The role of co-infection in the pathogenesis of acute SARS-CoV-2 infection and development of post-acute sequelae: A perspective

Infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) may lead to persistent symptoms and sequelae that range from mild impairment of daily activities to severe long-term disability or death (Seeßle et al., 2022; Peluso et al., 2022c; Yang et al., 2022; Peluso and Deeks, 2022a; Mehandru and Merad, 2022). These symptoms, which relate to one or more organ systems and may be ongoing, relapsing, or new, define a multi-syndromic entity referred to as post-acute sequelae of SARS-CoV-2 infection (PASC). The World Health Organization describes PASC (or ‘long COVID’ or ‘post-COVID-19’) as a condition occurring in individuals with a history of probable or confirmed SARS-CoV-2 infection, 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 (https://www.who.int/europe/news-room/fact-sheets/item/post-covid-19-condition). The US National Academies (National Academies of Sciences E, and Medicine et al., 2024) describe long COVID as a set of signs, symptoms, and conditions that continue or develop after initial infection, are present for 4 weeks or more, may be multisystemic, and present with relapsing-remitting patterns. Sequelae associated with other viral infections include the induction by infection of antibodies that enhance disease after subsequent reinfections, as is the case with dengue virus infections (Katzelnick et al., 2017). During the first months of the COVID-19 pandemic, the possibility of antibody-dependent enhancement (ADE) of disease associated with SARS-CoV-2 antibodies was a major concern for vaccine development. In fact, ADE has been documented for SARS-CoV-1 infections in laboratory and animal studies (Karthik et al., 2020). Nevertheless, there have been no documented cases of ADE in humans infected with SARS-CoV-2. The possibility that ADE might be involved in some of the PASC symptoms is therefore quite remote.

The worldwide burden of PASC is staggering: estimates of its incidence have ranged between 65 and 400 million by the end of 2023 (Davis et al., 2023). Although they incorporate risk reductions associated with roll-out of COVID-19 vaccines and reduced virulence of infection with newer SARS-CoV-2 strains (Al-Aly et al., 2022; Antonelli et al., 2022; Cortellini et al., 2023), these estimates may be conservative as they only represent cases arising from symptomatic infection (Davis et al., 2023). Given the burden, the potential effects of PASC on health, quality of life, and life expectancy are of concern worldwide. Finding causative or exacerbating mechanisms of PASC should be a public health priority.

PASC is of unknown etiology, presents heterogeneous clinical phenotypes, potentially impacts multiple organs, and is likely multifactorial. Affected organ systems include the neurological system, the gastrointestinal system, heart, lung, pancreas, and the reproductive system (Davis et al., 2023). Other organs, as well as blood vessels and the immune system, may also be affected (Davis et al., 2023; Altmann et al., 2023). While emerging data point to various major potential drivers of PASC (Peluso and Deeks, 2022a; Mehandru and Merad, 2022; Davis et al., 2023; Castanares-Zapatero et al., 2022), several causative hypotheses of PASC involve microbes or microbial products. For example, SARS-CoV-2 itself may persist in tissues after extrapulmonary viral dissemination during acute infection, resulting in lasting antigenic stimulus, inflammation, aberrant immune responses, and tissue damage (Altmann et al., 2023; Swank et al., 2023; Natarajan et al., 2022; Peluso et al., 2022b; Cheung et al., 2022; Acosta-Ampudia et al., 2022; Peluso et al., 2021b; Phetsouphanh et al., 2022). In addition to SARS-CoV-2, reactivation of latent viruses such as Epstein-Barr virus (EBV) and herpes simplex or herpes zoster viruses may be associated with PASC. Additionally, gut microbial dysbiosis and subsequent bacterial translocation to liver or other organs can lead to sustained inflammation, immune dysregulation, and tissue damage (Davis et al., 2023; Altmann et al., 2023; Peluso et al., 2023; Giron et al., 2022; Gold et al., 2021; Klein et al., 2023; Su et al., 2022; Grobbelaar et al., 2021; De Michele et al., 2022; Zuo et al., 2020). Moreover, it is well documented that co-infections exacerbate the severity of acute SARS-CoV-2 infection and worsen its outcome (Musuuza et al., 2021; Patton et al., 2023; Feldman and Anderson, 2021; Sreenath et al., 2021). Thus, it is tempting to consider the possibility that acute and chronic infectious diseases occurring prior to, during, or after acute SARS-CoV-2 infection may contribute to PASC development and phenotypic presentation. Understanding microbial contribution to PASC might dramatically improve our capabilities to diagnose and treat PASC, and to prevent it.

