The molecular microenvironment of coronaviral replicase complexes provides functional and spatial links between conserved cellular processes and viral RNA synthesis, and highlights potential targets for the development of novel antivirals.
Phylogenetic and computational methods reveal that at least two seasonal coronaviruses are evolving adaptively in the region of the viral spike protein exposed to the human humoral immune system.
The HCoV-229E coronavirus S-protein accommodates extensive mutational change and possesses hydrophilic subunit interfaces in the S2 region, features that provide new insights into immune evasion, cross-species transmission and membrane fusion.
SARS-CoV-2 has evolved to cleverly mimic the FURIN-cleavage site in human ENaC-α, unlike any prior coronavirus strain, shedding new light on the Acute Respiratory Distress Syndrome (ARDS) in COVID-19 patients.
SARS-CoV-2 receptor ACE2 is expressed in nasal olfactory epithelia, tongue keratinocytes and small intestine enterocytes, connected with the COVID-19 patient phenotypes such as anosmia and diarrhea.
MERS-CoV infections in the Arabian Peninsula are the result of several hundred spillover events from viruses circulating in camels into the human population.
Key numbers about the biology of the SARS-CoV-2 virus and the infection of a single human host by the virus have been compiled from the peer-reviewed literature.
A high-throughput microscopy screen for drugs that modulate SARS-CoV-2 spike-mediated membrane fusion identifies an essential role for cholesterol in both virus entry and syncytia formation.
Gene expression analysis reveals a novel, integrated molecular mechanism for much of the pathogenesis of COVID-19 that provides therapeutic intervention points that can be addressed with existing approved pharmaceuticals.
