Nidovirales

Nidoviruses form a phylogenetically compact but diverse group of enveloped positive-stranded RNA viruses with the largest RNA genome known. They infect a broad range of hosts, including humans, other mammals, birds, fish, and shrimp. Nidovirus infection starts by binding to a receptor on the cell surface, and fusion of the viral and cellular membranes mediated by one of the major surface glycoproteins. Following genome uncoating, the translation of the two overlapping replicase open reading frames (ORFs) yields two large polyprotein precursors that undergo autoproteolysis to produce the mature nonstructural proteins that eventually assemble into a membrane-bound, replication–transcription complex. The complex, which also contains several cellular proteins, mediates negative-strand RNA synthesis, amplification of the genome RNA, and production of a nested set of subgenomic messenger RNAs (sg mRNAs). Whereas nidovirus genome replication proceeds through the synthesis of a full-length negative-strand RNA, transcription involves the synthesis of subgenome-length, negative-strand templates for mRNA synthesis. In arteriviruses and coronaviruses, and probably bafiniviruses, transcription involves a mechanism of discontinuous negative-strand synthesis (template switch) to equip each subgenomic RNA with a 5′ common leader sequence identical to the genomic 5′ end. Except for the largest torovirus sg RNA, torovirus and ronivirus sgRNAs do not share such a common leader sequence and discontinuous RNA synthesis does not appear to be involved in this case. New nidovirus particles are assembled in the cytoplasm. There is increasing evidence that nidovirus infections modify a variety of host cell functions and structures, and induce a variety of immune and stress responses.