In this review, we outline how various viral, bacterial, and fungal co-infections may induce or facilitate the development of PASC. To do so, we use the current, limited evidence on the association between PASC and certain co-infections (mostly viral), the current knowledge on the impact of viral, bacterial, and fungal infections on the severity of acute SARS-CoV-2, and biological plausibility criteria derived from our collective understanding of the pathogenesis of various infectious diseases. While, as of this writing, all possible associations we discuss are within the realm of biological plausibility, they are, of necessity, speculative, and compelling evidence for a causal association of PASC with any microbial infection remains to be obtained. Here, our goal is to present the current state of understanding of the candidate microorganisms in the context of SARS-CoV-2 infection in the hope of stimulating and informing future research into this still mysterious and often debilitating condition. While changes in the composition of commensal microbiota may also be related to PASC, the potential role of dysbiosis in PASC has already been discussed in many reviews (e.g. Raj et al., 2024; Guo et al., 2023; Norouzi Masir and Shirvaliloo, 2022), requires specific considerations and is not included in the present review.

Although some forms of PASC were first reported in the very early stages of the pandemic (Callard and Perego, 2021), the changing epidemiology of infectious diseases throughout the world during and after the COVID-19 pandemic suggests that other pathogens may have contributed to the pathophysiology of PASC. For example, 44 countries have experienced a 10-fold increase in the incidence of at least 13 infectious diseases relative to the pre-pandemic baseline (http://www.airfinity.com/articles/global-surge-in-infectious-diseases-as-over-40-countries-report-outbreaks-10). Several non-mutually exclusive explanations have been proposed for this phenomenon (Figure 1). First, interruptions of public health measures may explain the emergence of some infections. For example, declining vaccine rates during the pandemic due to disrupted supply chains and limited immunization are likely to be major factors for increases in measles, polio, and whooping cough. Similarly, increases in tuberculosis cases may be related to the collapse of public health infrastructure, resulting in delayed diagnosis and treatment and failure of infection control measures (reviewed in Marco et al., 2024). Second, immune mechanisms may have contributed to a dramatic increase in respiratory viral infections, particularly in children (Rubin, 2024). One mechanism, popularized as ‘immunity theft’, describes a period of increased vulnerability to other infections following acute SARS-CoV-2 infection (Rubin, 2024). This mechanism is not only possible but probable, given that hyperinflammation of various microbial or viral origin is often followed by a period of immune suppression (Biswas and Lopez-Collazo, 2009; Libbey and Fujinami, 2002) and that PASC in children has been reported to give rise to prolonged periods of innate immune hyporesponsiveness (Khan et al., 2025). An alternative mechanism, known as ‘immunity debt’, which postulates a rebound of infections following a period of reduced exposure during lockdowns, widespread masking, and social distancing, has lost scientific support in favor of immune dysfunction hypotheses (Needle and Russell, 2023). Third, changes in temperature and rainfall patterns due to climate change may enable the spread of water- and mosquito-borne diseases such as cholera and dengue (Feinmann, 2024). A link between climate change and COVID-19 itself has been proposed (Ford et al., 2022), the implications of which are beyond the scope of the present article.

Figure 1

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While causal links between the emergence of other viral and bacterial infections and the development of PASC have yet to be established, it is possible that the interactions of SARS-CoV-2 and other pathogens lead to PASC either directly or indirectly. For example (and as discussed below in more detail), SARS-CoV-2-induced immune dysregulation may increase susceptibility to other infections. Conversely, increased incidence of other infections may directly induce organ dysfunction or elicit immune dysregulation, leading to persistence of SARS-CoV-2 in the tissues. Regardless of the responsible mechanisms, further study of the interactions of SARS-CoV-2 and other pathogens, and their role in the development of PASC, is warranted.

