, ejaculation difficulties, and reduced libido. The risk of Long COVID was higher among women, ethnic minorities, those with lower socio-economic status, smokers, obese individuals, and those with underlying health conditions, and increased with decreasing age (Subramanian et al., 2022). In contrast, Long COVID affects 7.3% of 3042 US survey respondents, equivalent to 18.8 million adults. Impacts on daily activities were severe for 25.3% of those with Long COVID and 28.9% had SARS-CoV-2 infection over a year ago. Women, those with comorbidities, and those unvaccinated or not boosted were at higher risk (Robertson et al., 2022). Studies from the USA and Europe have found that the prevalence of Long COVID is higher among women and those with multiple chronic conditions (Chen et al., 2022; Fernández-de-Las-Peñas et al., 2022; Robertson et al., 2022; Thompson et al., 2022). However, there is variation in risk factor data due to differences in study design, population studied, and definition of Long COVID. Often, studies lack a COVID-free control group, focus on hospitalized or healthcare-seeking populations, and have different definitions of Long COVID. These studies emphasize the high burden of Long COVID and the need for further research on its prevalence and risk factors.

The clinical manifestations of PASC vary widely. Common PASC symptoms include fatigue, dyspnea, cough, ‘brain fog’, headaches, sleep disturbance, impaired smell and taste, palpitations, chest pain, and orthostatic dizziness (Davis et al., 2021; Hernandez-Romieu et al., 2022; Ozonoff et al., 2022; Sneller et al., 2022; Sudre et al., 2021). Using machine-learning algorithms, Estiri et al. uncovered 33 phenotypes of PASC and it is likely that multiple different pathophysiologic mechanisms account for this heterogeneity (Estiri et al., 2021). Indeed, detailed multi-omic profiling of COVID-19 patients revealed unique associations between immunological signatures and specific PASC endotypes (Su et al., 2022). Future mechanistic studies will need to recognize the heterogeneity of the disorder. PASC is more common in individuals who suffered a severe vs mild acute COVID-19 illness (Hernandez-Romieu et al., 2022; LaVergne et al., 2021; Xie et al., 2021). In such patients, the illness shares features of post-intensive care syndrome (PICS) (Rawal et al., 2017) and findings observed in survivors of the SARS and MERS coronavirus epidemics (Greenhalgh et al., 2020; Tansey et al., 2007). Pathophysiologic mechanisms in this group may include the effects of SARS-CoV-2 infection, reactivation of other viruses such as the Epstein–Barr virus (EBV), autoimmunity, incomplete recovery from acute organ injury (e.g., lung, heart, kidney, brain, thrombosis), effects of treatments (e.g., mechanical ventilation, steroids), and exacerbation of pre-existing conditions (e.g., pre-diabetes, CKD, CHF). However, individuals with mild COVID-19 (Augustin et al., 2021; Estiri et al., 2021), and even individuals with no serologic evidence of prior SARS-CoV-2 infection (Krishna et al., 2022; Sneller et al., 2022), can experience PASC symptoms, suggesting that some features of PASC may represent responses to the stress of the pandemic, for example, social isolation, anxiety, loss of friends or family, work stress, and financial stress, in addition to the viral infection itself. The prevalence of PASC appears to be lower in the more recent COVID ‘waves’, especially with the Omicron variant, and lower in people who were vaccinated prior to contracting COVID-19 (Azzolini et al., 2022; Zisis et al., 2022), suggesting that SARS-CoV-2 variants, availability of newer treatments and immune responses may impact the pathogenesis of PASC. For example, recent research suggests that the use of nirmatrelvir/ritonavir during acute SARS-CoV-2 infection reduces the risk of PASC regardless of vaccination status or history of prior infection (Xie et al., 2022). Long COVID may also manifest as residual or new organ dysfunction which could be the result of acute organ injury during the COVID-19 infection, for example, ARDS, acute kidney injury, or myocarditis, or the result of chronic inflammation, ED, or autoimmunity triggered by the infection. The high incidence of new-onset type I diabetes after COVID-19 infection, for example, could be due to direct viral injury of pancreatic beta cells, induction of autoimmunity to beta cells or glucose-regulating pathways or decreases in peripheral insulin sensitivity associated with chronic inflammation that is exhibited in PASC patients (Barrett et al., 2022; Rubino et al., 2020). There are commonalities of clinical manifestations and symptoms between COVID-19 and Long COVID-19 that require detailed mechanistic understandings (Davis et al., 2021; Mehandru and Merad, 2022).

Many PASC features resemble (ME/CFS), which is also commonly preceded by viral infections, prompting some to ask whether PASC and ME/CFS are similar diseases (Bornstein et al., 2022; Tate et al., 2022). Fatigue, exertion intolerance, and post-exertional malaise are among the most frequent symptoms cited for PASC. These same symptoms manifesting in PASC patients had been designated as ‘core criteria’ of ME/CFS by the National Academy of Medicine in a 2015 report (https://batemanhornecenter.org/wp-content/uploads/filebase/providers/Recognizing-PVS-and-Tools-ECHO-5_3_2022-V2.pdf). It is estimated that about half of people with Long COVID will meet the criteria for ME/CFS, whether they are given that specific diagnosis or not. It is also important to note the multiple types of tissues and organs adversely affected by ME/CFS including cardiovascular problems, central nervous system (CNS), immune system disturbances, ion transport dysfunction, cell energy metabolism, GI dysfunction, cognitive impairment, myalgia, arthralgia, orthostatic intolerance, and chronic inflammation (Rasa et al., 2018), are also commonly reported in PASC patients. The trigger for COVID-19 is the SARS-CoV-2 infection. ME/CFS is a complex disease frequently triggered by an infection with EBV (the virus that causes mononucleosis) or parvovirus B19 even though various other viral and nonviral triggers have also been reported (Chu et al., 2019; Fluge et al., 2021; Jason et al., 2022; Sotzny et al., 2018). The evidence is clear that in COVID-19 and potentially in PASC patients, the initial SARS-CoV-2 infection resurrects latent viruses such as EBV (Fluge et al., 2021), which could trigger ME/CFS. Although EBV has been associated with post-viral fatigue in ME/CFS, the mechanisms leading to post-viral fatigue syndrome and Long COVID (PASC) are unresolved. The similarities raise two questions: Do these two multi-symptomatic diseases share common molecular and pathophysiological pathways in their disruption of homeostasis post-infection? Although the triggers may be different, because of their overlapping symptoms, could there be a common pathobiological explanation? Indeed, the lessons learned from three decades of studying ME/CFS should help with identification of a variety of conceptually distinct medical comorbid conditions found in PASC.

Postural orthostatic tachycardia syndrome (POTS), which can be seen after other viral infections has also been observed in PASC and may point toward autoimmune dysfunction of the autonomic system, including autoantibodies to acetylcholine and adrenergic receptors (Blitshteyn and Whitelaw, 2021; Fluge et al., 2021). However, a recent German study reports that PASC is not associated with autoantibodies (Schultheiss et al., 2022). Nevertheless, SARS-CoV-2 may be responsible for PASC symptoms by activating the host’s immune response and leading to long-term autoantibody production. Autoantibodies were isolated in acute COVID-19 patients by several research teams including Wang et al. who used REAP to screen a group of 194 SARS-CoV-2-positive COVID-19 patients for autoantibodies against 2770 extracellular proteins. Results showed that COVID-19 patients had a significant increase in autoantibody reactivity compared to uninfected controls (Jiang et al., 2023; Wang et al., 2021). It is currently not well understood what role autoantibodies may play in the pathophysiology of Long COVID or PASC. Evidence linking autoantibodies to Long COVID as an etiological factor is limited and further research is needed to fully understand their role in the development of PASC. Similarities between PASC symptoms and those of Mast Cell Activation Syndrome (MCAS) have also been noted (Akin, 2017; Blitshteyn and Whitelaw, 2021; Schieffer and Schieffer, 2022).

Longitudinal studies need to be conducted to determine the similarities and differences between PASC and ME/CFS and other post-infectious syndromes by frequently collecting biological samples (as it is being implemented by the RECOVER study—https://recovercovid.org), and up-to-date information on the presence of the infectious agent and the severity of various symptoms. Such studies should also include continual laboratory studies of the immune system, metabolism, gene structure and function, and transcriptome, as well as tests of cognition, sleep, and the functioning of the nervous system, heart, and cardiovascular system.

Although the COVID-19 pandemic disproportionately affected patients who had comorbid diabetes mellitus, it is now clear from numerous studies across the globe that COVID-19 causes dysregulation of glucose homeostasis leading to new-onset hyperglycemia and type I diabetes (Genç et al., 2021) in patients with no previous risk factors for diabetes mellitus (Bode et al., 2020; Sathish et al., 2021c; Sathish and Chandrika Anton, 2021b; Tittel et al., 2020; Unsworth et al., 2020; Watson, 2022). New-onset COVID-induced type 1 or 2 diabetes has also been documented in children (Tittel et al., 2020; Trieu et al., 2021; Unsworth et al., 2020). This novel form of COVID-induced diabetes with anomalous glycemic parameters and heightened rates of DKA (diabetic ketoacidosis), occurs in severely ill patients with higher mortality rates and poorer outcomes compared to COVID-19 patients with pre-existing diabetes (Chandrashekhar Joshi and Pozzilli, 2022). The underlying pathobiological mechanism for this induced diabetes in COVID-19 patients has not been clearly delineated although it is suspected that SARS-CoV-2 could damage the beta cells of the pancreas and precipitate insulin resistance (Aluganti Narasimhulu and Singla, 2022). There are some plausible mechanisms that underlie this new diabetes onset. SARS-CoV-2 infection can damage beta cells or increase glucose levels via oxidative stress and inflammation; the virus can also bind the angiotensin-converting enzyme receptor 2 (ACE2), on acinar cells and cause tissue detriment and pulmonary fibrosis via increasing concentration of the fibrosis-promoting Angiotensin II (Morganstein et al., 2021) and hyperglycemia can inhibit lymphocyte proliferation to repair the tissue damage. The initial binding of the virus to ACE2 requires the presence of transmembrane serine protease 2 (TMPRSS2), a protein that is regulated by androgens. The ACE2 mRNA is also expressed in several endocrine glands, including the pancreas, ovaries, testes, and thyroid gland (Lazartigues et al., 2020). At postmortem, both follicular and parafollicular cells of the thyroid gland were extensively damaged in patients who died of COVID (Wei et al., 2007). These systems, which are physiologically regulated by ACE2 upon viral infection, induce acute cardiopulmonary failure, and coagulopathy. Furthermore, the overexpression of the ACE2 receptor can deregulate these systems and cause cardiovascular instability (renin–angiotensin system), acute inflammatory pulmonary edema (kinin–kallikrein system), and thromboembolism (coagulation system) (Sidarta-Oliveira et al., 2020). In fact, ACE2 gene therapy in gene knockout mice promoted better survival and function of the beta cells, as well as improved glucose homeostasis (Bindom et al., 2010). Additionally, a downregulation of the transcription factor REST (RE1-silencing transcription factor) observed in COVID-19 patients is linked to the altered gene expression of glucose and lipid metabolism involving apelin, myostatin myeloperoxidase (peptides and proteins important for the insulin signaling pathway) (He et al., 2021). COVID-19 patients also harbored upregulated short-chain fatty acids, propionic acid, and isobutyric acid, which are possibly linked to insulin resistance (He et al., 2021).

Stress is another factor that can be induced by a viral infection, which causes elevated glucose levels in subjects with diabetes via the secretion of glucocorticoids and catecholamines contributing to further impairment of the immune system (Wang et al., 2020). In addition, the incidence of DKA observed in COVID-induced diabetic patients was unusually high in the absence of autoantibodies suggesting that acute viral-induced pancreatic damage might have occurred (Li et al., 2020b; Vellanki and Umpierrez GE - Center ofDiabetes and Metabolism, Emory University School of Medicine, 2021). There are also a few reports of cases that have described autoantibody-negative insulin-dependent diabetes (Hollstein et al., 2020; Kuchay et al., 2020). Mechanistically, the consequence of stress caused by SARS-CoV-2 infection may be explained by the stimulation of a signaling pathway designated as the integrated stress response (ISR) that promotes the activation of a family of serine/threonine kinases that is, double-stranded RNA-dependent protein kinase (PKR) and PKR-like ER kinase (PERK), and the subsequent induction of serine phosphorylation of insulin receptor substrates (IRS) which leads to downregulation of the insulin signaling pathway. Both the viral components (RNA or proteins) of SARS-CoV-2 and ‘cytokine storm’, which activates a family of serine/threonine kinases linked to the ISR and is represented by pro-inflammatory cytokines such as IL-6 and tumor necrosis factor (TNF-α, can cause insulin resistance Santos et al., 2021). Moreover, insulin resistance can be caused by the downregulation of insulin receptors in skeletal muscle via virally induced interferon gamma (IFN-γ) (Sestan et al., 2018). This could be an additional contributor to the insulin resistance syndrome that has been described in COVID-induced diabetes patients.

There are also several other postulated mechanisms including molecular mimicry, that may explain the rise in autoimmune diabetes following COVID-19 infection. SARS-CoV-2 also downregulates ACE2, which degrades Angiotensin II. These mechanisms of unrestricted actions of Angiotensin II lead to deleterious effects including inflammatory activity by increasing the infiltration of macrophages and monocytes, reducing blood flow to pancreatic islets, and promoting the instability of the beta cells leading to glycemic dysregulation (Carlsson et al., 1998; Chee et al., 2020; Montezano et al., 2014). There is emerging evidence showing that the new-onset diabetes is also a feature of Long COVID (Sathish et al., 2021a) even though the precise mechanism might be multifaceted. It is essential to collect biospecimens to design mechanistic studies that might shed light on the underlying causes precipitating the various types of symptoms experienced by Long COVID sufferers and specifically to follow-up COVID-related diabetes patients by implementing longitudinal and prospective cohort studies to distinguish between COVID-induced diabetes from conventional diabetes. There is a digital registry that is specifically designed to establish the extent and characteristics of new-onset, COVID-19-related diabetes, and to investigate its pathogenesis and outcomes (http://covidiab.e-dendrite.com).

The upper respiratory system is the primary site of the SARS-CoV-2 viral infection. In the scenario of an excessive inflammatory response, the consequence can be irreversible lung fibrosis and the compromise of respiratory effector function (Tanni et al., 2021). Fibrotic remodeling with characteristic findings consists of fibroblast proliferation, micro-honeycombing, and airspace obliteration, which were uncovered in pulmonary postmortem findings in a series of COVID-19 cases (Grosse et al., 2020). This suggested a link to respiratory distress syndrome (ARDS) as a long-term complication of COVID-19. In addition to ARDS, fibrotic remodeling resulting in respiratory symptoms can originate from pathologic conditions including dyspnea, and even from hospitalization, intensive care unit stays, use of high-flow oxygen support, and need for mechanical ventilation (Grillo et al., 2021). Additional mechanisms include epithelial and endothelial to mesenchymal transition and the ‘cytokine storm’. Prolonged exposure to supplemental oxygen is known to lead to increased oxidative stress and could maintain the inflammatory status favorable for activation of post-COVID-19 pulmonary fibrosis (George et al., 2020). A fraction of PASC patients present with fatigue, exercise limitation, persistent chest pain, and breathlessness. These symptoms may be caused in part by compromised cardiorespiratory function, lung vascular damage in microvessels, and hemodynamic complications such as resolved thrombus (Kosuge et al., 2012; Yaméogo et al., 2011). Fatigue and breathlessness may also be caused by chronic overstimulation of the ergoreflex, activated by exercise to centrally couple ventilation and cardiovascular function to exercise intensity (Sze et al., 2022). Exaggerated ergoreflex leads to excessive response relative to work performed, and to the sensation of breathlessness and fatigue. The hypercatabolic state, cytokine storm, and stimulation of the renin–angiotensin–aldosterone system by SARS-CoV-2 use of ACE2 to facilitate cell entry might cause a reduction in skeletal muscle mass and function, excessive ergoreflex, and sensations of fatigue and breathlessness (Medina-Enríquez et al., 2020). Further study of the mechanistic involvement and interactions between respiratory systems and extrapulmonary systems with reciprocal crosstalk and influence is needed.

Pulmonary dysfunctions are among the most destructive events associated with impaired immune responses caused by SARS-CoV-2 infection. The resulting cytokine storm activates defense events that stimulate biochemical pathways that eventually lead to the production of tissue injury markers and the collapse of lung tissue (Piazza et al., 2020; Sakr et al., 2020; Sidarta-Oliveira et al., 2020). These hematological changes form pulmonary thrombi and capillary microthrombi, which may represent thromboembolism instead of thrombosis in bone marrow emboli and septic pulmonary thromboembolism (Ackermann et al., 2020; D’Errico et al., 2020; Grosse et al., 2020; Khan et al., 2020). Transcriptomic analyses of coexpression data from human lung cells have shown that there are three physiological systems directly involved in the pathogenesis of COVID-19: (1) the kinin–kallikrein system; (2) the renin–system angiotensin; and (3) the coagulation system coexpressed with the ACE2 receptor in alveolar cells (Sidarta-Oliveira et al., 2020). These systems, which are physiologically regulated by ACE2 upon viral infection of the lungs, induce acute cardiovascular failure, coagulopathy, acute inflammatory pulmonary edema (kinin–kallikrein system), and thromboembolism (coagulation system) (Sidarta-Oliveira et al., 2020). Hyperinflammation induced by immunopathogenic, and biochemical mechanisms of SARS-CoV-2 suggests that cytokines and chemokines contribute to alveolar endothelial damage that promotes apoptosis of alveolar cells (pneumocyte type I) and degeneration of pulmonary pneumocyte type II alveolar cells (Hussman, 2020). These cell types are operationally connected via narrow junctions that control the transfer of ions, minerals, and fluid through the epithelium (Ackermann et al., 2020). SARS-CoV-2 infects ACE2-expressing pneumocyte type II cells, which act as epithelial immune cells and produce TNF, IL-6, IL-1β, and MCP-1.

Figure 1 depicts the initial entry of SARS-CoV-2 into the host cell by binding to ACE2 receptor in the respiratory tract and causing disruption of homeostasis by persisting in several organ systems and leading to the eventual development of PASC in a subset of patients. The depiction is for immunological, neurological, and pulmonary dysregulations, which may likely contribute to the hyperactivation of monocyte-derived macrophages in both acute and post-acute phases of the disease. Type I IFN-γ production is delayed leading to increased sensing of microbial threats. This in turn enhances the release of monocyte chemokines by alveolar epithelial cells (pneumocyte types 1 and 2), which direct blood monocytes into the lungs. There are several signaling molecules that induce monocytes to differentiate into pro-inflammatory macrophages via activation of Janus kinase (JAK)–signal transducer and activator of transcription (STAT) pathways. Activated T cells and natural killer cells enhance the recruitment and stimulation of macrophages (derived from monocytes) through the production of granulocyte–macrophage colony-stimulating factor (GM-CSF), IFN-γ, and TNF (see Figure 1).

