C — Coronaviruses
Coronaviruses are enveloped, positive-sense single-stranded RNA viruses with the largest known RNA viral genomes (~30 kb). Their spike (S) glycoprotein mediates receptor binding and fusion. For example, SARS-CoV-2 uses ACE2 and TMPRSS2 for entry into cells.
Replication occurs in the cytoplasm within double-membrane vesicles derived from the endoplasmic reticulum. A viral RNA-dependent RNA polymerase synthesizes full-length genomes and subgenomic mRNAs via discontinuous transcription. Notably, coronaviruses encode a proofreading exonuclease (nsp14), which enhances replication fidelity compared to other RNA viruses.
Pathogenesis involves both viral cytopathic effects and dysregulated host immune responses. Early infection targets respiratory epithelium. Severe disease is associated with hyperinflammation, endothelial dysfunction, thrombosis, and impaired interferon responses. Viral proteins such as nsp1 and ORF6 antagonize innate immunity.
Clinically, coronaviruses range from endemic strains causing mild upper respiratory infections to highly pathogenic strains (SARS-CoV, MERS-CoV, SARS-CoV-2) causing pneumonia, ARDS, and multisystem involvement. Research areas include spike evolution, zoonotic spillover, antiviral targets (e.g., polymerase inhibitors), and long-term sequelae such as post-acute COVID syndromes.
Coronaviruses are enveloped, positive-sense single-stranded RNA viruses with the largest known RNA viral genomes (~30 kb). Their spike (S) glycoprotein mediates receptor binding and fusion. For example, SARS-CoV-2 uses ACE2 and TMPRSS2 for entry into cells.
Replication occurs in the cytoplasm within double-membrane vesicles derived from the endoplasmic reticulum. A viral RNA-dependent RNA polymerase synthesizes full-length genomes and subgenomic mRNAs via discontinuous transcription. Notably, coronaviruses encode a proofreading exonuclease (nsp14), which enhances replication fidelity compared to other RNA viruses.
Pathogenesis involves both viral cytopathic effects and dysregulated host immune responses. Early infection targets respiratory epithelium. Severe disease is associated with hyperinflammation, endothelial dysfunction, thrombosis, and impaired interferon responses. Viral proteins such as nsp1 and ORF6 antagonize innate immunity.
Clinically, coronaviruses range from endemic strains causing mild upper respiratory infections to highly pathogenic strains (SARS-CoV, MERS-CoV, SARS-CoV-2) causing pneumonia, ARDS, and multisystem involvement. Research areas include spike evolution, zoonotic spillover, antiviral targets (e.g., polymerase inhibitors), and long-term sequelae such as post-acute COVID syndromes.