Below, we briefly review current evidence on the role of SARS-CoV-2 persistence in tissues as a driver of PASC (Figure 2, top row). In the following sections, we discuss how, in the presence or absence of persistent SARS-CoV-2, other microorganisms may favor the development of PASC or exacerbate its severity. The discussion of causative relationships between PASC and co- or secondary infections requires considering multiple and intertwined elements. These include: (i) the type of co-infection (e.g. acute vs chronic, de novo infection vs reactivation of latent infection); (ii) mechanisms of pathogenesis, i.e., how infection with other agents may favor PASC development or worsen its severity and duration; (iii) temporal relationships, i.e., when co- or secondary infections have occurred relative to the acute SARS-CoV-2 infection, and (iv) the anatomical location of the infection.

Figure 2

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SARS-CoV-2 is transmitted through respiratory droplets and targets ciliated epithelial cells in the nasal cavity, trachea, and lungs by utilizing the cellular receptor angiotensin-converting enzyme 2 (ACE2) (Ahn et al., 2021; Jayaweera et al., 2020; Lamers and Haagmans, 2022; Jackson et al., 2022; Fraser et al., 2023). Infection limited to the upper respiratory tract is generally associated with milder disease outcomes, whereas dissemination to the lungs, in particular infection of the bronchi, bronchioles, and alveoli, can cause pneumonia, severe disease, acute respiratory distress syndrome, and death (Lamers and Haagmans, 2022). In addition, infected cells can be found in many other tissues throughout the body, particularly in vascular tissues. Studies in humans have described roles for type I and III interferons (IFNs), inflammatory cytokines (IL-6, TNF-α, IL-1β), innate immune cells (monocytes, pDCs, cDCs, natural killer cells), antibodies (IgG, sIgA, neutralizing antibodies), and adaptive immune cells (B cells, CD8⁺ and CD4⁺ T cells) in both pathogenesis and clearance of SARS-CoV-2 infection within the respiratory tract (Sievers et al., 2024; Harne et al., 2023).

The term infection can have a wide-ranging definition when referring to cells or tissues that harbor SARS-CoV-2 virus. This ambiguity often leads to varying interpretations of whether persistent SARS-CoV-2 infection is the cause of PASC symptoms. The definition of infection is rooted in the concept of tropism, which refers to the ability of a virus to infect a particular cell type or tissue. SARS-CoV-2 infection itself requires that a cell type expresses the ACE2 receptor, which can be ubiquitously expressed on cells within the respiratory tract and extrapulmonary tissues (Hamming et al., 2004; Ortiz et al., 2020). Historically, scientists relied on a rigorous definition of infection, which involved demonstrating the production of a virus in a cell type either by measurement of infectious virus (e.g. plaque assay, focus forming assay, outgrowth assay) or electron microscopy to visualize virions. These techniques are often difficult to perform or require specialized facilities/equipment. Alternatively, infection is defined in the literature by the presence of viral antigen, viral RNA using in situ hybridization or highly sensitive quantitative reverse transcription PCR (qRT-PCR), or viral sequencing. With these now routine, but less rigorous definitions, caution must be taken to avoid over-interpreting the impact that infection can have on PASC symptoms. For instance, viral antigen can persist for several weeks to months without any active virus replication in cells. Similarly, qRT-PCR or viral sequencing data can be from residual RNA in a particular cell type or tissue that has yet to be cleared following infection. In this section, we will look at findings within the respiratory tract in the context of acute and persistent SARS-CoV-2 infection.

To better understand SARS-CoV-2 persistence, it is important to consider the known cellular targets of SARS-CoV-2 during acute infection. Extensive studies using in vitro and in vivo (e.g. mice, hamsters, and nonhuman primates) infection models and specimens from infected humans have identified key cellular targets of SARS-CoV-2 infection. In the upper respiratory tract, SARS-CoV-2 infects the olfactory epithelium, mainly sustentacular cells, which can result in its rapid and gross desquamation (Khan et al., 2021; Verma et al., 2022). The resulting anosmia, defined by the loss of the senses of smell and taste, was described early in the pandemic and recognized as a profound neurological manifestation of COVID-19 (Tsukahara et al., 2023). A recent study suggests that a transition from the olfactory to the respiratory epithelium from the ancestral variants (e.g. WA1 and Delta) to the Omicron variants may account for the reduced incidence of anosmia in the Omicron era (Chen et al., 2024). Within the trachea, SARS-CoV-2 can infect epithelial cells of the mucosa, including goblet, ciliated, and basal cells. In the lungs, SARS-CoV-2 infects epithelial cells of the bronchi/bronchioles, including basal, ciliated, type II pneumocytes (ATII), and club cells (Hou et al., 2020). Other studies have identified macrophage subsets, including interstitial macrophages and alveolar macrophages, as potential targets of infection based on the presence of viral antigen or viral RNA (Huot et al., 2023; Wu et al., 2024). However, this observation may be a result of either phagocytosed infected cell debris or abortive infection, defined by a likely block in virus replication. The impact of SARS-CoV-2 infection of macrophages is not yet clear but may lead to dysregulated airway repair mechanisms (Wendisch et al., 2021). Macrophages have also been identified as potential targets of persisting SARS-CoV-2 (Huot et al., 2023).