Figure 1

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Alveolar macrophages lead to the activation and release of cytokine and chemokine and aggregation of neutrophils and monocytes that produce toxic mediators resulting in the death of the alveolar cells, fibrin deposition, hyaline membrane formation, the influx of red blood cells, alveolar edema, and dyspnea (Ackermann et al., 2020; Al-Khawaga and Abdelalim, 2020).

Whole-transcriptome sequencing of postmortem lung tissue from COVID-19 patients reveals two distinct molecular signatures: Lung damage caused by a massive metabolic reprogramming due to the upregulation of the unfolded protein response, steroid biosynthesis, and complement activation; and secondarily, ‘cytokine release syndrome’ (CRS) represented by the upregulation of cytokines such as IL-1 and CCL19, but absence of complement activation (Budhraja et al., 2022). Although most patients cleared the viral infection, they succumbed to acute dysbiosis overrepresented by Staphylococcus cohnii in ‘classical’ patients and Pasteurella multocida in CRS patients (Budhraja et al., 2022).

The association between insulin resistance and lung dysfunction in humans has also been documented in the literature. Another recent study confirmed other previous studies that revealed that the insulin/insulin-like growth factor 1 (IGF) signaling pathway, which plays an important role in energy metabolism, is impaired in organs and tissues of severe COVID-19 patients (Shin et al., 2022). AKT/mTOR/MAPK pathway and ligand/receptor interactions that initiate cellular signaling through IRS/PI3K lie downstream of insulin/IGF signaling pathway but are also additional molecular pathways that are associated with energy uptake and utilization. An impaired IGF pathway engenders insulin resistance or abnormal insulin/IGF response, which also leads to an enhanced metabolic syndrome manifestation such as diabetes, hyperglycemia, hyperlipidemia, and obesity. A COVID-19-impaired insulin/IGF signaling pathway is also associated with the downregulation of various metabolic pathways including the citrate cycle, lipid metabolism, beta-oxidation, amino acid metabolism, carbohydrate metabolism, and respiratory electron transport chain affecting the adipose tissue, liver, lungs, and pancreas resulting in the development of multiorgan dysfunction (Shin et al., 2022).

Chest pain, dyspnea, and heart palpitations are some of the key symptoms that draw attention to the cardiovascular system (Gluckman et al., 2022). However, cardiovascular disease (CVD) also includes congenital heart disease, coronary artery disease, hypertension (HTN), peripheral artery disease, stroke, and heart failure. Regardless of the severity of COVID-19, many patients have a complicated course of COVID-19 with regard to CVD. This is especially true for viral pneumonia (remembering that COVID-19 is primarily a respiratory infectious disease) that may result in severe systemic inflammation, acute myocardial infarction (MI), acute heart failure, cardiac arrest, venous thromboembolism (VTE), tachyarrhythmias, and stroke (Baldi et al., 2020; Basso et al., 2020; Gao et al., 2020; Lala et al., 2020; Parohan et al., 2020; Shi et al., 2020; Wallentin et al., 2020; Zhou et al., 2020). In a single-centered observational study, up to 329 days following diagnosis with COVID-19, approximately 75% reported persistent cardiac symptoms (Gluckman et al., 2022). In the absence of validated biomarkers for PASC, imaging evidence using cardiac magnetic resonance (CMR) was obtained for myocardial inflammation, pericardial enhancement, and diffuse myocardial edema. Similarly, various abnormalities on CMR as well positron emission tomography have been reported in COVID-19 patients, even in the absence of cardiac symptoms (Hanneman et al., 2022; Puntmann et al., 2020). There are indicators of CVD such as cardiomyocyte injury, quantified by cardiac troponin (cTn) concentrations, heart failure, quantified by N-terminal pro B-type natriuretic peptide (NT-proBNP), and hemodynamic cardiac stress, quantified by natriuretic peptide concentrations that were detected in COVID-19 patients (Flores et al., 2019; Lala et al., 2020; Mueller et al., 2021; Parohan et al., 2020; Shi et al., 2020; Zhou et al., 2020). The potential mechanisms underlying elevations in acute cTn and therefore myocardial injury from non-ischemic causes in COVID-19 patients include direct effect on myocardial cells via ACE2 receptor, cytokine storm, and hypoxia-induced apoptosis as well as myocarditis, Takotsubo syndrome, and pulmonary embolism. The rise in cTn from ischemic causes in COVID-19 patients include type I MI, and type II MI comprising shock, hypoxia, and tachycardia (Mueller et al., 2021).

SARS-CoV-2 can infect the brain, causing neuroinflammation (Pan et al., 2020). Moreover, inflammation elsewhere in the body can activate the innate immune system (Figure 1) in the brain via both humoral and retrograde neural signals, largely involving the vagus nerve (Poon et al., 2015; VanElzakker, 2013). Different study model systems such as autopsies, animals and organoids used to study the infective potential of the SARS-CoV-2 virus show that SARS-CoV-2 can reach and infect neurons and cells of the CNS and produce neuroinflammation (Matschke et al., 2020; Song et al., 2020). Neuropsychological symptoms are frequent in PASC survivors of COVID-19 who often experience lingering neurological symptoms analogous to cancer-therapy-related cognitive impairment, which involves white matter microglial reactivity and consequent neural dysregulation. SARS-CoV-2 infection has been shown to affect white-matter-selective microglial reactivity in mice and humans by impairing hippocampal neurogenesis, decreasing oligodendrocytes, and promoting myelin loss with a concomitant increase in CSF cytokines/chemokines including CCL11 (Fernández-Castañeda et al., 2022a). Accordingly, cognitive impairment manifested even with mild COVID symptoms parallel the neuropathophysiology that is observed in people with cancer therapy (Fernández-Castañeda et al., 2022b). The question remains: How does the virus manage to get to the brain? One potential pathway to reach the CNS is via hematogenous dissemination from severely infected upper and lower respiratory system by way of systemic inflammation that raises the permeability of blood–brain barrier (BBB) and permit circulating non-BBB-crossing molecules to adversely affect brain function (Proal and VanElzakker, 2021). More importantly for PASC, during acute infection this porousness can also allow for viral neuroinvasion that may persist past the acute infection phase. Although the mechanism is not well known, this neuroinvasion can occur directly or indirectly through host immune cells infected with the virus and are actively transported into the CNS (Dando et al., 2014; Lauer et al., 2018). A large MRI registry study that examined changes in the brain before and a mean of 141 days following SAR-CoV-2 identified reductions global brain size and gray matter thickness in orbitofrontal cortex/parahippocampal gyrus. Importantly, the study also identified increased markers of tissue damage in regions associated with the primary olfactory cortex following infection. These data suggest that COVID-19 has profound impact on the brain, especially the olfactory cortex, which may explain changes of taste and smell and may indicate CNS infection from direct extension from the olfactory system (Douaud et al., 2022).

The extrapulmonary disease that SARS-CoV-2 inflicts upon the body also extends to the GI tract where there is evidence that the virus may persist where the ACE2 receptor is highly expressed (Settanni et al., 2021). Given that the severity of COVID-19 is typically engendered by a set of comorbidities such as HTN, diabetes, obesity, and/or advanced age, the GI symptoms, such as diarrhea, vomiting, or abdominal pain during the early phases of the disease can be debilitating (Lamers et al., 2020). Symptoms can last for years as is the case for post-infectious irritable bowel syndrome (PI-IBS), which is punctuated by the persistence of abdominal discomfort, bloating and diarrhea that continue despite clearance of the inciting pathogen, usually bacterial origin (Dunlop et al., 2003; Kim et al., 2006; Settanni et al., 2021). Again, the culprit in all these acute and post-acute COVID-19 symptoms including the impairment of bowel physiology may be a dysregulation of ACE2-mediated functions due to a competitive mechanism of the virus on ACE2 receptor or from a downregulation of its anti-inflammatory activity. To date, there is a dearth of data on the GI sequelae of SARS-CoV-2 infection. This may be due to the uncertainty over COVID-19’s path of action on the gut physiology.

While much of our current understanding of PASC comes from adults, one of the first PASC phenotypes occurred in children. Shortly after the emergence of SARS-CoV-2, rare cases of multisystem inflammatory syndrome in children (MIS-C) were documented (Riphagen et al., 2020). It is now understood that MIS-C occurs weeks after SARS-CoV-2 infection and is characterized by persistent fevers, massive inflammation, and multiorgan involvement including long-term neurologic complications. The most striking clinical manifestation is profound myocardial dysfunction resulting in shock; however, extracardiac organ system dysfunction is also common, particularly GI (Cheung et al., 2020; Feldstein et al., 2020; Riphagen et al., 2020). The mechanisms which underlie MIS-C are not fully understood but emerging evidence points toward immune system dysfunction. Acute MIS-C is defined by massive elevations in inflammatory cytokines, particularly those related to myeloid recruitment and mucosal immunity (Consiglio et al., 2020; Gruber et al., 2020). The production of autoreactive antibodies is also characteristic of acute MIS-C with antibodies specific for endothelial proteins detected in many patients (Consiglio et al., 2020; Gruber et al., 2020; Ramaswamy et al., 2021). Aberrant activation of T cells is a consistent finding as well (Vella et al., 2021), with a potentially pathognomonic role for biased expansions of T cell clones (Porritt et al., 2021). Activated T lymphocyte cell expansions resemble those seen following bacterial superantigen stimulation with additional evidence suggesting that motifs from the SARS-CoV-2 spike protein may be capable of promoting autoimmunity (Noval Rivas et al., 2022). These immune derangements along with elevated biomarkers suggesting mucosal barrier breakdown have been linked to detectable antigenic persistence in circulation (Yonker et al., 2021), suggesting an additional role for viral persistence in the pathogenesis of MIS-C. Treatment for MIS-C has included steroids, intravenous immunoglobulin, and monoclonal antibodies targeting IL-6 and IL-1Ra (Feldstein et al., 2020). Fortunately, following treatment for MIS-C, short to mid-range reported health outcomes have been excellent (Farooqi et al., 2021; Matsubara et al., 2022). Pediatric PASC outside of MIS-C has been more difficult to quantify, with estimates ranging from 4% to 25% of previously infected children experiencing PASC symptoms (Izquierdo-Pujol et al., 2022). Risk factors for development of pediatric PASC include severity of acute infection, younger age (<5 years), and presence of chronic health conditions (Rao et al., 2022). In case reports or small series, endothelial damage and encephalomyelitis have been identified in children with PASC (Buonsenso et al., 2021; Lindan et al., 2021) but underlying mechanisms remain undefined. Based on our current knowledge of MIS-C and the evidence that pediatric immune responses to SARS-CoV-2 are distinct from adults (Pierce et al., 2020; Weisberg et al., 2021; Yoshida et al., 2022), understanding immune responses in pediatric PASC must be prioritized. To better characterize pediatric PASC subtypes and define the mechanisms giving rise to persistent symptomatology, awareness, and identification followed by study enrollment of relatively rare cases is critical to maximize our ability to understand and treat this emerging pediatric health threat.

What are PASC factors? When can the factors be assayed in the course of disease progression? Are these factors interrelated or independent? What are the immune and genomic signatures of PASC? What is the eventual public disease burden of PASC? What does PASC mean for patients and what can be done about it? The unknowns about PASC are too numerous to list. We still do not know if there is a correlation between PASC and the duration/frequency/severity of the initial SARS-CoV-2 infection. Also, the subsequent iterations of the virus (i.e., omicron variants) with factors like age, gender, demographics, and comorbidities are not clear. The longitudinal collection of biospecimens and deep phenotyping of PASC subjects in the RECOVER study will provide a rich set of resources to answer key prognostic, epidemiologic and pathophysiologic questions about PASC and will serve as a platform for testing interventions to prevent or treat PASC.

We urgently need comprehensive epidemiologic studies via surveys/questionnaires and by interrogating the electronic health record databases and through longitudinal study enrollment that allow for a more complete understanding of the prevalence ad incidence of PASC within various populations. Furthermore, comprehensive examination of blood and tissues using synergistic methods such as proteomics, metabolomics, transcriptomics, viral nucleic acid and protein testing, and virus-specific and auto-reactive antibody characterization will be needed. Additionally, comprehensive immunophenotyping of PASC can be performed to identify cell markers and to provide further pathophysiologic understanding of the interplay between immune responses, inflammation, and PASC phenotypes. It must also be noted that the mechanisms underlying Long COVID/PASC may not be uniform across all individuals. Among the more prominent sociodemographic and clinical risk factors, the severity of acute COVID-19 infection, female sex, advanced age, pre-existing diabetes mellitus, more than five early symptoms, early dyspnea, and prior psychiatric disorders have been identified (Carfì et al., 2020; Subramanian et al., 2022; Yong, 2021). Additional variables that need to be considered include the variant of SARS-CoV-2 infection and those who develop PASC and the role of vaccination and antiviral therapy in acute infection (Antonelli et al., 2022; Ledford, 2022). Double-vaccinated participants with COVID-19 caused by the Omicron BA.1, BA.4, and BA.5 variants were less likely to develop PASC, as compared to those infected by the Delta variant. It is also likely that most of the symptoms and pathologies associated with COVID-19 persist in Long COVID perhaps because of the spike protein, which is also the target of the vaccination. The currently known and suspected mechanisms and molecular features for COVID and potentially for Long COVID/PASC pathologies are shown in Table 1.

There are various hypotheses underlying Long COVID/PASC symptoms. The first points to the immune system going haywire after the initial virus infection, triggering a long-lasting inflammatory response that inflicts havoc on multiple organ systems. The second hypothesis is that this long-lasting inflammation may be due to the continued presence of virus or viral particles in organs such as the gut but may also be due to the reactivation of latent pathogens such as EBV, the most common cause of mononucleosis. The third hypothesis states that COVID-19 elicits a radical response analogous to an autoimmune disease that causes antibodies to target and destroy the body’s own tissues. The fourth leading hypothesis stipulates the formation of microclots, tiny blood clots that cause coagulopathy and lead to thrombosis. Therefore, the conclusion from this review on tissue damage is that there may be more than a single mechanism in motion for Long COVID (PASC) patients who experience a constellation of symptoms. Certain mechanisms may dominate over others in individual patients. There may be potential biomarkers or signaling pathways for different tissues or organs affected as well as therapeutic applications mostly in the form of inhibitors of the presumptive biomarkers of various tissues presented in Table 1, that could be employed for PASC sufferers until the underlying individual or collective mechanisms giving rise to their symptoms are clearly delineated. Furthermore, there is an urgent need to design experimental protocols that can distinctively identify the underlying mechanisms or pathways that are responsible for the clinical manifestations exhibited by Long COVID or PASC patients.

Authorship has been determined according to ICMJE recommendations.

1. 1. Ackermann M
   2. Verleden SE
   3. Kuehnel M
   4. Haverich A
   5. Welte T
   6. Laenger F
   7. Vanstapel A
   8. Werlein C
   9. Stark H
   10. Tzankov A
   11. Li WW
   12. Li VW
   13. Mentzer SJ
   14. Jonigk D

   (2020) Pulmonary vascular endothelialitis, thrombosis, and angiogenesis in covid-19

   New England Journal of Medicine 383:120–128.

   https://doi.org/10.1056/NEJMoa2015432

   • Google Scholar
2. 1. Ahamed J
   2. Laurence J

   (2022) Long COVID endotheliopathy: hypothesized mechanisms and potential therapeutic approaches

   The Journal of Clinical Investigation 132:e161167.

   https://doi.org/10.1172/JCI161167

   • PubMed
   • Google Scholar
3. 1. Aird WC

   (2007) Phenotypic heterogeneity of the endothelium: II. representative vascular beds

   Circulation Research 100:174–190.

   https://doi.org/10.1161/01.RES.0000255690.03436.ae

   • PubMed
   • Google Scholar
4. 1. Akin C

   (2017) Mast cell activation syndromes

   The Journal of Allergy and Clinical Immunology 140:349–355.

   https://doi.org/10.1016/j.jaci.2017.06.007

   • PubMed
   • Google Scholar
5. 1. Akpek M

   (2022) Does COVID-19 cause hypertension?

   Angiology 73:682–687.

   https://doi.org/10.1177/00033197211053903

   • Google Scholar
6. 1. Al-Khawaga S
   2. Abdelalim EM

   (2020) Potential application of mesenchymal stem cells and their exosomes in lung injury: an emerging therapeutic option for COVID-19 patients

   Stem Cell Research & Therapy 11:437–446.

   https://doi.org/10.1186/s13287-020-01963-6

   • Google Scholar
7. 1. Al-Kuraishy HM
   2. Al-Gareeb AI
   3. Qusti S
   4. Alshammari EM
   5. Gyebi GA
   6. Batiha GE-S

   (2021) Covid-19-induced dysautonomia: A menace of sympathetic storm

   ASN Neuro 13:17590914211057635.

   https://doi.org/10.1177/17590914211057635

   • PubMed
   • Google Scholar
8. 1. Al-Ramadan A
   2. Rabab’h O
   3. Shah J
   4. Gharaibeh A

   (2021) Acute and post-acute neurological complications of COVID-19

   Neurology International 13:102–119.

   https://doi.org/10.3390/neurolint13010010

   • Google Scholar
9. 1. Aluganti Narasimhulu C
   2. Singla DK

   (2022) Mechanisms of COVID-19 pathogenesis in diabetes

   American Journal of Physiology.Heart and Circulatory Physiology 323:H403–H420.

   https://doi.org/10.1152/ajpheart.00204.2022

   • Google Scholar
10. 1. Amenta EM
    2. Spallone A
    3. Rodriguez-Barradas MC
    4. El Sahly HM
    5. Atmar RL
    6. Kulkarni PA

    (2020) Postacute COVID-19: an overview and approach to classification

    Open Forum Infectious Diseases 7:faa509.

    https://doi.org/10.1093/ofid/ofaa509

    • Google Scholar
11. 1. Antonelli M
    2. Pujol JC
    3. Spector TD
    4. Ourselin S
    5. Steves CJ

    (2022) Risk of long COVID associated with delta versus omicron variants of SARS-cov-2

    Lancet 399:2263–2264.

    https://doi.org/10.1016/S0140-6736(22)00941-2

    • PubMed
    • Google Scholar
12. 1. Augustin M
    2. Schommers P
    3. Stecher M
    4. Dewald F
    5. Gieselmann L
    6. Gruell H
    7. Horn C
    8. Vanshylla K
    9. Cristanziano VD
    10. Osebold L
    11. Roventa M
    12. Riaz T
    13. Tschernoster N
    14. Altmueller J
    15. Rose L
    16. Salomon S
    17. Priesner V
    18. Luers JC
    19. Albus C
    20. Rosenkranz S
    21. Gathof B
    22. Fätkenheuer G
    23. Hallek M
    24. Klein F
    25. Suárez I
    26. Lehmann C

    (2021) Post-COVID syndrome in non-hospitalised patients with COVID-19: a longitudinal prospective cohort study

    The Lancet Regional Health. Europe 6:100122.

    https://doi.org/10.1016/j.lanepe.2021.100122

    • PubMed
    • Google Scholar
13. 1. Awogbindin IO
    2. Ben-Azu B
    3. Olusola BA
    4. Akinluyi ET
    5. Adeniyi PA
    6. Di Paolo T
    7. Tremblay MÈ

