Coronaviruses in the Limelight

Abstract

For ∼ years after their first description by Tyrrell and Byneo in 1965 [1], the field of human coronaviruses (HCoVs) was pretty dull. There were classic early descriptions of their respiratory pathogenicity in volunteer studies [2, 3], and there were seroepidemiologic studies of the 2 most easily studied strains, HCoV-229E and HCoV-OC43 [4–6]. Efforts to implicate HCoVs in diseases of the gastrointestinal tract were largely unsuccessful, with the possible exception of a postulated role in necrotizing enterocolitis of newborns [7]. During this time, the fields of animal CoVs and of the molecular biology of CoVs were, in contrast, buzzing. CoVs were discovered in large numbers and were implicated in a rich variety of animal diseases in multiple species. Diseases as widely varying as progressive peritonitis, nephritis, acute and chronic hepatitis, and subacute encephalitis were described, along with the more traditional respiratory and gastrointestinal syndromes, and pathogenesis was explained through broad mixtures of viral cytopathogenicity, immunologic damage, and genetic susceptibilities. The CoV genome proved to be the largest of all of the RNA viruses and to have a unique strategy of replication, with transcription and protein production occurring through a nested set of mRNA molecules [8].