The persistence of SARS-CoV-2 spike protein several months after a PCR-confirmed test has become a central tenet in the pathology of PASC. In a RECOVER-led multi-cohort study, SARS-CoV-2 spike can be detected in the blood for up to 14 months with around 50% of those experiencing persistent cardiopulmonary, musculoskeletal, and neurological symptoms also showing spike in the blood (Swank et al., 2024). It is also important to note that around 20% of asymptomatic individuals also showed circulating spike for up to 7 months post-recovery. It is not clear from this study whether a delay in viral clearance within the lungs or viral persistence in extrapulmonary tissues is the cause of persistent spike antigen in the blood. Autopsy studies have observed SARS-CoV-2 antigen and viral RNA in several extrapulmonary tissues, central nervous system, and the brain (Stein et al., 2022; Deinhardt-Emmer et al., 2021; Maffia-Bizzozero et al., 2023; Pesti et al., 2023). A longitudinal cohort study found that persistent inflammation characterized by type II interferon signaling and neutrophil activation was observed in individuals experiencing SARS-CoV-2 symptoms for more than 2 months (Talla et al., 2023).

Various types of co-infection (i.e. those coincident with active SARS-CoV-2) may be implicated in the development or exacerbation of PASC. These include:

• acute infections by respiratory or other pathogens (e.g. influenza virus, respiratory syncytial virus [RSV], measles virus, adenovirus, Staphylococcus aureus, streptococci, Hemophilus spp., Moraxella spp., Klebsiella pneumoniae, Acinetobacter, Pseudomonas, Aspergillus).

• chronic infections (e.g. human immunodeficiency virus [HIV], cytomegalovirus [CMV], tuberculosis) and reactivation of latent infections (e.g. EBV, varicella zoster virus [VZV], or latent tuberculosis).

Our in-depth understanding of the pathogenesis of many infectious diseases points to the biological plausibility of various direct pathophysiological mechanisms such as PASC drivers. For example, co-infections may predispose to PASC development by inducing altered organ function, immune dysregulation, autoimmunity, and organ damage (Box 1). Of note, noxious effects may be reciprocal, with pre-existing and concurrent co-infections worsening SARS-CoV-2 infection outcome and post-acute sequelae, and SARS-CoV-2 infection increasing the risk of superinfections during acute COVID-19 and post-acute secondary infections. While this is a burgeoning area of research, few studies have been able to make causal links between co-infections and PASC pathology. The following section is speculative, but we highlight how temporal and anatomical locations, as well as chronic infections, may influence the development of PASC.

Infection with any pathogen – may it be viruses, bacteria, and/or fungi – may precede, occur concurrently with (or soon after), or follow the onset of acute SARS-CoV-2 infection (Figure 2). Development of PASC may be induced or facilitated by pre-existing and/or latent infections, via dysregulated immune responses and/or dysfunctional organ systems. New infections and reactivation of latent infections that develop during (or soon after) acute SARS-CoV-2 infection may potentiate PASC by worsening histopathology and/or immune dysregulation. Furthermore, new or reactivated secondary infections may occur in the weeks or months following SARS-CoV-2 infection. In this case, it may be envisioned that SARS-CoV-2-induced immune dysregulation increases susceptibility to secondary infections or that, conversely, the effects of SARS-CoV-2 infection are exacerbated by immune dysregulation by ensuing infections, or both.