    (2021) Microglial implications in SARS-cov-2 infection and COVID-19: lessons from viral RNA neurotropism and possible relevance to parkinson’s disease

    Frontiers in Cellular Neuroscience 15:670298.

    https://doi.org/10.3389/fncel.2021.670298

    • PubMed
    • Google Scholar
14. 1. Azzolini E
    2. Levi R
    3. Sarti R
    4. Pozzi C
    5. Mollura M
    6. Mantovani A
    7. Rescigno M

    (2022) Association between bnt162b2 vaccination and long COVID after infections not requiring hospitalization in health care workers

    JAMA 328:676–678.

    https://doi.org/10.1001/jama.2022.11691

    • PubMed
    • Google Scholar
15. 1. Baig AM
    2. Khaleeq A
    3. Ali U
    4. Syeda H

    (2020) Evidence of the COVID-19 virus targeting the CNS: tissue distribution, host-virus interaction, and proposed neurotropic mechanisms

    ACS Chemical Neuroscience 11:995–998.

    https://doi.org/10.1021/acschemneuro.0c00122

    • PubMed
    • Google Scholar
16. 1. Baldi E
    2. Sechi GM
    3. Mare C
    4. Canevari F
    5. Brancaglione A
    6. Primi R
    7. Klersy C
    8. Palo A
    9. Contri E
    10. Ronchi V
    11. Beretta G
    12. Reali F
    13. Parogni P
    14. Facchin F
    15. Bua D
    16. Rizzi U
    17. Bussi D
    18. Ruggeri S
    19. Oltrona Visconti L
    20. Savastano S
    21. Lombardia CARe Researchers

    (2020) Out-of-hospital cardiac arrest during the covid-19 outbreak in italy

    The New England Journal of Medicine 383:496–498.

    https://doi.org/10.1056/NEJMc2010418

    • PubMed
    • Google Scholar
17. 1. Barrett CE
    2. Koyama AK
    3. Alvarez P
    4. Chow W
    5. Lundeen EA
    6. Perrine CG
    7. Pavkov ME
    8. Rolka DB
    9. Wiltz JL
    10. Bull-Otterson L
    11. Gray S
    12. Boehmer TK
    13. Gundlapalli AV
    14. Siegel DA
    15. Kompaniyets L
    16. Goodman AB
    17. Mahon BE
    18. Tauxe RV
    19. Remley K
    20. Saydah S

    (2022) Risk for newly diagnosed diabetes >30 days after SARS-cov-2 infection among persons aged

    MMWR.Morbidity and Mortality Weekly Report 71:59–65.

    https://doi.org/10.15585/mmwr.mm7102e2

    • Google Scholar
18. 1. Basso C
    2. Leone O
    3. Rizzo S
    4. De Gaspari M
    5. van der Wal AC
    6. Aubry MC
    7. Bois MC
    8. Lin PT
    9. Maleszewski JJ
    10. Stone JR

    (2020) Pathological features of COVID-19-associated myocardial injury: a multicentre cardiovascular pathology study

    European Heart Journal 41:3827–3835.

    https://doi.org/10.1093/eurheartj/ehaa664

    • PubMed
    • Google Scholar
19. 1. Bindom SM
    2. Hans CP
    3. Xia H
    4. Boulares AH
    5. Lazartigues E

    (2010) Angiotensin I-converting enzyme type 2 (ACE2) gene therapy improves glycemic control in diabetic mice

    Diabetes 59:2540–2548.

    https://doi.org/10.2337/db09-0782

    • PubMed
    • Google Scholar
20. 1. Bisaccia G
    2. Ricci F
    3. Recce V
    4. Serio A
    5. Iannetti G
    6. Chahal AA
    7. Ståhlberg M
    8. Khanji MY
    9. Fedorowski A
    10. Gallina S

    (2021) Post-acute sequelae of COVID-19 and cardiovascular autonomic dysfunction: what do we know?

    Journal of Cardiovascular Development and Disease 8:156.

    https://doi.org/10.3390/jcdd8110156

    • PubMed
    • Google Scholar
21. 1. Blanco-Melo D
    2. Nilsson-Payant BE
    3. Liu W-C
    4. Uhl S
    5. Hoagland D
    6. Møller R
    7. Jordan TX
    8. Oishi K
    9. Panis M
    10. Sachs D
    11. Wang TT
    12. Schwartz RE
    13. Lim JK
    14. Albrecht RA
    15. tenOever BR

    (2020) Imbalanced host response to SARS-cov-2 drives development of COVID-19

    Cell 181:1036–1045.

    https://doi.org/10.1016/j.cell.2020.04.026

    • PubMed
    • Google Scholar
22. 1. Blitshteyn S
    2. Whitelaw S

    (2021) Postural orthostatic tachycardia syndrome (POTS) and other autonomic disorders after COVID-19 infection: A case series of 20 patients

    Immunologic Research 69:205–211.

    https://doi.org/10.1007/s12026-021-09185-5

    • Google Scholar
23. 1. Bode B
    2. Garrett V
    3. Messler J
    4. McFarland R
    5. Crowe J
    6. Booth R
    7. Klonoff DC

    (2020) Glycemic characteristics and clinical outcomes of COVID-19 patients hospitalized in the united states

    Journal of Diabetes Science and Technology 14:813–821.

    https://doi.org/10.1177/1932296820924469

    • Google Scholar
24. 1. Boisramé-Helms J
    2. Kremer H
    3. Schini-Kerth V
    4. Meziani F

    (2013) Endothelial dysfunction in sepsis

    Current Vascular Pharmacology 11:150–160.

    https://doi.org/10.2174/1570161111311020005

    • PubMed
    • Google Scholar
25. 1. Bornstein SR
    2. Voit-Bak K
    3. Donate T
    4. Rodionov RN
    5. Gainetdinov RR
    6. Tselmin S
    7. Kanczkowski W
    8. Muller GM
    9. Achleitner M
    10. Wang J
    11. Licinio J
    12. Bauer M
    13. Young AH
    14. Thuret S
    15. Bechmann N
    16. Straube R

    (2022) Chronic post-COVID-19 syndrome and chronic fatigue syndrome: is there a role for extracorporeal apheresis?

    Molecular Psychiatry 27:34–37.

    https://doi.org/10.1038/s41380-021-01148-4

    • Google Scholar
26. 1. Budhraja A
    2. Basu A
    3. Gheware A
    4. Abhilash D
    5. Rajagopala S
    6. Pakala S
    7. Sumit M
    8. Ray A
    9. Subramaniam A
    10. Mathur P
    11. Nambirajan A
    12. Kumar S
    13. Gupta R
    14. Wig N
    15. Trikha A
    16. Guleria R
    17. Sarkar C
    18. Gupta I
    19. Jain D

    (2022) Molecular signature of postmortem lung tissue from COVID-19 patients suggests distinct trajectories driving mortality

    Disease Models & Mechanisms 15:dmm049572.

    https://doi.org/10.1242/dmm.049572

    • PubMed
    • Google Scholar
27. 1. Buijsers B
    2. Yanginlar C
    3. de Nooijer A
    4. Grondman I
    5. Maciej-Hulme ML
    6. Jonkman I
    7. Janssen NAF
    8. Rother N
    9. de Graaf M
    10. Pickkers P
    11. Kox M
    12. Joosten LAB
    13. Nijenhuis T
    14. Netea MG
    15. Hilbrands L
    16. van de Veerdonk FL
    17. Duivenvoorden R
    18. de Mast Q
    19. van der Vlag J

    (2020) Increased plasma heparanase activity in COVID-19 patients

    Frontiers in Immunology 11:575047.

    https://doi.org/10.3389/fimmu.2020.575047

    • PubMed
    • Google Scholar
28. 1. Buonsenso D
    2. Di Giuda D
    3. Sigfrid L
    4. Pizzuto DA
    5. Di Sante G
    6. De Rose C
    7. Lazzareschi I
    8. Sali M
    9. Baldi F
    10. Chieffo DPR
    11. Munblit D
    12. Valentini P

    (2021) Evidence of lung perfusion defects and ongoing inflammation in an adolescent with post-acute sequelae of SARS-cov-2 infection

    The Lancet. Child & Adolescent Health 5:677–680.

    https://doi.org/10.1016/S2352-4642(21)00196-6

    • PubMed
    • Google Scholar
29. 1. Camargo-Martínez W
    2. Lozada-Martínez I
    3. Escobar-Collazos A
    4. Navarro-Coronado A
    5. Moscote-Salazar L
    6. Pacheco-Hernández A
    7. Janjua T
    8. Bosque-Varela P

    (2021) Post-COVID 19 neurological syndrome: implications for sequelae’s treatment

    Journal of Clinical Neuroscience 88:219–225.

    https://doi.org/10.1016/j.jocn.2021.04.001

    • PubMed
    • Google Scholar
30. 1. Carfì A
    2. Bernabei R
    3. Landi F
    4. Gemelli Against COVID-19 Post-Acute Care Study Group

    (2020) Persistent symptoms in patients after acute COVID-19

    JAMA 324:603–605.

    https://doi.org/10.1001/jama.2020.12603

    • PubMed
    • Google Scholar
31. 1. Carlsson PO
    2. Berne C
    3. Jansson L

    (1998) Angiotensin II and the endocrine pancreas: effects on islet blood flow and insulin secretion in rats

    Diabetologia 41:127–133.

    https://doi.org/10.1007/s001250050880

    • Google Scholar
32. 1. Carod-Artal FJ

    (2021) Post-COVID-19 syndrome: epidemiology, diagnostic criteria and pathogenic mechanisms involved.[Sindrome post-COVID-19: epidemiologia, criterios diagnosticos y mecanismos patogenicos implicados]

    Revista de Neurologia 72:384–396.

    https://doi.org/10.33588/rn.7211.2021230

    • PubMed
    • Google Scholar
33. 1. Carretero OA
    2. Oparil S

    (2000) Essential hypertension: part I: definition and etiology

    Circulation 101:329–335.

    https://doi.org/10.1161/01.cir.101.3.329

    • Google Scholar
34. 1. Castanares-Zapatero D
    2. Chalon P
    3. Kohn L
    4. Dauvrin M
    5. Detollenaere J
    6. Maertens de Noordhout C
    7. Primus-de Jong C
    8. Cleemput I
    9. Van den Heede K

    (2022) Pathophysiology and mechanism of long COVID: A comprehensive review

    Annals of Medicine 54:1473–1487.

    https://doi.org/10.1080/07853890.2022.2076901

    • PubMed
    • Google Scholar
35. 1. Chandrashekhar Joshi S
    2. Pozzilli P

    (2022) COVID-19 induced diabetes: A novel presentation

    Diabetes Research and Clinical Practice 191:110034.

    https://doi.org/10.1016/j.diabres.2022.110034

    • PubMed
    • Google Scholar
36. 1. Charfeddine S
    2. Ibn Hadj Amor H
    3. Jdidi J
    4. Torjmen S
    5. Kraiem S
    6. Hammami R
    7. Bahloul A
    8. Kallel N
    9. Moussa N
    10. Touil I
    11. Ghrab A
    12. Elghoul J
    13. Meddeb Z
    14. Thabet Y
    15. Kammoun S
    16. Bouslama K
    17. Milouchi S
    18. Abdessalem S
    19. Abid L

    (2021) Long COVID 19 syndrome: is it related to microcirculation and endothelial dysfunction? insights from TUN-endcov study

    Frontiers in Cardiovascular Medicine 8:745758.

    https://doi.org/10.3389/fcvm.2021.745758

    • PubMed
    • Google Scholar
37. 1. Chee YJ
    2. Ng SJH
    3. Yeoh E

    (2020) Diabetic ketoacidosis precipitated by covid-19 in a patient with newly diagnosed diabetes mellitus

    Diabetes Research and Clinical Practice 164:108166.

    https://doi.org/10.1016/j.diabres.2020.108166

    • PubMed
    • Google Scholar
38. 1. Chen G
    2. Li X
    3. Gong Z
    4. Xia H
    5. Wang Y
    6. Wang X
    7. Huang Y
    8. Barajas-Martinez H
    9. Hu D

    (2021) Hypertension as a sequela in patients of SARS-cov-2 infection

    PLOS ONE 16:e0250815.

    https://doi.org/10.1371/journal.pone.0250815

    • PubMed
    • Google Scholar
39. 1. Chen C
    2. Haupert SR
    3. Zimmermann L
    4. Shi X
    5. Fritsche LG
    6. Mukherjee B

    (2022) Global prevalence of post-coronavirus disease 2019 (COVID-19) condition or long COVID: a meta-analysis and systematic review

    The Journal of Infectious Diseases 226:1593–1607.

    https://doi.org/10.1093/infdis/jiac136

    • PubMed
    • Google Scholar
40. 1. Cheung EW
    2. Zachariah P
    3. Gorelik M
    4. Boneparth A
    5. Kernie SG
    6. Orange JS
    7. Milner JD

    (2020) Multisystem inflammatory syndrome related to COVID-19 in previously healthy children and adolescents in New York City

    JAMA 324:294–296.

    https://doi.org/10.1001/jama.2020.10374

    • PubMed
    • Google Scholar
41. 1. Choutka J
    2. Jansari V
    3. Hornig M
    4. Iwasaki A

    (2022) Unexplained post-acute infection syndromes

    Nature Medicine 28:911–923.

    https://doi.org/10.1038/s41591-022-01810-6

    • PubMed
    • Google Scholar
42. 1. Chu L
    2. Valencia IJ
    3. Garvert DW
    4. Montoya JG

    (2019) Onset patterns and course of myalgic encephalomyelitis/chronic fatigue syndrome

    Frontiers in Pediatrics 7:12.

    https://doi.org/10.3389/fped.2019.00012

    • PubMed
    • Google Scholar
43. 1. Cipelli R
    2. Harries L
    3. Okuda K
    4. Yoshihara S
    5. Melzer D
    6. Galloway T

    (2014) Bisphenol A modulates the metabolic regulator oestrogen-related receptor-α in T-cells

    Reproduction 147:419–426.

    https://doi.org/10.1530/REP-13-0423

    • PubMed
    • Google Scholar
44. 1. Clarke SA
    2. Abbara A
    3. Dhillo WS

    (2022) Impact of COVID-19 on the endocrine system: a mini-review

    Endocrinology 163:bqab203.

    https://doi.org/10.1210/endocr/bqab203

    • PubMed
    • Google Scholar
45. 1. Consiglio CR
    2. Cotugno N
    3. Sardh F
    4. Pou C
    5. Amodio D
    6. Rodriguez L
    7. Tan Z
    8. Zicari S
    9. Ruggiero A
    10. Pascucci GR
    11. Santilli V
    12. Campbell T
    13. Bryceson Y
    14. Eriksson D
    15. Wang J
    16. Marchesi A
    17. Lakshmikanth T
    18. Campana A
    19. Villani A
    20. Rossi P
    21. Landegren N
    22. Palma P
    23. Brodin P
    24. CACTUS Study Team

    (2020) The immunology of multisystem inflammatory syndrome in children with COVID-19

    Cell 183:968–981.

    https://doi.org/10.1016/j.cell.2020.09.016

    • PubMed
    • Google Scholar
46. 1. Cortés-Telles A
    2. López-Romero S
    3. Figueroa-Hurtado E
    4. Pou-Aguilar YN
    5. Wong AW
    6. Milne KM
    7. Ryerson CJ
    8. Guenette JA

    (2021) Pulmonary function and functional capacity in COVID-19 survivors with persistent dyspnoea

    Respiratory Physiology & Neurobiology 288:103644.

    https://doi.org/10.1016/j.resp.2021.103644

    • PubMed
    • Google Scholar
47. 1. Couleau N
    2. Falla J
    3. Beillerot A
    4. Battaglia E
    5. D’Innocenzo M
    6. Plançon S
    7. Laval-Gilly P
    8. Bennasroune A

    (2015) Effects of endocrine disruptor compounds, alone or in combination, on human macrophage-like THP-1 cell response

    PLOS ONE 10:e0131428.

    https://doi.org/10.1371/journal.pone.0131428

    • PubMed
    • Google Scholar
48. 1. Dando SJ
    2. Mackay-Sim A
    3. Norton R
    4. Currie BJ
    5. St John JA
    6. Ekberg JAK
    7. Batzloff M
    8. Ulett GC
    9. Beacham IR

    (2014) Pathogens penetrating the central nervous system: infection pathways and the cellular and molecular mechanisms of invasion

    Clinical Microbiology Reviews 27:691–726.

    https://doi.org/10.1128/CMR.00118-13

    • PubMed
    • Google Scholar
49. 1. Davis HE
    2. Assaf GS
    3. McCorkell L
    4. Wei H
    5. Low RJ
    6. Re’em Y
    7. Redfield S
    8. Austin JP
    9. Akrami A

    (2021) Characterizing long COVID in an international cohort: 7 months of symptoms and their impact

    EClinicalMedicine 38:101019.

    https://doi.org/10.1016/j.eclinm.2021.101019

    • PubMed
    • Google Scholar
50. 1. D’Errico S
    2. Zanon M
    3. Montanaro M
    4. Radaelli D
    5. Sessa F
    6. Di Mizio G
    7. Montana A
    8. Corrao S
    9. Salerno M
    10. Pomara C

    (2020) More than pneumonia: distinctive features of SARS-cov-2 infection from autopsy findings to clinical implications: a systematic review

    Microorganisms 8:1642.

    https://doi.org/10.3390/microorganisms8111642

    • PubMed
    • Google Scholar
51. 1. Douaud G
    2. Lee S
    3. Alfaro-Almagro F
    4. Arthofer C
    5. Wang C
    6. McCarthy P
    7. Lange F
    8. Andersson JLR
    9. Griffanti L
    10. Duff E
    11. Jbabdi S
    12. Taschler B
    13. Keating P
    14. Winkler AM
    15. Collins R
    16. Matthews PM
    17. Allen N
    18. Miller KL
    19. Nichols TE
    20. Smith SM

    (2022) SARS-cov-2 is associated with changes in brain structure in UK Biobank

    Nature 604:697–707.

    https://doi.org/10.1038/s41586-022-04569-5

    • PubMed
    • Google Scholar
52. 1. Doykov I
    2. Hällqvist J
    3. Gilmour KC
    4. Grandjean L
    5. Mills K
    6. Heywood WE

    (2020) “The long tail of covid-19” - the detection of a prolonged inflammatory response after a SARS-cov-2 infection in asymptomatic and mildly affected patients

    F1000Research 9:1349.

    https://doi.org/10.12688/f1000research.27287.2

    • PubMed
    • Google Scholar
53. 1. Doyle ME
    2. Appleton A
    3. Liu Q-R
    4. Yao Q
    5. Mazucanti CH
    6. Egan JM

    (2021) Human type II taste cells express angiotensin-converting enzyme 2 and are infected by severe acute respiratory syndrome coronavirus 2 (SARS-cov-2)

    The American Journal of Pathology 191:1511–1519.

    https://doi.org/10.1016/j.ajpath.2021.05.010

    • PubMed
    • Google Scholar
54. 1. Drucker DJ

    (2020) Coronavirus infections and type 2 diabetes-shared pathways with therapeutic implications

    Endocrine Reviews 41:bnaa011.