An additional set of considerations relates to anatomical location. As mentioned above, PASC may target various end organs such as the lungs, heart, and brain (Altmann et al., 2023). The lungs are a primary target organ during SARS-CoV-2 infection, and respiratory symptoms are important sequelae of PASC. It stands to reason, therefore, that respiratory infections due to other pathogens, including viruses, bacteria, and fungi, may modify risk factors for the development of PASC (Figure 3). For example, pre-existing acute or chronic inflammation, tissue damage, or impaired lung function may predate SARS-CoV-2 infection. Similarly, concurrent or post-acute co-infection with other pathogens may result in worsened inflammation, immunosuppression, immune dysregulation, or exacerbated tissue damage. In turn, these co-infections may then predispose to the development of respiratory PASC and associate dyspnea, fatigue, and cough. Below, we discuss some of the respiratory pathogens that may most conceivably contribute to PASC development.

Figure 3

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PASC may also be characterized by systemic symptomatology and/or the involvement of multiple organs. This is particularly relevant, since the ACE2 receptor, which is the cellular receptor by which SARS-CoV-2 enters cells, is widely distributed throughout the body. Systemic co-infections may play a causative/facilitating role in at least two different ways. One is by damaging mucosal barriers, with consequent microbial translocation and subepithelial immune activation, leading to systemic inflammation, endothelial damage, and compromised organ systems. The example of intestinal co-infections (or changes in gut microbiota) and gut lining damage as PASC drivers is depicted in Figure 4A, but systemic disease caused by bacterial and angioinvasive fungal infections (discussed above) could drive similar changes.

Figure 4

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Another mechanism of pathogenesis of systemic PASC relates to the reactivation of latent viruses, such as EBV. It can be envisioned that SARS-CoV-2 infection may facilitate EBV reactivation in the Peyer’s patches in the gut (Figure 4A) or in lymphoid tissue elsewhere (Figure 4B), resulting in either viral shedding and direct tissue damage, systemic damage secondary to EBV-induced immune dysregulation or pathogenic transformation of B cells that may traffic to anatomical regions outside the areas of initial viral reactivation (Figure 4B). Thus, co-infections may be drivers of PASC, either at the site of infection or systemically, and induce a wide range of clinical phenotypes.

Animal models, including mice, hamsters, and nonhuman primates (NHPs), have been used to study the pathogenesis, immunity, transmission, and protection against SARS-CoV-2 infection. These models have been essential for preclinical development and testing of countermeasures, which include vaccines, monoclonal antibodies, and direct-acting antivirals (Boras et al., 2021; Corbett et al., 2020; Guebre-Xabier et al., 2020; Hansen et al., 2020; He et al., 2021; Pruijssers et al., 2020; Tian et al., 2021; van Doremalen et al., 2020; Vogel et al., 2021).

Mice, hamsters, and NHPs have been used to define the contributions of the innate immune response, including type I IFNs, pro-inflammatory and anti-inflammatory cytokines (IL-6, TNF-α, IL-1β, IL-10, IL-2), and innate cell-mediated responses (macrophages, monocytes, neutrophils, eosinophils, natural killer cells), and the adaptive immune response (humoral, B cells, and T cells) in modulating protection against SARS-CoV-2 (Case et al., 2025). These animal models are now being leveraged to replicate facets of long COVID and serve as platforms for mechanistic studies and therapeutic development. Several review articles have been published describing animal models of gastrointestinal, neurological, and cardiovascular PASC and will not be discussed in this review (Vanderheiden and Diamond, 2025; Chung et al., 2025; Dai et al., 2025). We highlight how animal models are being used to study pulmonary sequelae and viral persistence.

Pulmonary sequelae, such as lung fibrosis and chronic inflammation, have been prominently observed during the recovery phase following SARS-CoV-2 infection of mice. For instance, infection of standard laboratory strains with a mouse-adapted SARS-CoV-2 strain (MA10) has been shown to cause chronic pulmonary epithelial and immune cell dysfunction with fibrosis, as well as sustained lung inflammation, injury, and airway wall thickening (Dinnon et al., 2022). Sustained neutrophil activation and extracellular trap formation (Giannakopoulos et al., 2024), complement (Perico et al., 2023), dysregulated macrophage-CD8⁺ T cell signaling axis (Narasimhan et al., 2024), and fibroblast-intrinsic CD147 (Wu et al., 2022) have been shown to contribute to SARS-CoV-2-induced progressive pulmonary fibrosis. Further, therapeutics including antivirals and monoclonal antibodies have been shown to reduce lung fibrosis and disease severity (Dinnon et al., 2022; Wu et al., 2022; Kolloli et al., 2023; Zhang et al., 2024).