    https://doi.org/10.1210/endrev/bnaa011

    • PubMed
    • Google Scholar
55. 1. Dunlop SP
    2. Jenkins D
    3. Spiller RC

    (2003) Distinctive clinical, psychological, and histological features of postinfective irritable bowel syndrome

    The American Journal of Gastroenterology 98:1578–1583.

    https://doi.org/10.1111/j.1572-0241.2003.07542.x

    • PubMed
    • Google Scholar
56. 1. Escher R
    2. Breakey N
    3. Lammle B

    (2020) Severe COVID-19 infection associated with endothelial activation

    Thrombosis Research 190:62.

    https://doi.org/10.1016/j.thromres.2020.04.014

    • Google Scholar
57. 1. Escorihuela RM
    2. Capdevila L
    3. Castro JR
    4. Zaragoza MC
    5. Maurel S
    6. Alegre J
    7. Castro-Marrero J

    (2020) Reduced heart rate variability predicts fatigue severity in individuals with chronic fatigue syndrome/myalgic encephalomyelitis

    Journal of Translational Medicine 18:184.

    https://doi.org/10.1186/s12967-019-02184-z

    • Google Scholar
58. 1. Estiri H
    2. Strasser ZH
    3. Brat GA
    4. Semenov YR

    (2021) Evolving phenotypes of non-hospitalized patients that indicate long COVID

    BMC Medicine 19:249.

    https://doi.org/10.1186/s12916-021-02115-0

    • Google Scholar
59. 1. Evans PC
    2. Rainger GE
    3. Mason JC
    4. Guzik TJ
    5. Osto E
    6. Stamataki Z
    7. Neil D
    8. Hoefer IE
    9. Fragiadaki M
    10. Waltenberger J
    11. Weber C
    12. Bochaton-Piallat M-L
    13. Bäck M

    (2020) Endothelial dysfunction in COVID-19: A position paper of the ESC working group for atherosclerosis and vascular biology, and the ESC council of basic cardiovascular science

    Cardiovascular Research 116:2177–2184.

    https://doi.org/10.1093/cvr/cvaa230

    • PubMed
    • Google Scholar
60. 1. Farooqi KM
    2. Chan A
    3. Weller RJ
    4. Mi J
    5. Jiang P
    6. Abrahams E
    7. Ferris A
    8. Krishnan US
    9. Pasumarti N
    10. Suh S
    11. Shah AM
    12. DiLorenzo MP
    13. Zachariah P
    14. Milner JD
    15. Rosenzweig EB
    16. Gorelik M
    17. Anderson BR
    18. Columbia University Interdisciplinary MIS-C Follow-up Program and the CUIMC Pediatric/Adult Congenital Heart Research Collaborative

    (2021) Longitudinal outcomes for multisystem inflammatory syndrome in children

    Pediatrics 148:e2021051155.

    https://doi.org/10.1542/peds.2021-051155

    • PubMed
    • Google Scholar
61. 1. Feldstein LR
    2. Rose EB
    3. Horwitz SM
    4. Collins JP
    5. Newhams MM
    6. Son MBF
    7. Newburger JW
    8. Kleinman LC
    9. Heidemann SM
    10. Martin AA
    11. Singh AR
    12. Li S
    13. Tarquinio KM
    14. Jaggi P
    15. Oster ME
    16. Zackai SP
    17. Gillen J
    18. Ratner AJ
    19. Walsh RF
    20. Fitzgerald JC
    21. Keenaghan MA
    22. Alharash H
    23. Doymaz S
    24. Clouser KN
    25. Giuliano JS Jr
    26. Gupta A
    27. Parker RM
    28. Maddux AB
    29. Havalad V
    30. Ramsingh S
    31. Bukulmez H
    32. Bradford TT
    33. Smith LS
    34. Tenforde MW
    35. Carroll CL
    36. Riggs BJ
    37. Gertz SJ
    38. Daube A
    39. Lansell A
    40. Coronado Munoz A
    41. Hobbs CV
    42. Marohn KL
    43. Halasa NB
    44. Patel MM
    45. Randolph AG
    46. Overcoming COVID-19 Investigators
    47. CDC COVID-19 Response Team

    (2020) Multisystem inflammatory syndrome in U.S. children and adolescents

    The New England Journal of Medicine 383:334–346.

    https://doi.org/10.1056/NEJMoa2021680

    • PubMed
    • Google Scholar
62. 1. Feng Y
    2. Fang Z
    3. Liu B
    4. Zheng X

    (2019) P38Mapk plays a pivotal role in the development of acute respiratory distress syndrome

    Clinics 74:e509.

    https://doi.org/10.6061/clinics/2019/e509

    • PubMed
    • Google Scholar
63. 1. Fernández-Castañeda A
    2. Lu P
    3. Geraghty AC
    4. Song E
    5. Lee MH
    6. Wood J
    7. O’Dea MR
    8. Dutton S
    9. Shamardani K
    10. Nwangwu K
    11. Mancusi R
    12. Yalçın B
    13. Taylor KR
    14. Acosta-Alvarez L
    15. Malacon K
    16. Keough MB
    17. Ni L
    18. Woo PJ
    19. Contreras-Esquivel D
    20. Toland AMS
    21. Gehlhausen JR
    22. Klein J
    23. Takahashi T
    24. Silva J
    25. Israelow B
    26. Lucas C
    27. Mao T
    28. Peña-Hernández MA
    29. Tabachnikova A
    30. Homer RJ
    31. Tabacof L
    32. Tosto-Mancuso J
    33. Breyman E
    34. Kontorovich A
    35. McCarthy D
    36. Quezado M
    37. Vogel H
    38. Hefti MM
    39. Perl DP
    40. Liddelow S
    41. Folkerth R
    42. Putrino D
    43. Nath A
    44. Iwasaki A
    45. Monje M

    (2022a) Mild respiratory COVID can cause multi-lineage neural cell and myelin dysregulation

    Cell 185:2452–2468.

    https://doi.org/10.1016/j.cell.2022.06.008

    • PubMed
    • Google Scholar
64. Preprint

    1. Fernández-Castañeda A
    2. Lu P
    3. Geraghty AC
    4. Song E
    5. Lee MH

    (2022b) Mild Respiratory SARS-Cov-2 Infection Can Cause Multi-Lineage Cellular Dysregulation and Myelin Loss in the Brain

    bioRxiv.

    https://doi.org/10.1101/2022.01.07.475453

    • Google Scholar
65. 1. Fernández-de-Las-Peñas C
    2. Palacios-Ceña D
    3. Gómez-Mayordomo V
    4. Cuadrado ML
    5. Florencio LL

    (2021) Defining post-COVID symptoms (post-acute COVID, long COVID, persistent post-COVID): an integrative classification

    International Journal of Environmental Research and Public Health 18:2621.

    https://doi.org/10.3390/ijerph18052621

    • PubMed
    • Google Scholar
66. 1. Fernández-de-Las-Peñas C
    2. Pellicer-Valero OJ
    3. Navarro-Pardo E
    4. Palacios-Ceña D
    5. Florencio LL
    6. Guijarro C
    7. Martín-Guerrero JD

    (2022) Symptoms experienced at the acute phase of SARS-cov-2 infection as risk factor of long-term post-COVID symptoms: the LONG-COVID-EXP-CM multicenter study

    International Journal of Infectious Diseases 116:241–244.

    https://doi.org/10.1016/j.ijid.2022.01.007

    • PubMed
    • Google Scholar
67. 1. Flores D
    2. Walter J
    3. Wussler D
    4. Kozhuharov N
    5. Nowak A
    6. Dinort J
    7. Badertscher P
    8. Martin J
    9. Sabti Z
    10. Lavallaz J

    (2019)

    Direct comparison of high-sensitivity cardiac troponin T and I for prediction of mortality in patients with pneumonia

    J Clin Chem Lab Med 2:1000131.

    • Google Scholar
68. 1. Fluge Ø
    2. Tronstad KJ
    3. Mella O

    (2021) Pathomechanisms and possible interventions in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)

    The Journal of Clinical Investigation 131:e150377.

    https://doi.org/10.1172/JCI150377

    • PubMed
    • Google Scholar
69. 1. Frere JJ
    2. Serafini RA
    3. Pryce KD
    4. Zazhytska M
    5. Oishi K
    6. Golynker I
    7. Panis M
    8. Zimering J
    9. Horiuchi S
    10. Hoagland DA
    11. Møller R
    12. Ruiz A
    13. Kodra A
    14. Overdevest JB
    15. Canoll PD
    16. Borczuk AC
    17. Chandar V
    18. Bram Y
    19. Schwartz R
    20. Lomvardas S
    21. Zachariou V
    22. tenOever BR

    (2022) SARS-cov-2 infection in hamsters and humans results in lasting and unique systemic perturbations after recovery

    Science Translational Medicine 14:eabq3059.

    https://doi.org/10.1126/scitranslmed.abq3059

    • PubMed
    • Google Scholar
70. 1. Gao C
    2. Wang Y
    3. Gu X
    4. Shen X
    5. Zhou D
    6. Zhou S
    7. Huang J-A
    8. Cao B
    9. Guo Q
    10. Community-Acquired Pneumonia–China Network

    (2020) Association between cardiac injury and mortality in hospitalized patients infected with avian influenza A (H7N9) virus

    Critical Care Medicine 48:451–458.

    https://doi.org/10.1097/CCM.0000000000004207

    • PubMed
    • Google Scholar
71. 1. Genç S
    2. Evren B
    3. Bozbay A
    4. Aydın EŞ
    5. Genç Ö

    (2021) Could covid-19trigger type 1 diabetes? presentation of covid-19 case presented withdiabetic ketoacidosis

    Acta Endocrinol 1:532–536.

    https://doi.org/10.4183/aeb.2021.532

    • PubMed
    • Google Scholar
72. 1. Gentile S
    2. Strollo F
    3. Mambro A
    4. Ceriello A

    (2020) COVID-19, ketoacidosis and new-onset diabetes: are there possible cause and effect relationships among them?

    Diabetes, Obesity & Metabolism 22:2507–2508.

    https://doi.org/10.1111/dom.14170

    • PubMed
    • Google Scholar
73. 1. George PM
    2. Wells AU
    3. Jenkins RG

    (2020) Pulmonary fibrosis and COVID-19: the potential role for antifibrotic therapy

    The Lancet. Respiratory Medicine 8:807–815.

    https://doi.org/10.1016/S2213-2600(20)30225-3

    • PubMed
    • Google Scholar
74. 1. Giron LB
    2. Peluso MJ
    3. Ding J
    4. Kenny G
    5. Zilberstein NF
    6. Koshy J
    7. Hong KY
    8. Rasmussen H
    9. Miller GE
    10. Bishehsari F
    11. Balk RA
    12. Moy JN
    13. Hoh R
    14. Lu S
    15. Goldman AR
    16. Tang HY
    17. Yee BC
    18. Chenna A
    19. Winslow JW
    20. Petropoulos CJ
    21. Kelly JD
    22. Wasse H
    23. Martin JN
    24. Liu Q
    25. Keshavarzian A
    26. Landay A
    27. Deeks SG
    28. Henrich TJ
    29. Abdel-Mohsen M

    (2022) Markers of fungal translocation are elevated during post-acute sequelae of SARS-cov-2 and induce NF-κB signaling

    JCI Insight 7:e164813.

    https://doi.org/10.1172/jci.insight.164813

    • PubMed
    • Google Scholar
75. 1. Giustino G
    2. Pinney SP
    3. Lala A
    4. Reddy VY
    5. Johnston-Cox HA
    6. Mechanick JI
    7. Halperin JL
    8. Fuster V

    (2020) Coronavirus and cardiovascular disease, myocardial injury, and arrhythmia: JACC focus seminar

    Journal of the American College of Cardiology 76:2011–2023.

    https://doi.org/10.1016/j.jacc.2020.08.059

    • PubMed
    • Google Scholar
76. 1. Gluckman TJ
    2. Bhave NM
    3. Allen LA
    4. Chung EH
    5. Spatz ES
    6. Ammirati E
    7. Baggish AL
    8. Bozkurt B
    9. Cornwell WK
    10. Harmon KG
    11. Kim JH
    12. Lala A
    13. Levine BD
    14. Martinez MW
    15. Onuma O
    16. Phelan D
    17. Puntmann VO
    18. Rajpal S
    19. Taub PR
    20. Verma AK
    21. Writing Committee

    (2022) 2022 ACC expert consensus decision pathway on cardiovascular sequelae of COVID-19 in adults: myocarditis and other myocardial involvement, post-acute sequelae of SARS-cov-2 infection, and return to play: a report of the american college of cardiology solution set oversight committee

    Journal of the American College of Cardiology 79:1717–1756.

    https://doi.org/10.1016/j.jacc.2022.02.003

    • PubMed
    • Google Scholar
77. 1. Gottschalk CG
    2. Peterson D
    3. Armstrong J
    4. Knox K
    5. Roy A

    (2023) Potential molecular mechanisms of chronic fatigue in long haul COVID and other viral diseases

    Infectious Agents and Cancer 18:7.

    https://doi.org/10.1186/s13027-023-00485-z

    • PubMed
    • Google Scholar
78. 1. Greenhalgh T
    2. Knight M
    3. A’Court C
    4. Buxton M
    5. Husain L

    (2020) Management of post-acute covid-19 in primary care

    BMJ 370:m3026.

    https://doi.org/10.1136/bmj.m3026

    • PubMed
    • Google Scholar
79. 1. Griffin DO
    2. Jensen A
    3. Khan M
    4. Chin J
    5. Chin K
    6. Saad J
    7. Parnell R
    8. Awwad C
    9. Patel D

    (2020) Pulmonary embolism and increased levels of d-dimer in patients with coronavirus disease

    Emerging Infectious Diseases 26:1941–1943.

    https://doi.org/10.3201/eid2608.201477

    • PubMed
    • Google Scholar
80. 1. Grillo F
    2. Barisione E
    3. Ball L
    4. Mastracci L
    5. Fiocca R

    (2021) Lung fibrosis: an undervalued finding in COVID-19 pathological series

    The Lancet.Infectious Diseases 21:e72.

    https://doi.org/10.1016/S1473-3099(20)30582-X

    • Google Scholar
81. 1. Grimes JM
    2. Grimes KV

    (2020) P38 MAPK inhibition: A promising therapeutic approach for COVID-19

    Journal of Molecular and Cellular Cardiology 144:63–65.

    https://doi.org/10.1016/j.yjmcc.2020.05.007

    • PubMed
    • Google Scholar
82. 1. Groff D
    2. Sun A
    3. Ssentongo AE
    4. Ba DM
    5. Parsons N
    6. Poudel GR
    7. Lekoubou A
    8. Oh JS
    9. Ericson JE
    10. Ssentongo P
    11. Chinchilli VM

    (2021) Short-term and long-term rates of postacute sequelae of SARS-cov-2 infection: A systematic review

    JAMA Network Open 4:e2128568.

    https://doi.org/10.1001/jamanetworkopen.2021.28568

    • Google Scholar
83. 1. Grosse C
    2. Grosse A
    3. Salzer HJF
    4. Dünser MW
    5. Motz R
    6. Langer R

    (2020) Analysis of cardiopulmonary findings in COVID-19 fatalities: high incidence of pulmonary artery thrombi and acute suppurative bronchopneumonia

    Cardiovascular Pathology 49:107263.

    https://doi.org/10.1016/j.carpath.2020.107263

    • PubMed
    • Google Scholar
84. 1. Gruber CN
    2. Patel RS
    3. Trachtman R
    4. Lepow L
    5. Amanat F
    6. Krammer F
    7. Wilson KM
    8. Onel K
    9. Geanon D
    10. Tuballes K
    11. Patel M
    12. Mouskas K
    13. O’Donnell T
    14. Merritt E
    15. Simons NW
    16. Barcessat V
    17. Del Valle DM
    18. Udondem S
    19. Kang G
    20. Gangadharan S
    21. Ofori-Amanfo G
    22. Laserson U
    23. Rahman A
    24. Kim-Schulze S
    25. Charney AW
    26. Gnjatic S
    27. Gelb BD
    28. Merad M
    29. Bogunovic D

    (2020) Mapping systemic inflammation and antibody responses in multisystem inflammatory syndrome in children (MIS-C)

    Cell 183:982–995.

    https://doi.org/10.1016/j.cell.2020.09.034

    • PubMed
    • Google Scholar
85. 1. Gunning WT
    2. Kvale H
    3. Kramer PM
    4. Karabin BL
    5. Grubb BP

    (2019) Postural orthostatic tachycardia syndrome is associated with elevated G-protein coupled receptor autoantibodies

    Journal of the American Heart Association 8:e013602.

    https://doi.org/10.1161/JAHA.119.013602

    • PubMed
    • Google Scholar
86. 1. Guo X-ZJ
    2. Thomas PG

    (2017) New fronts emerge in the influenza cytokine storm

    Seminars in Immunopathology 39:541–550.

    https://doi.org/10.1007/s00281-017-0636-y

    • PubMed
    • Google Scholar
87. 1. Haffke M
    2. Freitag H
    3. Rudolf G
    4. Seifert M
    5. Doehner W
    6. Scherbakov N
    7. Hanitsch L
    8. Wittke K
    9. Bauer S
    10. Konietschke F
    11. Paul F
    12. Bellmann-Strobl J
    13. Kedor C
    14. Scheibenbogen C
    15. Sotzny F

    (2022) Endothelial dysfunction and altered endothelial biomarkers in patients with post-COVID-19 syndrome and chronic fatigue syndrome (ME/CFS)

    Journal of Translational Medicine 20:138.

    https://doi.org/10.1186/s12967-022-03346-2

    • PubMed
    • Google Scholar
88. 1. Halushka MK
    2. Vander Heide RS

    (2021) Myocarditis is rare in COVID-19 autopsies: cardiovascular findings across 277 postmortem examinations

    Cardiovascular Pathology 50:107300.

    https://doi.org/10.1016/j.carpath.2020.107300

    • Google Scholar
89. 1. Hamming I
    2. Timens W
    3. Bulthuis MLC
    4. Lely AT
    5. Navis GJ
    6. van Goor H

    (2004) Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus: A first step in understanding SARS pathogenesis

    The Journal of Pathology 203:631–637.

    https://doi.org/10.1002/path.1570

    • PubMed
    • Google Scholar
90. 1. Hamming I
    2. Cooper ME
    3. Haagmans BL
    4. Hooper NM
    5. Korstanje R
    6. Osterhaus AD
    7. Timens W
    8. Turner AJ
    9. Navis G
    10. Goor H

    (2007) The emerging role of ACE2 in physiology and disease

    The Journal of Pathology 212:1–11.

    https://doi.org/10.1002/path.2162

    • Google Scholar
91. 1. Hanneman K
    2. Houbois C
    3. Schoffel A
    4. Gustafson D
    5. Iwanochko RM
    6. Wintersperger BJ
    7. Chan R
    8. Fish JE
    9. Howe KL
    10. Thavendiranathan P

    (2022) Combined cardiac fluorodeoxyglucose-positron emission tomography/magnetic resonance imaging assessment of myocardial injury in patients who recently recovered from COVID-19

    JAMA Cardiology 7:298–308.

    https://doi.org/10.1001/jamacardio.2021.5505

    • Google Scholar
92. 1. Harmer D
    2. Gilbert M
    3. Borman R
    4. Clark KL

    (2002) Quantitative mrna expression profiling of ACE 2, a novel homologue of angiotensin converting enzyme

    FEBS Letters 532:107–110.

    https://doi.org/10.1016/s0014-5793(02)03640-2

    • PubMed
    • Google Scholar
93. 1. He X
    2. Liu C
    3. Peng J
    4. Li Z
    5. Li F
    6. Wang J
    7. Hu A
    8. Peng M
    9. Huang K
    10. Fan D
    11. Li N
    12. Zhang F
    13. Cai W
    14. Tan X
    15. Hu Z
    16. Deng X
    17. Li Y
    18. Mo X
    19. Li L
    20. Lei C

    (2021) COVID-19 induces new-onset insulin resistance and lipid metabolic dysregulation via regulation of secreted metabolic factors

    Signal Transduction and Targeted Therapy 6:427.

    https://doi.org/10.1038/s41392-021-00822-x

    • Google Scholar
94. 1. Hernandez-Romieu AC
    2. Carton TW
    3. Saydah S
    4. Azziz-Baumgartner E
    5. Boehmer TK
    6. Garret NY
    7. Bailey LC
    8. Cowell LG
    9. Draper C
    10. Mayer KH
    11. Nagavedu K
    12. Puro JE
    13. Rasmussen SA
    14. Trick WE
    15. Wanga V
    16. Chevinsky JR
    17. Jackson BR
    18. Goodman AB
    19. Cope JR
    20. Gundlapalli AV
    21. Block JP

    (2022) Prevalence of select new symptoms and conditions among persons aged younger than 20 years and 20 years or older at 31 to 150 days after testing positive or negative for SARS-cov-2

    JAMA Network Open 5:e2147053.

    https://doi.org/10.1001/jamanetworkopen.2021.47053

    • PubMed
    • Google Scholar
95. 1. Hollstein T
    2. Schulte DM
    3. Schulz J
    4. Glück A
    5. Ziegler AG
    6. Bonifacio E
    7. Wendorff M
    8. Franke A
    9. Schreiber S
    10. Bornstein SR
    11. Laudes M

    (2020) Autoantibody-negative insulin-dependent diabetes mellitus after sars-cov-2 infection: a case report

    Nature Metabolism 2:1021–1024.

    https://doi.org/10.1038/s42255-020-00281-8

    • PubMed
    • Google Scholar
96. 1. Holmes E
    2. Wist J
    3. Masuda R
    4. Lodge S
    5. Nitschke P
    6. Kimhofer T
    7. Loo RL
    8. Begum S
    9. Boughton B
    10. Yang R
    11. Morillon A-C
    12. Chin S-T
    13. Hall D
    14. Ryan M
    15. Bong S-H
    16. Gay M
    17. Edgar DW
    18. Lindon JC
    19. Richards T
    20. Yeap BB
    21. Pettersson S
    22. Spraul M
    23. Schaefer H
    24. Lawler NG
    25. Gray N
    26. Whiley L
    27. Nicholson JK

    (2021) Incomplete systemic recovery and metabolic phenoreversion in post-acute-phase nonhospitalized COVID-19 patients: implications for assessment of post-acute COVID-19 syndrome

    Journal of Proteome Research 20:3315–3329.

    https://doi.org/10.1021/acs.jproteome.1c00224

    • PubMed
    • Google Scholar
97. 1. Hussman JP

    (2020) Cellular and molecular pathways of COVID-19 and potential points of therapeutic intervention

    Frontiers in Pharmacology 11:1169.

    https://doi.org/10.3389/fphar.2020.01169

    • PubMed
    • Google Scholar
98. 1. Izquierdo-Pujol J
    2. Moron-Lopez S
    3. Dalmau J
    4. Gonzalez-Aumatell A
    5. Carreras-Abad C
    6. Mendez M
    7. Rodrigo C
    8. Martinez-Picado J

    (2022) Post COVID-19 condition in children and adolescents: an emerging problem

    Frontiers in Pediatrics 10:894204.

    https://doi.org/10.3389/fped.2022.894204

    • PubMed
    • Google Scholar
99. 1. Jason LA
    2. Cotler J
    3. Islam MF
    4. Furst J
    5. Katz BZ

    (2022) Predictors for developing severe myalgic encephalomyelitis/chronic fatigue syndrome following infectious mononucleosis

    Journal of Rehabilitation Therapy 4:1–5.

    https://doi.org/10.29245/2767-5122/2021/1.1129

    • PubMed
    • Google Scholar
100. 1. Jiang W
     2. Johnson D
     3. Adekunle R
     4. Heather H
     5. Xu W
     6. Cong X
     7. Wu X
     8. Fan H
     9. Andersson LM
     10. Robertson J
     11. Gisslén M

     (2023) COVID-19 is associated with bystander polyclonal autoreactive B cell activation as reflected by a broad autoantibody production, but none is linked to disease severity

     Journal of Medical Virology 95:e28134.

     https://doi.org/10.1002/jmv.28134

     • PubMed
     • Google Scholar
101. 1. Jin B
     2. Singh R
     3. Ha SE
     4. Zogg H
     5. Park PJ
     6. Ro S

     (2021) Pathophysiological mechanisms underlying gastrointestinal symptoms in patients with COVID-19

     World Journal of Gastroenterology 27:2341–2352.

     https://doi.org/10.3748/wjg.v27.i19.2341

     • PubMed
     • Google Scholar
102. 1. Jonigk D
     2. Werlein C
     3. Lee PD
     4. Kauczor H-U
     5. Länger F
     6. Ackermann M

     (2022) Pulmonary and systemic pathology in COVID-19—holistic pathological analyses

     Deutsches Arzteblatt International 119:429–435.

     https://doi.org/10.3238/arztebl.m2022.0231

     • PubMed
     • Google Scholar
103. 1. Jose RJ
     2. Manuel A

     (2020) COVID-19 cytokine storm: the interplay between inflammation and coagulation

     The Lancet. Respiratory Medicine 8:e46–e47.

     https://doi.org/10.1016/S2213-2600(20)30216-2

     • PubMed
     • Google Scholar
104. 1. Jud P
     2. Kessler HH
     3. Brodmann M

     (2021) Case report: changes of vascular reactivity and arterial stiffness in a patient with covid-19 infection

     Frontiers in Cardiovascular Medicine 8:671669.

     https://doi.org/10.3389/fcvm.2021.671669

     • PubMed
     • Google Scholar
105. 1. Kaltsas G
     2. Vgontzas A
     3. Chrousos G

     (2010) Fatigue, endocrinopathies, and metabolic disorders

     PM & R 2:393–398.

     https://doi.org/10.1016/j.pmrj.2010.04.011

     • PubMed
     • Google Scholar
106. 1. Khan M
     2. Khan H
     3. Khan S
     4. Nawaz M

     (2020) Epidemiological and clinical characteristics of coronavirus disease (COVID-19) cases at a screening clinic during the early outbreak period: a single-centre study

     Journal of Medical Microbiology 69:1114–1123.

     https://doi.org/10.1099/jmm.0.001231

     • PubMed
     • Google Scholar
107. 1. Kim HS
     2. Kim MS
     3. Ji SW
     4. Park H

     (2006)

     The development of irritable bowel syndrome after shigella infection: 3 year follow-up study

     The Korean Journal of Gastroenterology = Taehan Sohwagi Hakhoe Chi 47:300–305.

     • PubMed
     • Google Scholar
108. 1. Kosuge M
     2. Ebina T
     3. Hibi K
     4. Tsukahara K
     5. Iwahashi N
     6. Gohbara M
     7. Matsuzawa Y
     8. Okada K
     9. Morita S
     10. Umemura S
     11. Kimura K

     (2012) Differences in negative T waves among acute coronary syndrome, acute pulmonary embolism, and takotsubo cardiomyopathy

     European Heart Journal. Acute Cardiovascular Care 1:349–357.

     https://doi.org/10.1177/2048872612466790

     • PubMed
     • Google Scholar
109. 1. Krishna BA
     2. Lim EY
     3. Mactavous L
     4. Team NB
     5. Lyons PA
     6. Doffinger R
     7. Bradley JR
     8. Smith KGC
     9. Sinclair J
     10. Matheson NJ
     11. Lehner PJ
     12. Wills MR
     13. Sithole N

     (2022) Evidence of previous SARS-cov-2 infection in seronegative patients with long COVID

     EBioMedicine 81:104129.

     https://doi.org/10.1016/j.ebiom.2022.104129

     • PubMed
     • Google Scholar
110. 1. Kuchay MS
     2. Reddy PK
     3. Gagneja S
     4. Mathew A
     5. Mishra SK

     (2020) Short term follow-up of patients presenting with acute onset diabetes and diabetic ketoacidosis during an episode of COVID-19

     Diabetes & Metabolic Syndrome 14:2039–2041.

     https://doi.org/10.1016/j.dsx.2020.10.015

     • PubMed
     • Google Scholar
111. 1. Lala A
     2. Johnson KW
     3. Januzzi JL
     4. Russak AJ
     5. Paranjpe I
     6. Richter F
     7. Zhao S
     8. Somani S
     9. Van Vleck T
     10. Vaid A
     11. Chaudhry F
     12. De Freitas JK
     13. Fayad ZA
     14. Pinney SP
     15. Levin M
     16. Charney A
     17. Bagiella E
     18. Narula J
     19. Glicksberg BS
     20. Nadkarni G
     21. Mancini DM
     22. Fuster V
     23. Mount Sinai COVID Informatics Center

     (2020) Prevalence and impact of myocardial injury in patients hospitalized with COVID-19 infection

     Journal of the American College of Cardiology 76:533–546.

     https://doi.org/10.1016/j.jacc.2020.06.007

     • PubMed
     • Google Scholar
112. 1. Lamers MM
     2. Beumer J
     3. van der Vaart J
     4. Knoops K
     5. Puschhof J
     6. Breugem TI
     7. Ravelli RBG
     8. Paul van Schayck J
     9. Mykytyn AZ
     10. Duimel HQ
     11. van Donselaar E
     12. Riesebosch S
     13. Kuijpers HJH
     14. Schipper D
     15. van de Wetering WJ
     16. de Graaf M
     17. Koopmans M
     18. Cuppen E
     19. Peters PJ
     20. Haagmans BL
     21. Clevers H

     (2020) SARS-cov-2 productively infects human gut enterocytes

     Science 369:50–54.

     https://doi.org/10.1126/science.abc1669

     • PubMed
     • Google Scholar
113. 1. Lauer AN
     2. Tenenbaum T
     3. Schroten H
     4. Schwerk C

     (2018) The diverse cellular responses of the choroid plexus during infection of the central nervous system

     American Journal of Physiology. Cell Physiology 314:C152–C165.

     https://doi.org/10.1152/ajpcell.00137.2017

     • PubMed
     • Google Scholar
114. 1. LaVergne SM
     2. Stromberg S
     3. Baxter BA
     4. Webb TL
     5. Dutt TS
     6. Berry K
     7. Tipton M
     8. Haberman J
     9. Massey BR
     10. McFann K
     11. Alnachoukati O
     12. Zier L
     13. Heacock T
     14. Ebel GD
     15. Henao-Tamayo M
     16. Dunn J
     17. Ryan EP

     (2021) A longitudinal SARS-cov-2 biorepository for COVID-19 survivors with and without post-acute sequelae

     BMC Infectious Diseases 21:677.

     https://doi.org/10.1186/s12879-021-06359-2

     • PubMed
     • Google Scholar
115. 1. Lazartigues E
     2. Qadir MMF
     3. Mauvais-Jarvis F

     (2020) Endocrine significance of SARS-cov-2’s reliance on ACE2

     Endocrinology 161:bqaa108.

     https://doi.org/10.1210/endocr/bqaa108

     • PubMed
     • Google Scholar
116. 1. Ledford H

     (2022) How common is long COVID? why studies give different answers

     Nature 606:852–853.

     https://doi.org/10.1038/d41586-022-01702-2

     • PubMed
     • Google Scholar
117. 1. Lee JC
     2. Nallani R
     3. Cass L
     4. Bhalla V
     5. Chiu AG
     6. Villwock JA

     (2021) A systematic review of the neuropathologic findings of post-viral olfactory dysfunction: implications and novel insight for the COVID-19 pandemic

     American Journal of Rhinology & Allergy 35:323–333.

     https://doi.org/10.1177/1945892420957853

     • Google Scholar
118. 1. Li Q
     2. Verma IM

     (2002) NF-kappab regulation in the immune system

     Nature Reviews.Immunology 2:725–734.

     https://doi.org/10.1038/nri910

     • Google Scholar
119. 1. Li YC
     2. Bai WZ
     3. Hashikawa T

     (2020a) The neuroinvasive potential of SARS-cov2 may play a role in the respiratory failure of COVID-19 patients

     Journal of Medical Virology 92:552–555.

     https://doi.org/10.1002/jmv.25728

     • Google Scholar
120. 1. Li J
     2. Wang X
     3. Chen J
     4. Zuo X
     5. Zhang H
     6. Deng A

     (2020b) COVID-19 infection may cause ketosis and ketoacidosis

     Diabetes, Obesity & Metabolism 22:1935–1941.

     https://doi.org/10.1111/dom.14057

     • PubMed
     • Google Scholar
121. 1. Lindan CE
     2. Mankad K
     3. Ram D
     4. Kociolek LK
     5. Silvera VM
     6. Boddaert N
     7. Stivaros SM
     8. Palasis S
     9. Group APC

     (2021) Neuroimaging manifestations in children with SARS-cov-2 infection: A multinational, multicentre collaborative study

     The Lancet. Child & Adolescent Health 5:167–177.

     https://doi.org/10.1016/S2352-4642(20)30362-X

     • PubMed
     • Google Scholar
122. 1. Lippi G
     2. Wong J
     3. Henry BM

     (2020) Hypertension in patients with coronavirus disease 2019 (COVID-19): a pooled analysis

     Polish Archives of Internal Medicine 130:304–309.

     https://doi.org/10.20452/pamw.15272

     • PubMed
     • Google Scholar
123. 1. Liu PP
     2. Blet A
     3. Smyth D
     4. Li H

     (2020a) The science underlying COVID-19: implications for the cardiovascular system

     Circulation 142:68–78.

     https://doi.org/10.1161/CIRCULATIONAHA.120.047549

     • PubMed
     • Google Scholar
124. 1. Liu Y
     2. Lv J
     3. Liu J
     4. Li M
     5. Xie J
     6. Lv Q
     7. Deng W
     8. Zhou N
     9. Zhou Y
     10. Song J
     11. Wang P
     12. Qin C
     13. Tong WM
     14. Huang B

     (2020b) Mucus production stimulated by IFN-ahr signaling triggers hypoxia of COVID-19

     Cell Research 30:1078–1087.

     https://doi.org/10.1038/s41422-020-00435-z

     • PubMed
     • Google Scholar
125. 1. Liu YH
     2. Chen Y
     3. Wang QH
     4. Wang LR
     5. Jiang L
     6. Yang Y
     7. Chen X
     8. Li Y
     9. Cen Y
     10. Xu C
     11. Zhu J
     12. Li W
     13. Wang YR
     14. Zhang LL
     15. Liu J
     16. Xu ZQ
     17. Wang YJ

     (2022) One-Year trajectory of cognitive changes in older survivors of COVID-19 in Wuhan, China: a longitudinal cohort study

     JAMA Neurology 79:509–517.

     https://doi.org/10.1001/jamaneurol.2022.0461

     • PubMed
     • Google Scholar
126. 1. Mantovani A
     2. Morrone MC
     3. Patrono C
     4. Santoro MG
     5. Schiaffino S
     6. Remuzzi G
     7. Bussolati G

     (2022) Long covid: where we stand and challenges ahead

     Cell Death and Differentiation 29:1891–1900.

     https://doi.org/10.1038/s41418-022-01052-6

     • Google Scholar
127. 1. Matschke J
     2. Lütgehetmann M
     3. Hagel C
     4. Sperhake JP
     5. Schröder AS
     6. Edler C
     7. Mushumba H
     8. Fitzek A
     9. Allweiss L
     10. Dandri M
     11. Dottermusch M
     12. Heinemann A
     13. Pfefferle S
     14. Schwabenland M
     15. Sumner Magruder D
     16. Bonn S
     17. Prinz M
     18. Gerloff C
     19. Püschel K
     20. Krasemann S
     21. Aepfelbacher M
     22. Glatzel M

     (2020) Neuropathology of patients with COVID-19 in germany: A post-mortem case series

     The Lancet. Neurology 19:919–929.

     https://doi.org/10.1016/S1474-4422(20)30308-2

     • PubMed
     • Google Scholar
128. 1. Matsubara D
     2. Chang J
     3. Kauffman HL
     4. Wang Y
     5. Nadaraj S
     6. Patel C
     7. Paridon SM
     8. Fogel MA
     9. Quartermain MD
     10. Banerjee A

     (2022) Longitudinal assessment of cardiac outcomes of multisystem inflammatory syndrome in children associated with COVID-19 infections

     Journal of the American Heart Association 11:e023251.

     https://doi.org/10.1161/JAHA.121.023251

     • Google Scholar
129. 1. McFarland AJ
     2. Yousuf MS
     3. Shiers S
     4. Price TJ

     (2021) Neurobiology of SARS-cov-2 interactions with the peripheral nervous system: implications for COVID-19 and pain

     Pain Reports 6:e885.

     https://doi.org/10.1097/PR9.0000000000000885

     • Google Scholar
130. 1. Medina-Enríquez MM
     2. Lopez-León S
     3. Carlos-Escalante JA
     4. Aponte-Torres Z
     5. Cuapio A
     6. Wegman-Ostrosky T

     (2020) ACE2: the molecular doorway to SARS-cov-2

     Cell & Bioscience 10:148.

     https://doi.org/10.1186/s13578-020-00519-8

     • PubMed
     • Google Scholar
131. 1. Mehandru S
     2. Merad M

     (2022) Pathological sequelae of long-haul COVID

     Nature Immunology 23:194–202.

     https://doi.org/10.1038/s41590-021-01104-y

     • PubMed
     • Google Scholar
132. 1. Michelen M
     2. Manoharan L
     3. Elkheir N
     4. Cheng V
     5. Dagens A
     6. Hastie C
     7. O’Hara M
     8. Suett J
     9. Dahmash D
     10. Bugaeva P
     11. Rigby I
     12. Munblit D
     13. Harriss E
     14. Burls A
     15. Foote C
     16. Scott J
     17. Carson G
     18. Olliaro P
     19. Sigfrid L
     20. Stavropoulou C

     (2021) Characterising long COVID: A living systematic review

     BMJ Global Health 6:e005427.

     https://doi.org/10.1136/bmjgh-2021-005427

     • PubMed
     • Google Scholar
133. 1. Montezano AC
     2. Nguyen Dinh Cat A
     3. Rios FJ
     4. Touyz RM

     (2014) Angiotensin II and vascular injury

     Current Hypertension Reports 16:431–432.