Persistent SARS-CoV-2 reservoirs that remain hidden in various tissues have been postulated to drive chronic inflammation and symptoms long after acute infection. One of the challenges with animal models is that SARS-CoV-2 is rapidly cleared following acute infection, which has made it difficult to study viral persistence. CD4⁺ and CD8⁺ T cells have been shown to be recruited to the upper and lower respiratory tract following SARS-CoV-2 infection in mice (Kar et al., 2024). Antibody-based depletion of T cells resulted in persistent infectious virus in the upper respiratory tract, but not lungs, for more than a month. This finding demonstrates that T cells are required for preventing viral persistence in the respiratory tract. Treatment with antivirals cleared viral persistence in the upper respiratory tract (Lieber et al., 2024). In a reductionist model, intravenous delivery of the SARS-CoV-2 spike protein led to neuroinflammation within the skull-meninges-brain axis and induced anxiety-like behavior in mice (Rong et al., 2024).

Animal models should continue to be used to develop deeper mechanistic insight to the pathophysiology of PASC. There are many factors that should be considered, including age, sex, host genetics, immunological status (e.g. pre-existing vaccine or infection-induced immunity), metabolic state, sequential and/or co-infections with other heterologous pathogens, obesity, and diabetes. We should attempt to use models that appropriately recapitulate acute infection, pathogenesis, immune responses, and recovery observed in humans.

Here, we reviewed data regarding the interactions of pathogenic microorganisms with SARS-CoV-2 infection and the possibility that co-infections are associated with the development of PASC. Co-infections important to PASC can be pre-existing, reactivated during or after acute infection, or infect de novo along a wide time range. The relationship between SARS-CoV-2 and other co-infecting microorganisms may be multifaceted. On one hand, SARS-CoV-2 infection might exacerbate immunological dysfunctions caused by previous infections with other pathogens. On the other hand, immune dysregulation and tissue damage during SARS-CoV-2 infection might trigger reactivation of latent infections or predispose to severe disease from the subsequent encounter with other pathogens. In addition, co-infections might trigger severe manifestations and sequelae of SARS-CoV-2 infection that may not occur in the absence of co-infection. Moreover, various co-infections might have different consequences for PASC manifestations. Depending on the pathogen, the time between infections, and the presence of other predisposing host and environmental factors, co-infection-related effects may be organ-specific and/or have systemic implications, giving rise to a wide spectrum of sequelae of SARS-CoV-2 infection and diverse PASC symptoms. Given the multitude of clinical phenotypes and potential mechanistic drivers, small epidemiological and tissue or blood-based mechanistic studies are insufficient to demonstrate the causal roles of any given co-infection in PASC development. As a result, these studies should be complemented with large longitudinal studies, such as the RECOVER initiative, which have the potential to assess the association of various co-infections with PASC or specific PASC phenotypes across a wide cross-section of the population. A better understanding of pathogen-specific associations of co-infections with PASC will be critical in the development of appropriate diagnosis of long COVID patients. This, in turn, will help find PASC therapies tailored according to the specific underlying mechanism.

Due to the large heterogeneity of PASC phenotypes and the various co-variates that might drive them, including co-morbidities, genetic predisposition, previous exposure to various agents, and, as discussed in this manuscript, co-infections, we propose a framework to best conduct PASC research, which allows for informed comparisons among studies, so that advances can be achieved leading to specific therapies for the affected patients (Box 2). This framework involves the participation of clinicians, microbiologists, immunologists, pathologists, statisticians, bioinformaticians, machine learning and AI experts, patient advocates, regulators, and funders to ensure not only that samples are collected from large longitudinal studies, such as the RECOVER initiative, but also that the appropriate information is collected to address the multiple variables that can drive PASC symptoms, and that samples are analyzed in a comprehensive and comparative way to best establish correlates of disease and to generate hypotheses to further investigate possible therapies. With this framework, clinical trials targeting specific mechanisms identified in subsets of PASC patients, related or not related to co-infections, are likely to be more informative than clinical trials in PASC patients without a clear hypothesis on the underlying causes of their symptoms. In this respect, the development of animal models of PASC that investigate the impact of co-infections will also be of significant help for the discovery of preventive measures and therapies to mitigate the sequelae associated with SARS-CoV-2 infection. The implementation of adequate clinical strategies based on a better understanding of the factors associated with PASC, including the impact of co-infections, will pave the way for finding treatments that mitigate the development of PASC.

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