     https://doi.org/10.1007/s11906-014-0431-2

     • PubMed
     • Google Scholar
134. 1. Morganstein T
     2. Haidar Z
     3. Trivlidis J
     4. Azuelos I
     5. Huang MJ
     6. Eidelman DH
     7. Baglole CJ

     (2021) Involvement of the ACE2/ang- (1-7) /masr axis in pulmonary fibrosis: implications for COVID-19

     International Journal of Molecular Sciences 22:12955.

     https://doi.org/10.3390/ijms222312955

     • PubMed
     • Google Scholar
135. 1. Mueller C
     2. Giannitsis E
     3. Jaffe AS
     4. Huber K
     5. Mair J
     6. Cullen L
     7. Hammarsten O
     8. Mills NL
     9. Mockel M
     10. Krychtiuk K
     11. Thygesen K
     12. Lindahl B

     (2021) Cardiovascular biomarkers in patients with COVID-19

     European Heart Journal 10:310–319.

     https://doi.org/10.1093/ehjacc/zuab009

     • Google Scholar
136. 1. Nalbandian A
     2. Sehgal K
     3. Gupta A
     4. Madhavan MV
     5. McGroder C
     6. Stevens JS
     7. Cook JR
     8. Nordvig AS
     9. Shalev D
     10. Sehrawat TS
     11. Ahluwalia N
     12. Bikdeli B
     13. Dietz D
     14. Der-Nigoghossian C
     15. Liyanage-Don N
     16. Rosner GF
     17. Bernstein EJ
     18. Mohan S
     19. Beckley AA
     20. Seres DS
     21. Choueiri TK
     22. Uriel N
     23. Ausiello JC
     24. Accili D
     25. Freedberg DE
     26. Baldwin M
     27. Schwartz A
     28. Brodie D
     29. Garcia CK
     30. Elkind MSV
     31. Connors JM
     32. Bilezikian JP
     33. Landry DW
     34. Wan EY

     (2021) Post-acute COVID-19 syndrome

     Nature Medicine 27:601–615.

     https://doi.org/10.1038/s41591-021-01283-z

     • PubMed
     • Google Scholar
137. 1. Nelson MJ
     2. Bahl JS
     3. Buckley JD
     4. Thomson RL
     5. Davison K

     (2019) Evidence of altered cardiac autonomic regulation in myalgic Encephalomyelitis/Chronic fatigue syndrome: a systematic review and meta-analysis

     Medicine 98:e17600.

     https://doi.org/10.1097/MD.0000000000017600

     • PubMed
     • Google Scholar
138. 1. Noval Rivas M
     2. Porritt RA
     3. Cheng MH
     4. Bahar I
     5. Arditi M

     (2022) Multisystem inflammatory syndrome in children and long COVID: the SARS-cov-2 viral superantigen hypothesis

     Frontiers in Immunology 13:941009.

     https://doi.org/10.3389/fimmu.2022.941009

     • PubMed
     • Google Scholar
139. 1. Oronsky B
     2. Larson C
     3. Hammond TC
     4. Oronsky A
     5. Kesari S
     6. Lybeck M
     7. Reid TR

     (2023) A review of persistent post-COVID syndrome (PPCS)

     Clinical Reviews in Allergy & Immunology 64:66–74.

     https://doi.org/10.1007/s12016-021-08848-3

     • PubMed
     • Google Scholar
140. 1. Osburn WO
     2. Smith K
     3. Yanek L
     4. Amat-Alcaron N
     5. Thiemann DR
     6. Cox AL
     7. Leucker TM
     8. Lowenstein CJ

     (2022) Markers of endothelial cell activation are associated with the severity of pulmonary disease in COVID-19

     PLOS ONE 17:e0268296.

     https://doi.org/10.1371/journal.pone.0268296

     • PubMed
     • Google Scholar
141. 1. O’Shea JJ
     2. Schwartz DM
     3. Villarino AV
     4. Gadina M
     5. McInnes IB
     6. Laurence A

     (2015) The JAK-STAT pathway: impact on human disease and therapeutic intervention

     Annual Review of Medicine 66:311–328.

     https://doi.org/10.1146/annurev-med-051113-024537

     • PubMed
     • Google Scholar
142. 1. Ostergaard L

     (2021) Sars cov-2 related microvascular damage and symptoms during and after COVID-19: consequences of capillary transit-time changes, tissue hypoxia and inflammation

     Physiological Reports 9:e14726.

     https://doi.org/10.14814/phy2.14726

     • PubMed
     • Google Scholar
143. 1. Ozonoff A
     2. Schaenman J
     3. Jayavelu ND
     4. Milliren CE
     5. Calfee CS
     6. Cairns CB
     7. Kraft M
     8. Baden LR
     9. Shaw AC
     10. Krammer F
     11. van Bakel H
     12. Esserman DA
     13. Liu S
     14. Sesma AF
     15. Simon V
     16. Hafler DA
     17. Montgomery RR
     18. Kleinstein SH
     19. Levy O
     20. Bime C
     21. Haddad EK
     22. Erle DJ
     23. Pulendran B
     24. Nadeau KC
     25. Davis MM
     26. Hough CL
     27. Messer WB
     28. Higuita NIA
     29. Metcalf JP
     30. Atkinson MA
     31. Brakenridge SC
     32. Corry D
     33. Kheradmand F
     34. Ehrlich LIR
     35. Melamed E
     36. McComsey GA
     37. Sekaly R
     38. Diray-Arce J
     39. Peters B
     40. Augustine AD
     41. Reed EF
     42. Altman MC
     43. Becker PM
     44. Rouphael N
     45. IMPACC study group members

     (2022) Phenotypes of disease severity in a cohort of hospitalized COVID-19 patients: results from the IMPACC study

     EBioMedicine 83:104208.

     https://doi.org/10.1016/j.ebiom.2022.104208

     • PubMed
     • Google Scholar
144. 1. Pablos JL
     2. Galindo M
     3. Carmona L
     4. Lledó A
     5. Retuerto M
     6. Blanco R
     7. Gonzalez-Gay MA
     8. Martinez-Lopez D
     9. Castrejón I
     10. Alvaro-Gracia JM
     11. Fernández Fernández D
     12. Mera-Varela A
     13. Manrique-Arija S
     14. Mena Vázquez N
     15. Fernandez-Nebro A
     16. RIER Investigators Group
     17. RIER investigators group

     (2020) Clinical outcomes of hospitalised patients with COVID-19 and chronic inflammatory and autoimmune rheumatic diseases: a multicentric matched cohort study

     Annals of the Rheumatic Diseases 79:1544–1549.

     https://doi.org/10.1136/annrheumdis-2020-218296

     • PubMed
     • Google Scholar
145. 1. Pan R
     2. Zhang Q
     3. Anthony SM
     4. Zhou Y
     5. Zou X
     6. Cassell M
     7. Perlman S

     (2020) Oligodendrocytes that survive acute coronavirus infection induce prolonged inflammatory responses in the CNS

     PNAS 117:15902–15910.

     https://doi.org/10.1073/pnas.2003432117

     • PubMed
     • Google Scholar
146. 1. Parohan M
     2. Yaghoubi S
     3. Seraji A

     (2020) Cardiac injury is associated with severe outcome and death in patients with coronavirus disease 2019 (COVID-19) infection: a systematic review and meta-analysis of observational studies

     European Heart Journal. Acute Cardiovascular Care 9:665–677.

     https://doi.org/10.1177/2048872620937165

     • PubMed
     • Google Scholar
147. 1. Pellegrini JAS
     2. Rech TH
     3. Schwarz P
     4. de Oliveira ACT
     5. Vieceli T
     6. Moraes RB
     7. Sekine L
     8. Viana MV

     (2021) Incidence of venous thromboembolism among patients with severe COVID-19 requiring mechanical ventilation compared to other causes of respiratory failure: a prospective cohort study

     Journal of Thrombosis and Thrombolysis 52:482–492.

     https://doi.org/10.1007/s11239-021-02395-6

     • PubMed
     • Google Scholar
148. 1. Perlis RH
     2. Santillana M
     3. Ognyanova K
     4. Safarpour A
     5. Lunz Trujillo K
     6. Simonson MD
     7. Green J
     8. Quintana A
     9. Druckman J
     10. Baum MA
     11. Lazer D

     (2022) Prevalence and correlates of long COVID symptoms among US adults

     JAMA Network Open 5:e2238804.

     https://doi.org/10.1001/jamanetworkopen.2022.38804

     • PubMed
     • Google Scholar
149. 1. Petersen MS
     2. Kristiansen MF
     3. Hanusson KD
     4. Foldbo BM
     5. Danielsen ME
     6. Á Steig B
     7. Gaini S
     8. Strøm M
     9. Weihe P

     (2022) Prevalence of long COVID in a national cohort: longitudinal measures from disease onset until 8 months’ follow-up

     International Journal of Infectious Diseases 122:437–441.

     https://doi.org/10.1016/j.ijid.2022.06.031

     • PubMed
     • Google Scholar
150. 1. Piazza G
     2. Campia U
     3. Hurwitz S
     4. Snyder JE
     5. Rizzo SM
     6. Pfeferman MB
     7. Morrison RB
     8. Leiva O
     9. Fanikos J
     10. Nauffal V
     11. Almarzooq Z
     12. Goldhaber SZ

     (2020) Registry of arterial and venous thromboembolic complications in patients with COVID-19

     Journal of the American College of Cardiology 76:2060–2072.

     https://doi.org/10.1016/j.jacc.2020.08.070

     • PubMed
     • Google Scholar
151. 1. Pierce CA
     2. Preston-Hurlburt P
     3. Dai Y
     4. Aschner CB
     5. Cheshenko N
     6. Galen B
     7. Garforth SJ
     8. Herrera NG
     9. Jangra RK
     10. Morano NC
     11. Orner E
     12. Sy S
     13. Chandran K
     14. Dziura J
     15. Almo SC
     16. Ring A
     17. Keller MJ
     18. Herold KC
     19. Herold BC

     (2020) Immune responses to SARS-cov-2 infection in hospitalized pediatric and adult patients

     Science Translational Medicine 12:eabd5487.

     https://doi.org/10.1126/scitranslmed.abd5487

     • PubMed
     • Google Scholar
152. 1. Poon DCH
     2. Ho YS
     3. Chiu K
     4. Wong HL
     5. Chang RCC

     (2015) Sickness: from the focus on cytokines, prostaglandins, and complement factors to the perspectives of neurons

     Neuroscience and Biobehavioral Reviews 57:30–45.

     https://doi.org/10.1016/j.neubiorev.2015.07.015

     • PubMed
     • Google Scholar
153. 1. Porritt RA
     2. Paschold L
     3. Rivas MN
     4. Cheng MH
     5. Yonker LM
     6. Chandnani H
     7. Lopez M
     8. Simnica D
     9. Schultheiß C
     10. Santiskulvong C
     11. Van Eyk J
     12. McCormick JK
     13. Fasano A
     14. Bahar I
     15. Binder M
     16. Arditi M

     (2021) Hla class I-associated expansion of TRBV11-2 T cells in multisystem inflammatory syndrome in children

     The Journal of Clinical Investigation 131:e146614.

     https://doi.org/10.1172/JCI146614

     • PubMed
     • Google Scholar
154. 1. Proal AD
     2. VanElzakker MB

     (2021) Long COVID or post-acute sequelae of COVID-19 (PASC): an overview of biological factors that may contribute to persistent symptoms

     Frontiers in Microbiology 12:698169.

     https://doi.org/10.3389/fmicb.2021.698169

     • PubMed
     • Google Scholar
155. 1. Puntmann VO
     2. Carerj ML
     3. Wieters I
     4. Fahim M
     5. Arendt C
     6. Hoffmann J
     7. Shchendrygina A
     8. Escher F
     9. Vasa-Nicotera M
     10. Zeiher AM
     11. Vehreschild M
     12. Nagel E

     (2020) Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from coronavirus disease 2019 (COVID-19)

     JAMA Cardiology 5:1265–1273.

     https://doi.org/10.1001/jamacardio.2020.3557

     • PubMed
     • Google Scholar
156. 1. Rahman A
     2. Niloofa R
     3. Jayarajah U
     4. De Mel S
     5. Abeysuriya V
     6. Seneviratne SL

     (2021) Hematological abnormalities in COVID-19: a narrative review

     The American Journal of Tropical Medicine and Hygiene 104:1188–1201.

     https://doi.org/10.4269/ajtmh.20-1536

     • PubMed
     • Google Scholar
157. 1. Ramaswamy A
     2. Brodsky NN
     3. Sumida TS
     4. Comi M
     5. Asashima H
     6. Hoehn KB
     7. Li N
     8. Liu Y
     9. Shah A
     10. Ravindra NG
     11. Bishai J
     12. Khan A
     13. Lau W
     14. Sellers B
     15. Bansal N
     16. Guerrerio P
     17. Unterman A
     18. Habet V
     19. Rice AJ
     20. Catanzaro J
     21. Chandnani H
     22. Lopez M
     23. Kaminski N
     24. Dela Cruz CS
     25. Tsang JS
     26. Wang Z
     27. Yan X
     28. Kleinstein SH
     29. van Dijk D
     30. Pierce RW
     31. Hafler DA
     32. Lucas CL

     (2021) Immune dysregulation and autoreactivity correlate with disease severity in SARS-cov-2-associated multisystem inflammatory syndrome in children

     Immunity 54:1083–1095.

     https://doi.org/10.1016/j.immuni.2021.04.003

     • PubMed
     • Google Scholar
158. 1. Rao S
     2. Lee GM
     3. Razzaghi H
     4. Lorman V
     5. Mejias A
     6. Pajor NM
     7. Thacker D
     8. Webb R
     9. Dickinson K
     10. Bailey LC
     11. Jhaveri R
     12. Christakis DA
     13. Bennett TD
     14. Chen Y
     15. Forrest CB

     (2022) Clinical features and burden of postacute sequelae of SARS-cov-2 infection in children and adolescents

     JAMA Pediatrics 176:1000–1009.

     https://doi.org/10.1001/jamapediatrics.2022.2800

     • PubMed
     • Google Scholar
159. 1. Rasa S
     2. Nora-Krukle Z
     3. Henning N
     4. Eliassen E
     5. Shikova E
     6. Harrer T
     7. Scheibenbogen C
     8. Murovska M
     9. Prusty BK
     10. European Network on ME/CFS

     (2018) Chronic viral infections in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)

     Journal of Translational Medicine 16:268.

     https://doi.org/10.1186/s12967-018-1644-y

     • PubMed
     • Google Scholar
160. 1. Rawal G
     2. Yadav S
     3. Kumar R

     (2017) Post-intensive care syndrome: an overview

     Journal of Translational Internal Medicine 5:90–92.

     https://doi.org/10.1515/jtim-2016-0016

     • PubMed
     • Google Scholar
161. 1. Rimoldi SF
     2. Scherrer U
     3. Messerli FH

     (2014) Secondary arterial hypertension: when, who, and how to screen?

     European Heart Journal 35:1245–1254.

     https://doi.org/10.1093/eurheartj/eht534

     • PubMed
     • Google Scholar
162. 1. Riphagen S
     2. Gomez X
     3. Gonzalez-Martinez C
     4. Wilkinson N
     5. Theocharis P

     (2020) Hyperinflammatory shock in children during COVID-19 pandemic

     Lancet 395:1607–1608.

     https://doi.org/10.1016/S0140-6736(20)31094-1

     • Google Scholar
163. 1. Robertson MM
     2. Qasmieh SA
     3. Kulkarni SG
     4. Teasdale CA
     5. Jones H
     6. McNairy M
     7. Borrell LN
     8. Nash D

     (2022) The epidemiology of long COVID in US adults

     Clinical Infectious Diseases 1:ciac961.

     https://doi.org/10.1093/cid/ciac961

     • PubMed
     • Google Scholar
164. 1. Ronco C
     2. Reis T

     (2020) Kidney involvement in COVID-19 and rationale for extracorporeal therapies

     Nature Reviews.Nephrology 16:308–310.

     https://doi.org/10.1038/s41581-020-0284-7

     • Google Scholar
165. 1. Rossier BC
     2. Bochud M
     3. Devuyst O

     (2017) The hypertension pandemic: an evolutionary perspective

     Physiology 32:112–125.

     https://doi.org/10.1152/physiol.00026.2016

     • Google Scholar
166. 1. Rubino F
     2. Amiel SA
     3. et P
     4. Alberti G
     5. Bornstein S
     6. Eckel RH
     7. Mingrone G
     8. Boehm B
     9. Cooper ME
     10. Chai Z
     11. Del Prato S
     12. Ji L
     13. Hopkins D
     14. Herman WH
     15. Khunti K
     16. Mbanya JC
     17. Renard E

     (2020) New-onset diabetes in covid-19

     The New England Journal of Medicine 383:789–790.

     https://doi.org/10.1056/NEJMc2018688

     • Google Scholar
167. 1. Sabroe I
     2. Parker LC
     3. Dower SK
     4. Whyte MKB

     (2008) The role of TLR activation in inflammation

     The Journal of Pathology 214:126–135.

     https://doi.org/10.1002/path.2264

     • PubMed
     • Google Scholar
168. 1. Sadanandam A
     2. Bopp T
     3. Dixit S
     4. Knapp D
     5. Emperumal CP
     6. Vergidis P
     7. Rajalingam K
     8. Melcher A
     9. Kannan N

     (2020) A blood transcriptome-based analysis of disease progression, immune regulation, and symptoms in coronavirus-infected patients

     Cell Death Discovery 6:141.

     https://doi.org/10.1038/s41420-020-00376-x

     • PubMed
     • Google Scholar
169. 1. Sahin BE
     2. Celikbilek A
     3. Kocak Y
     4. Saltoglu GT
     5. Konar NM
     6. Hizmali L

     (2022) Plasma biomarkers of brain injury in COVID-19 patients with neurological symptoms

     Journal of the Neurological Sciences 439:120324.

     https://doi.org/10.1016/j.jns.2022.120324

     • PubMed
     • Google Scholar
170. 1. Sakr Y
     2. Giovini M
     3. Leone M
     4. Pizzilli G
     5. Kortgen A
     6. Bauer M
     7. Tonetti T
     8. Duclos G
     9. Zieleskiewicz L
     10. Buschbeck S
     11. Ranieri VM
     12. Antonucci E

     (2020) Pulmonary embolism in patients with coronavirus disease-2019 (COVID-19) pneumonia: a narrative review

     Annals of Intensive Care 10:124.

     https://doi.org/10.1186/s13613-020-00741-0

     • PubMed
     • Google Scholar
171. 1. Santos A
     2. Magro DO
     3. Evangelista-Poderoso R
     4. Saad MJA

     (2021) Diabetes, obesity, and insulin resistance in COVID-19: molecular interrelationship and therapeutic implications

     Diabetology & Metabolic Syndrome 13:23.

     https://doi.org/10.1186/s13098-021-00639-2

     • PubMed
     • Google Scholar
172. 1. Sathish T
     2. Anton MC
     3. Sivakumar T

     (2021a) New-onset diabetes in “long COVID.”

     Journal of Diabetes 13:693–694.

     https://doi.org/10.1111/1753-0407.13187

     • PubMed
     • Google Scholar
173. 1. Sathish T
     2. Chandrika Anton M

     (2021b) Newly diagnosed diabetes in patients with mild to moderate COVID-19

     Diabetes & Metabolic Syndrome 15:569–571.

     https://doi.org/10.1016/j.dsx.2021.02.034

     • PubMed
     • Google Scholar
174. 1. Sathish T
     2. Kapoor N
     3. Cao Y
     4. Tapp RJ
     5. Zimmet P

     (2021c) Proportion of newly diagnosed diabetes in COVID-19 patients: A systematic review and meta-analysis

     Diabetes, Obesity & Metabolism 23:870–874.

     https://doi.org/10.1111/dom.14269

     • Google Scholar
175. 1. Scherbakov N
     2. Szklarski M
     3. Hartwig J
     4. Sotzny F
     5. Lorenz S
     6. Meyer A
     7. Grabowski P
     8. Doehner W
     9. Scheibenbogen C

     (2020) Peripheral endothelial dysfunction in myalgic encephalomyelitis/chronic fatigue syndrome

     ESC Heart Failure 7:1064–1071.

     https://doi.org/10.1002/ehf2.12633

     • Google Scholar
176. 1. Schieffer E
     2. Schieffer B

     (2022) The rationale for the treatment of long-covid symptoms - A cardiologist’s view

     Frontiers in Cardiovascular Medicine 9:992686.

     https://doi.org/10.3389/fcvm.2022.992686

     • PubMed
     • Google Scholar
177. 1. Schultheiss C
     2. Willscher E
     3. Paschold L
     4. Gottschick C
     5. Klee B
     6. Henkes SS
     7. Bosurgi L
     8. Dutzmann J
     9. Sedding D
     10. Frese T
     11. Girndt M
     12. Höll JI
     13. Gekle M
     14. Mikolajczyk R
     15. Binder M

     (2022) The IL-1β, IL-6, and TNF cytokine triad is associated with post-acute sequelae of COVID-19

     Cell Reports. Medicine 3:100663.

     https://doi.org/10.1016/j.xcrm.2022.100663

     • PubMed
     • Google Scholar
178. 1. Sestan M
     2. Marinović S
     3. Kavazović I
     4. Cekinović Đ
     5. Wueest S
     6. Turk Wensveen T
     7. Brizić I
     8. Jonjić S
     9. Konrad D
     10. Wensveen FM
     11. Polić B

     (2018) Virus-induced interferon-γ causes insulin resistance in skeletal muscle and derails glycemic control in obesity

     Immunity 49:164–177.

     https://doi.org/10.1016/j.immuni.2018.05.005

     • PubMed
     • Google Scholar
179. 1. Settanni CR
     2. Ianiro G
     3. Ponziani FR
     4. Bibbò S
     5. Segal JP
     6. Cammarota G
     7. Gasbarrini A

     (2021) COVID-19 as a trigger of irritable bowel syndrome: a review of potential mechanisms

     World Journal of Gastroenterology 27:7433–7445.

     https://doi.org/10.3748/wjg.v27.i43.7433

     • PubMed
     • Google Scholar
180. 1. Shaw BH
     2. Stiles LE
     3. Bourne K
     4. Green EA
     5. Shibao CA
     6. Okamoto LE
     7. Garland EM
     8. Gamboa A
     9. Diedrich A
     10. Raj V
     11. Sheldon RS
     12. Biaggioni I
     13. Robertson D
     14. Raj SR

     (2019) The face of postural tachycardia syndrome-insights from a large cross-sectional online community-based survey

     Journal of Internal Medicine 286:438–448.

     https://doi.org/10.1111/joim.12895

     • PubMed
     • Google Scholar
181. 1. Shi S
     2. Qin M
     3. Shen B
     4. Cai Y
     5. Liu T
     6. Yang F
     7. Gong W
     8. Liu X
     9. Liang J
     10. Zhao Q
     11. Huang H
     12. Yang B
     13. Huang C

     (2020) Association of cardiac injury with mortality in hospitalized patients with COVID-19 in wuhan, china

     JAMA Cardiology 5:802–810.

     https://doi.org/10.1001/jamacardio.2020.0950

     • PubMed
     • Google Scholar
182. 1. Shin J
     2. Toyoda S
     3. Nishitani S
     4. Onodera T
     5. Fukuda S
     6. Kita S
     7. Fukuhara A
     8. Shimomura I

     (2022) SARS-cov-2 infection impairs the insulin/IGF signaling pathway in the lung, liver, adipose tissue, and pancreatic cells via IRF1

     Metabolism 133:155236.

     https://doi.org/10.1016/j.metabol.2022.155236

     • PubMed
     • Google Scholar
183. 1. Sidarta-Oliveira D
     2. Jara CP
     3. Ferruzzi AJ
     4. Skaf MS
     5. Velander WH
     6. Araujo EP
     7. Velloso LA

     (2020) SARS-cov-2 receptor is co-expressed with elements of the kinin-kallikrein, renin-angiotensin and coagulation systems in alveolar cells

     Scientific Reports 10:19522.

     https://doi.org/10.1038/s41598-020-76488-2

     • PubMed
     • Google Scholar
184. 1. Silva Andrade B
     2. Siqueira S
     3. de Assis Soares WR
     4. de Souza Rangel F
     5. Santos NO
     6. Dos Santos Freitas A
     7. Ribeiro da Silveira P
     8. Tiwari S
     9. Alzahrani KJ
     10. Góes-Neto A
     11. Azevedo V
     12. Ghosh P
     13. Barh D

     (2021) Long-COVID and post-COVID health complications: an up-to-date review on clinical conditions and their possible molecular mechanisms

     Viruses 13:700.

     https://doi.org/10.3390/v13040700

     • PubMed
     • Google Scholar
185. 1. Sneller MC
     2. Liang CJ
     3. Marques AR
     4. Chung JY
     5. Shanbhag SM
     6. Fontana JR
     7. Raza H
     8. Okeke O
     9. Dewar RL
     10. Higgins BP
     11. Tolstenko K
     12. Kwan RW
     13. Gittens KR
     14. Seamon CA
     15. McCormack G
     16. Shaw JS
     17. Okpali GM
     18. Law M
     19. Trihemasava K
     20. Kennedy BD
     21. Shi V
     22. Justement JS
     23. Buckner CM
     24. Blazkova J
     25. Moir S
     26. Chun T-W
     27. Lane HC

     (2022) A longitudinal study of COVID-19 sequelae and immunity: baseline findings

     Annals of Internal Medicine 175:969–979.

     https://doi.org/10.7326/M21-4905

     • PubMed
     • Google Scholar
186. Preprint

     1. Song E
     2. Zhang C
     3. Israelow B
     4. Lu-Culligan A
     5. Prado AV
     6. Skriabine S
     7. Lu P
     8. Weizman OE
     9. Liu F
     10. Dai Y
     11. Szigeti-Buck K
     12. Yasumoto Y
     13. Wang G
     14. Castaldi C
     15. Heltke J
     16. Ng E
     17. Wheeler J
     18. Alfajaro MM
     19. Levavasseur E
     20. Fontes B
     21. Ravindra NG
     22. Van Dijk D
     23. Mane S
     24. Gunel M
     25. Ring A
     26. Kazmi SAJ
     27. Zhang K
     28. Wilen CB
     29. Horvath TL
     30. Plu I
     31. Haik S
     32. Thomas JL
     33. Louvi A
     34. Farhadian SF
     35. Huttner A
     36. Seilhean D
     37. Renier N
     38. Bilguvar K
     39. Iwasaki A

     (2020) Neuroinvasion of Sars-Cov-2 in Human and Mouse Brain

     bioRxiv.

     https://doi.org/10.1101/2020.06.25.169946

     • Google Scholar
187. 1. Song WJ
     2. Hui CKM
     3. Hull JH
     4. Birring SS
     5. McGarvey L
     6. Mazzone SB
     7. Chung KF

     (2021) Confronting COVID-19-associated cough and the post-COVID syndrome: role of viral neurotropism, neuroinflammation, and neuroimmune responses

     The Lancet. Respiratory Medicine 9:533–544.

     https://doi.org/10.1016/S2213-2600(21)00125-9

     • PubMed
     • Google Scholar
188. 1. Sotzny F
     2. Blanco J
     3. Capelli E
     4. Castro-Marrero J
     5. Steiner S
     6. Murovska M
     7. Scheibenbogen C
     8. European Network on ME/CFS EUROMENE

     (2018) Myalgic Encephalomyelitis/Chronic fatigue syndrome-evidence for an autoimmune disease

     Autoimmunity Reviews 17:601–609.

     https://doi.org/10.1016/j.autrev.2018.01.009

     • PubMed
     • Google Scholar
189. 1. Stefano GB
     2. Büttiker P
     3. Weissenberger S
     4. Ptacek R
     5. Wang F
     6. Esch T
     7. Bilfinger TV
     8. Raboch J
     9. Kream RM

     (2022) Biomedical perspectives of acute and chronic neurological and neuropsychiatric sequelae of COVID-19

     Current Neuropharmacology 20:1229–1240.

     https://doi.org/10.2174/1570159X20666211223130228

     • PubMed
     • Google Scholar
190. 1. Su Y
     2. Yuan D
     3. Chen DG
     4. Ng RH
     5. Wang K
     6. Choi J
     7. Li S
     8. Hong S
     9. Zhang R
     10. Xie J
     11. Kornilov SA
     12. Scherler K
     13. Pavlovitch-Bedzyk AJ
     14. Dong S
     15. Lausted C
     16. Lee I
     17. Fallen S
     18. Dai CL
     19. Baloni P
     20. Smith B
     21. Duvvuri VR
     22. Anderson KG
     23. Li J
     24. Yang F
     25. Duncombe CJ
     26. McCulloch DJ
     27. Rostomily C
     28. Troisch P
     29. Zhou J
     30. Mackay S
     31. DeGottardi Q
     32. May DH
     33. Taniguchi R
     34. Gittelman RM
     35. Klinger M
     36. Snyder TM
     37. Roper R
     38. Wojciechowska G
     39. Murray K
     40. Edmark R
     41. Evans S
     42. Jones L
     43. Zhou Y
     44. Rowen L
     45. Liu R
     46. Chour W
     47. Algren HA
     48. Berrington WR
     49. Wallick JA
     50. Cochran RA
     51. Micikas ME
     52. ISB-Swedish COVID-19 Biobanking Unit
     53. Wrin T
     54. Petropoulos CJ
     55. Cole HR
     56. Fischer TD
     57. Wei W
     58. Hoon DSB
     59. Price ND
     60. Subramanian N
     61. Hill JA
     62. Hadlock J
     63. Magis AT
     64. Ribas A
     65. Lanier LL
     66. Boyd SD
     67. Bluestone JA
     68. Chu H
     69. Hood L
     70. Gottardo R
     71. Greenberg PD
     72. Davis MM
     73. Goldman JD
     74. Heath JR

     (2022) Multiple early factors anticipate post-acute COVID-19 sequelae

     Cell 185:881–895.

     https://doi.org/10.1016/j.cell.2022.01.014

     • PubMed
     • Google Scholar
191. 1. Subramanian A
     2. Nirantharakumar K
     3. Hughes S
     4. Myles P
     5. Williams T
     6. Gokhale KM
     7. Taverner T
     8. Chandan JS
     9. Brown K
     10. Simms-Williams N
     11. Shah AD
     12. Singh M
     13. Kidy F
     14. Okoth K
     15. Hotham R
     16. Bashir N
     17. Cockburn N
     18. Lee SI
     19. Turner GM
     20. Gkoutos GV
     21. Aiyegbusi OL
     22. McMullan C
     23. Denniston AK
     24. Sapey E
     25. Lord JM
     26. Wraith DC
     27. Leggett E
     28. Iles C
     29. Marshall T
     30. Price MJ
     31. Marwaha S
     32. Davies EH
     33. Jackson LJ
     34. Matthews KL
     35. Camaradou J
     36. Calvert M
     37. Haroon S

     (2022) Symptoms and risk factors for long COVID in non-hospitalized adults

     Nature Medicine 28:1706–1714.

     https://doi.org/10.1038/s41591-022-01909-w

     • PubMed
     • Google Scholar
192. 1. Sudre CH
     2. Murray B
     3. Varsavsky T
     4. Graham MS
     5. Penfold RS
     6. Bowyer RC
     7. Pujol JC
     8. Klaser K
     9. Antonelli M
     10. Canas LS
     11. Molteni E
     12. Modat M
     13. Jorge Cardoso M
     14. May A
     15. Ganesh S
     16. Davies R
     17. Nguyen LH
     18. Drew DA
     19. Astley CM
     20. Joshi AD
     21. Merino J
     22. Tsereteli N
     23. Fall T
     24. Gomez MF
     25. Duncan EL
     26. Menni C
     27. Williams FMK
     28. Franks PW
     29. Chan AT
     30. Wolf J
     31. Ourselin S
     32. Spector T
     33. Steves CJ

     (2021) Author correction: attributes and predictors of long COVID

     Nature Medicine 27:1116.

     https://doi.org/10.1038/s41591-021-01361-2

     • PubMed
     • Google Scholar
193. 1. Sze S
     2. Pan D
     3. Moss AJ
     4. Ong CK
     5. Pareek M
     6. Squire IB
     7. Clark AL

     (2022) Overstimulation of the ergoreflex-A possible mechanism to explain symptoms in long COVID

     Frontiers in Cardiovascular Medicine 9:940832.

     https://doi.org/10.3389/fcvm.2022.940832

     • PubMed
     • Google Scholar
194. 1. Tanni SE
     2. Fabro AT
     3. de Albuquerque A
     4. Ferreira EVM
     5. Verrastro CGY
     6. Sawamura MVY
     7. Ribeiro SM
     8. Baldi BG

     (2021) Pulmonary fibrosis secondary to COVID-19: a narrative review

     Expert Review of Respiratory Medicine 15:791–803.

     https://doi.org/10.1080/17476348.2021.1916472

     • PubMed
     • Google Scholar
195. 1. Tansey CM
     2. Louie M
     3. Loeb M
     4. Gold WL
     5. Muller MP
     6. de Jager J
     7. Cameron JI
     8. Tomlinson G
     9. Mazzulli T
     10. Walmsley SL
     11. Rachlis AR
     12. Mederski BD
     13. Silverman M
     14. Shainhouse Z
     15. Ephtimios IE
     16. Avendano M
     17. Downey J
     18. Styra R
     19. Yamamura D
     20. Gerson M
     21. Stanbrook MB
     22. Marras TK
     23. Phillips EJ
     24. Zamel N
     25. Richardson SE
     26. Slutsky AS
     27. Herridge MS

     (2007) One-year outcomes and health care utilization in survivors of severe acute respiratory syndrome

     Archives of Internal Medicine 167:1312–1320.

     https://doi.org/10.1001/archinte.167.12.1312

     • PubMed
     • Google Scholar
196. 1. Tarentino AL
     2. Maley F

     (1975) A comparison of the substrate specificities of endo-beta-N-acetylglucosaminidases from streptomyces griseus and diplococcus pneumoniae

     Biochemical and Biophysical Research Communications 67:455–462.

     https://doi.org/10.1016/0006-291x(75)90337-x

     • PubMed
     • Google Scholar
197. 1. Tate W
     2. Walker M
     3. Sweetman E
     4. Helliwell A
     5. Peppercorn K
     6. Edgar C
     7. Blair A
     8. Chatterjee A

     (2022) Molecular mechanisms of neuroinflammation in ME/CFS and long COVID to sustain disease and promote relapses

     Frontiers in Neurology 13:877772.

     https://doi.org/10.3389/fneur.2022.877772

     • PubMed
     • Google Scholar
198. 1. Tay MZ
     2. Poh CM
     3. Rénia L
     4. MacAry PA
     5. Ng LFP

     (2020) The trinity of COVID-19: immunity, inflammation and intervention

     Nature Reviews. Immunology 20:363–374.

     https://doi.org/10.1038/s41577-020-0311-8

     • PubMed
     • Google Scholar
199. 1. Tergaonkar V
     2. Correa RG
     3. Ikawa M
     4. Verma IM

     (2005) Distinct roles of ikappab proteins in regulating constitutive NF-kappab activity

     Nature Cell Biology 7:921–923.

     https://doi.org/10.1038/ncb1296

     • PubMed
     • Google Scholar
200. 1. Teuwen LA
     2. Geldhof V
     3. Pasut A
     4. Carmeliet P

     (2020) COVID-19: the vasculature unleashed

     Nature Reviews. Immunology 20:389–391.

     https://doi.org/10.1038/s41577-020-0343-0

     • PubMed
     • Google Scholar
201. 1. Thompson EJ
     2. Williams DM
     3. Walker AJ
     4. Mitchell RE
     5. Niedzwiedz CL
     6. Yang TC
     7. Huggins CF
     8. Kwong ASF
     9. Silverwood RJ
     10. Di Gessa G
     11. Bowyer RCE
     12. Northstone K
     13. Hou B
     14. Green MJ
     15. Dodgeon B
     16. Doores KJ
     17. Duncan EL
     18. Williams FMK

     (2022) Long COVID burden and risk factors in 10 UK longitudinal studies and electronic health records

     Nature Communications 13:3528.

     https://doi.org/10.1038/s41467-022-30836-0

     • Google Scholar
202. 1. Tita AT
     2. Szychowski JM
     3. Boggess K
     4. Dugoff L
     5. Sibai B
     6. Lawrence K
     7. Hughes BL
     8. Bell J
     9. Aagaard K
     10. Edwards RK
     11. Gibson K
     12. Haas DM
     13. Plante L
     14. Metz T
     15. Casey B
     16. Esplin S
     17. Longo S
     18. Hoffman M
     19. Saade GR

     (2022) Treatment for mild chronic hypertension during pregnancy

     The New England Journal of Medicine 386:1781–1792.

     https://doi.org/10.1056/NEJMoa2201295

     • Google Scholar
203. 1. Tittel SR
     2. Rosenbauer J
     3. Kamrath C
     4. Ziegler J
     5. Reschke F
     6. Hammersen J
     7. Monkemoller K
     8. Pappa A
     9. Kapellen T
     10. Holl RW
     11. Initiative DPV

     (2020) Did the COVID-19 lockdown affect the incidence of pediatric type 1 diabetes in germany?

     Diabetes Care 43:e172–e173.

     https://doi.org/10.2337/dc20-1633

     • Google Scholar
204. 1. Toniolo S
     2. Scarioni M
     3. Di Lorenzo F
     4. Hort J
     5. Georges J
     6. Tomic S
     7. Nobili F
     8. Frederiksen KS
     9. Management Group of the EAN Dementia and Cognitive Disorders Scientific Panel

     (2021) Dementia and COVID-19, a bidirectional liaison: risk factors, biomarkers, and optimal health care

     Journal of Alzheimer’s Disease 82:883–898.

     https://doi.org/10.3233/JAD-210335

     • PubMed
     • Google Scholar
205. 1. Totura AL
     2. Whitmore A
     3. Agnihothram S
     4. Schäfer A
     5. Katze MG
     6. Heise MT
     7. Baric RS

     (2015) Toll-like receptor 3 signaling via TRIF contributes to a protective innate immune response to severe acute respiratory syndrome coronavirus infection

     MBio 6:e00638.

     https://doi.org/10.1128/mBio.00638-15

     • PubMed
     • Google Scholar
206. 1. Touyz RM
     2. Boyd MOE
     3. Guzik T
     4. Padmanabhan S
     5. McCallum L
     6. Delles C
     7. Mark PB
     8. Petrie JR
     9. Rios F
     10. Montezano AC
     11. Sykes R
     12. Berry C

     (2021) Cardiovascular and renal risk factors and complications associated with COVID-19

     CJC Open 3:1257–1272.

     https://doi.org/10.1016/j.cjco.2021.05.020

     • Google Scholar
207. 1. Townsend L
     2. Fogarty H
     3. Dyer A
     4. Martin-Loeches I
     5. Bannan C
     6. Nadarajan P
     7. Bergin C
     8. O’Farrelly C
     9. Conlon N
     10. Bourke NM
     11. Ward SE
     12. Byrne M
     13. Ryan K
     14. O’Connell N
     15. O’Sullivan JM
     16. Ni Cheallaigh C
     17. O’Donnell JS

     (2021) Prolonged elevation of D-dimer levels in convalescent COVID-19 patients is independent of the acute phase response

     Journal of Thrombosis and Haemostasis: JTH 19:1064–1070.

     https://doi.org/10.1111/jth.15267

     • Google Scholar
208. 1. Trasande L
     2. Zoeller RT
     3. Hass U
     4. Kortenkamp A
     5. Grandjean P
     6. Myers JP
     7. DiGangi J
     8. Hunt PM
     9. Rudel R
     10. Sathyanarayana S
     11. Bellanger M
     12. Hauser R
     13. Legler J
     14. Skakkebaek NE
     15. Heindel JJ

     (2016) Burden of disease and costs of exposure to endocrine disrupting chemicals in the european union: an updated analysis

     Andrology 4:565–572.

     https://doi.org/10.1111/andr.12178

     • Google Scholar
209. 1. Trieu C
     2. Sunil B
     3. Ashraf AP
     4. Cooper J
     5. Yarbrough A
     6. Pinninti S
     7. Boppana S

     (2021) SARS-cov-2 infection in hospitalized children with type 1 and type 2 diabetes

     Journal of Clinical & Translational Endocrinology 26:100271.

     https://doi.org/10.1016/j.jcte.2021.100271

     • Google Scholar
210. 1. Trimboli P
     2. Camponovo C
     3. Scappaticcio L
     4. Bellastella G
     5. Piccardo A
     6. Rotondi M

     (2021) Thyroid sequelae of COVID-19: A systematic review of reviews

     Reviews in Endocrine & Metabolic Disorders 22:485–491.

     https://doi.org/10.1007/s11154-021-09653-1

     • Google Scholar
211. 1. Unsworth R
     2. Wallace S
     3. Oliver NS
     4. Yeung S
     5. Kshirsagar A
     6. Naidu H
     7. Kwong RMW
     8. Kumar P
     9. Logan KM

     (2020) New-Onset type 1 diabetes in children during COVID-19: multicenter regional findings in the U.K

     Diabetes Care 43:e170–e171.

     https://doi.org/10.2337/dc20-1551

     • PubMed
     • Google Scholar
212. 1. van Campen CLMC
     2. Verheugt FWA
     3. Rowe PC
     4. Visser FC

     (2020) Cerebral blood flow is reduced in ME/CFS during head-up tilt testing even in the absence of hypotension or tachycardia: a quantitative, controlled study using Doppler echography

     Clinical Neurophysiology Practice 5:50–58.

     https://doi.org/10.1016/j.cnp.2020.01.003

     • PubMed
     • Google Scholar
213. 1. VanElzakker MB

     (2013) Chronic fatigue syndrome from vagus nerve infection: a psychoneuroimmunological hypothesis

     Medical Hypotheses 81:414–423.

     https://doi.org/10.1016/j.mehy.2013.05.034

     • PubMed
     • Google Scholar
214. 1. Vella LA
     2. Giles JR
     3. Baxter AE
     4. Oldridge DA
     5. Diorio C
     6. Kuri-Cervantes L
     7. Alanio C
     8. Pampena MB
     9. Wu JE
     10. Chen Z
     11. Huang YJ
     12. Anderson EM
     13. Gouma S
     14. McNerney KO
     15. Chase J
     16. Burudpakdee C
     17. Lee JH
     18. Apostolidis SA
     19. Huang AC
     20. Mathew D
     21. Kuthuru O
     22. Goodwin EC
     23. Weirick ME
     24. Bolton MJ
     25. Arevalo CP
     26. Ramos A
     27. Jasen CJ
     28. Conrey PE
     29. Sayed S
     30. Giannini HM
     31. D’Andrea K
     32. Meyer NJ
     33. Behrens EM
     34. Bassiri H
     35. Hensley SE
     36. Henrickson SE
     37. Teachey DT
     38. Betts MR
     39. Wherry EJ
     40. UPenn COVID Processing Unit

     (2021) Deep immune profiling of MIS-C demonstrates marked but transient immune activation compared to adult and pediatric COVID-19

     Science Immunology 6:57.

     https://doi.org/10.1126/sciimmunol.abf7570

     • PubMed
     • Google Scholar
215. 1. Vellanki P
     2. Umpierrez GE - Center ofDiabetes and Metabolism, Emory University School of Medicine

     (2021) Diabetic ketoacidosis risk during the COVID-19 pandemic

     The Lancet. Diabetes & Endocrinology 9:643–644.

     https://doi.org/10.1016/S2213-8587(21)00241-2

     • PubMed
     • Google Scholar
216. 1. Verdecchia P
     2. Reboldi G
     3. Cavallini C
     4. Mazzotta G
     5. Angeli F

     (2020) ACE-inhibitors, angiotensin receptor blockers and severe acute respiratory syndrome caused by coronavirus

     Giornale Italiano Di Cardiologia 21:321–327.

     https://doi.org/10.1714/3343.33127

     • PubMed
     • Google Scholar
217. 1. Wallentin L
     2. Lindbäck J
     3. Eriksson N
     4. Hijazi Z
     5. Eikelboom JW
     6. Ezekowitz MD
     7. Granger CB
     8. Lopes RD
     9. Yusuf S
     10. Oldgren J
     11. Siegbahn A

     (2020) Angiotensin-Converting enzyme 2 (ACE2) levels in relation to risk factors for COVID-19 in two large cohorts of patients with atrial fibrillation

     European Heart Journal 41:4037–4046.

     https://doi.org/10.1093/eurheartj/ehaa697

     • PubMed
     • Google Scholar
218. 1. Wang A
     2. Zhao W
     3. Xu Z
     4. Gu J

     (2020) Timely blood glucose management for the outbreak of 2019 novel coronavirus disease (COVID-19) is urgently needed

     Diabetes Research and Clinical Practice 162:108118.

     https://doi.org/10.1016/j.diabres.2020.108118

     • PubMed
     • Google Scholar
219. 1. Wang EY
     2. Mao T
     3. Klein J
     4. Dai Y
     5. Huck JD
     6. Jaycox JR
     7. Liu F
     8. Zhou T
     9. Israelow B
     10. Wong P
     11. Coppi A
     12. Lucas C
     13. Silva J
     14. Oh JE
     15. Song E
     16. Perotti ES
     17. Zheng NS
     18. Fischer S
     19. Campbell M
     20. Fournier JB
     21. Wyllie AL
     22. Vogels CBF
     23. Ott IM
     24. Kalinich CC
     25. Petrone ME
     26. Watkins AE
     27. Yale IMPACT Team
     28. Dela Cruz C
     29. Farhadian SF
     30. Schulz WL
     31. Ma S
     32. Grubaugh ND
     33. Ko AI
     34. Iwasaki A
     35. Ring AM

     (2021) Diverse functional autoantibodies in patients with COVID-19

     Nature 595:283–288.

     https://doi.org/10.1038/s41586-021-03631-y

     • PubMed
     • Google Scholar
220. 1. Watson C

     (2022) Diabetes risk rises after COVID, massive study finds

     Nature 1:e912.

     https://doi.org/10.1038/d41586-022-00912-y

     • PubMed
     • Google Scholar
221. 1. Webster G
     2. Patel AB
     3. Carr MR
     4. Rigsby CK
     5. Rychlik K
     6. Rowley AH
     7. Robinson JD

     (2021) Cardiovascular magnetic resonance imaging in children after recovery from symptomatic COVID-19 or MIS-C: a prospective study

     Journal of Cardiovascular Magnetic Resonance 23:86.

     https://doi.org/10.1186/s12968-021-00786-5

     • PubMed
     • Google Scholar
222. 1. Wei L
     2. Sun S
     3. Xu CH
     4. Zhang J
     5. Xu Y
     6. Zhu H
     7. Peh SC
     8. Korteweg C
     9. McNutt MA
     10. Gu J

     (2007) Pathology of the thyroid in severe acute respiratory syndrome

     Human Pathology 38:95–102.

     https://doi.org/10.1016/j.humpath.2006.06.011

     • PubMed
     • Google Scholar
223. 1. Weisberg SP
     2. Connors TJ
     3. Zhu Y
     4. Baldwin MR
     5. Lin W-H
     6. Wontakal S
     7. Szabo PA
     8. Wells SB
     9. Dogra P
     10. Gray J
     11. Idzikowski E
     12. Stelitano D
     13. Bovier FT
     14. Davis-Porada J
     15. Matsumoto R
     16. Poon MML
     17. Chait M
     18. Mathieu C
     19. Horvat B
     20. Decimo D
     21. Hudson KE
     22. Zotti FD
     23. Bitan ZC
     24. La Carpia F
     25. Ferrara SA
     26. Mace E
     27. Milner J
     28. Moscona A
     29. Hod E
     30. Porotto M
     31. Farber DL

     (2021) Distinct antibody responses to SARS-cov-2 in children and adults across the COVID-19 clinical spectrum

     Nature Immunology 22:25–31.

     https://doi.org/10.1038/s41590-020-00826-9

     • PubMed
     • Google Scholar
224. 1. Wirth KJ
     2. Scheibenbogen C

     (2021) Pathophysiology of skeletal muscle disturbances in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)

     Journal of Translational Medicine 19:162.

     https://doi.org/10.1186/s12967-021-02833-2

     • PubMed
     • Google Scholar
225. 1. Wong SW
     2. Fan BE
     3. Huang W
     4. Chia YW

     (2021) St-Segment elevation myocardial infarction in post-COVID-19 patients: a case series

     Annals of the Academy of Medicine, Singapore 50:425–430.

     https://doi.org/10.47102/annals-acadmedsg.202175

     • PubMed
     • Google Scholar
226. 1. Wostyn P

     (2021) COVID-19 and chronic fatigue syndrome: is the worst yet to come?

     Medical Hypotheses 146:110469.

     https://doi.org/10.1016/j.mehy.2020.110469

     • PubMed
     • Google Scholar
227. 1. Wu D
     2. Yang XO

     (2020) Th17 responses in cytokine storm of COVID-19: an emerging target of JAK2 inhibitor fedratinib

     Journal of Microbiology, Immunology, and Infection = Wei Mian Yu Gan Ran Za Zhi 53:368–370.

     https://doi.org/10.1016/j.jmii.2020.03.005

     • PubMed
     • Google Scholar
228. Preprint

     1. Wu K
     2. Zou J
     3. Chang HY

     (2020) RNA-GPS Predicts SARS-Cov-2 RNA Localization to Host Mitochondria and Nucleolus

     bioRxiv.

     https://doi.org/10.1101/2020.04.28.065201

     • Google Scholar
229. 1. Wu Q
     2. Coumoul X
     3. Grandjean P
     4. Barouki R
     5. Audouze K

     (2021) Endocrine disrupting chemicals and COVID-19 relationships: A computational systems biology approach

     Environment International 157:106232.

     https://doi.org/10.1016/j.envint.2020.106232

     • PubMed
     • Google Scholar
230. 1. Xie Y
     2. Bowe B
     3. Al-Aly Z

     (2021) Burdens of post-acute sequelae of COVID-19 by severity of acute infection, demographics and health status

     Nature Communications 12:6571.

     https://doi.org/10.1038/s41467-021-26513-3

     • PubMed
     • Google Scholar
231. Preprint

     1. Xie Y
     2. Choi T
     3. Al-Aly Z

     (2022) Nirmatrelvir and the risk of post-acute sequelae of COVID-19

     medRxiv.

     https://doi.org/10.1101/2022.11.03.22281783

     • Google Scholar
232. 1. Yaméogo NV
     2. Mbaye A
     3. Kagambèga LJ
     4. Diack B
     5. Pessinaba S
     6. Hakim R
     7. Ndiaye MB
     8. Bodian M
     9. Diao M
     10. Sow DD
     11. Kane M
     12. Kane A

     (2011) Pulmonary embolism mimicking acute anterior myocardial infarction: diagnostic trap

     Annales de Cardiologie et D’angeiologie 60:169–172.

     https://doi.org/10.1016/j.ancard.2010.12.011

     • PubMed
     • Google Scholar
233. 1. Ye Q
     2. Wang B
     3. Mao J

     (2020) The pathogenesis and treatment of the ` cytokine stor’' in COVID-19

     The Journal of Infection 80:607–613.

     https://doi.org/10.1016/j.jinf.2020.03.037

     • PubMed
     • Google Scholar
234. 1. Yong SJ

     (2021) Long COVID or post-COVID-19 syndrome: putative pathophysiology, risk factors, and treatments

     Infectious Diseases 53:737–754.

     https://doi.org/10.1080/23744235.2021.1924397

     • PubMed
     • Google Scholar
235. 1. Yonker LM
     2. Gilboa T
     3. Ogata AF
     4. Senussi Y
     5. Lazarovits R
     6. Boribong BP
     7. Bartsch YC
     8. Loiselle M
     9. Rivas MN
     10. Porritt RA
     11. Lima R
     12. Davis JP
     13. Farkas EJ
     14. Burns MD
     15. Young N
     16. Mahajan VS
     17. Hajizadeh S
     18. Lopez XIH
     19. Kreuzer J
     20. Morris R
     21. Martinez EE
     22. Han I
     23. Griswold K Jr
     24. Barry NC
     25. Thompson DB
     26. Church G
     27. Edlow AG
     28. Haas W
     29. Pillai S
     30. Arditi M
     31. Alter G
     32. Walt DR
     33. Fasano A

     (2021) Multisystem inflammatory syndrome in children is driven by zonulin-dependent loss of gut mucosal barrier

     The Journal of Clinical Investigation 131:e149633.

     https://doi.org/10.1172/JCI149633

     • PubMed
     • Google Scholar
236. 1. Yoshida M
     2. Worlock KB
     3. Huang N
     4. Lindeboom RGH
     5. Butler CR
     6. Kumasaka N
     7. Dominguez Conde C
     8. Mamanova L
     9. Bolt L
     10. Richardson L
     11. Polanski K
     12. Madissoon E
     13. Barnes JL
     14. Allen-Hyttinen J
     15. Kilich E
     16. Jones BC
     17. de Wilton A
     18. Wilbrey-Clark A
     19. Sungnak W
     20. Pett JP
     21. Weller J
     22. Prigmore E
     23. Yung H
     24. Mehta P
     25. Saleh A
     26. Saigal A
     27. Chu V
     28. Cohen JM
     29. Cane C
     30. Iordanidou A
     31. Shibuya S
     32. Reuschl A-K
     33. Herczeg IT
     34. Argento AC
     35. Wunderink RG
     36. Smith SB
     37. Poor TA
     38. Gao CA
     39. Dematte JE
     40. NU SCRIPT Study Investigators
     41. Reynolds G
     42. Haniffa M
     43. Bowyer GS
     44. Coates M
     45. Clatworthy MR
     46. Calero-Nieto FJ
     47. Göttgens B
     48. O’Callaghan C
     49. Sebire NJ
     50. Jolly C
     51. De Coppi P
     52. Smith CM
     53. Misharin AV
     54. Janes SM
     55. Teichmann SA
     56. Nikolić MZ
     57. Meyer KB

     (2022) Local and systemic responses to SARS-cov-2 infection in children and adults

     Nature 602:321–327.

     https://doi.org/10.1038/s41586-021-04345-x

     • PubMed
     • Google Scholar
237. 1. Yousif E
     2. Premraj S

     (2022) A review of long COVID with a special focus on its cardiovascular manifestations

     Cureus 14:e31933.

     https://doi.org/10.7759/cureus.31933

     • PubMed
     • Google Scholar
238. 1. Zachariah U
     2. Nair SC
     3. Goel A
     4. Balasubramanian KA
     5. Mackie I
     6. Elias E
     7. Eapen CE

     (2020) Targeting raised von willebrand factor levels and macrophage activation in severe COVID-19: consider low volume plasma exchange and low dose steroid

     Thrombosis Research 192:2.

     https://doi.org/10.1016/j.thromres.2020.05.001

     • PubMed
     • Google Scholar
239. 1. Zha D
     2. Fu M
     3. Qian Y

     (2022) Vascular endothelial glycocalyx damage and potential targeted therapy in COVID-19

     Cells 11:1972.

     https://doi.org/10.3390/cells11121972

     • PubMed
     • Google Scholar
240. 1. Zhang C
     2. Wu Z
     3. Li JW
     4. Zhao H
     5. Wang GQ

     (2020) Cytokine release syndrome in severe COVID-19: interleukin-6 receptor antagonist tocilizumab may be the key to reduce mortality

     International Journal of Antimicrobial Agents 55:105954.

     https://doi.org/10.1016/j.ijantimicag.2020.105954

     • PubMed
     • Google Scholar
241. 1. Zhao C
     2. Zhao W

     (2020) Nlrp3 inflammasome-A key player in antiviral responses

     Frontiers in Immunology 11:211.

     https://doi.org/10.3389/fimmu.2020.00211

     • PubMed
     • Google Scholar
242. 1. Zhou F
     2. Yu T
     3. Du R
     4. Fan G
     5. Liu Y
     6. Liu Z
     7. Xiang J
     8. Wang Y
     9. Song B
     10. Gu X
     11. Guan L
     12. Wei Y
     13. Li H
     14. Wu X
     15. Xu J
     16. Tu S
     17. Zhang Y
     18. Chen H
     19. Cao B

     (2020) Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study

     The Lancet 395:1054–1062.

     https://doi.org/10.1016/S0140-6736(20)30566-3

     • Google Scholar
243. 1. Zisis SN
     2. Durieux JC
     3. Mouchati C
     4. Perez JA
     5. McComsey GA

     (2022) The protective effect of coronavirus disease 2019 (COVID-19) vaccination on postacute sequelae of COVID-19: A multicenter study from A large national health research network

     Open Forum Infectious Diseases 9:fac228.

     https://doi.org/10.1093/ofid/ofac228

     • PubMed
     • Google Scholar
244. 1. Zou X
     2. Chen K
     3. Zou J
     4. Han P
     5. Hao J
     6. Han Z

     (2020) Single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to 2019-ncov infection

     Frontiers of Medicine 14:185–192.

     https://doi.org/10.1007/s11684-020-0754-0

     • PubMed
     • Google Scholar