Probably all coronaviruses replicate in epithelial cells of the respiratory and/or enteric tracts, though not necessarily producing clinical damage at those sites. Avian 1BV not only causes respiratory disease but can also damage gonads in both females and males, and causes serious kidney disease (dependent on the strain of virus, and to some extent on the breed of chicken). 1BV is able to replicate at virtually every epithelial surface in the host. Some coronaviruses have their most profound effect in the alimentary tract (e.g., porcine TGEV causes >90% mortality in neonatal pigs). Human coronaviruses are known to be associated with enteric and respiratory diseases (e.g., diarrhea), in addition to respiratory disease. SARS-CoV was also associated with diarrhea in humans, in addition to serious lung disease. Other coronaviruses, for example, MHV and porcine HEV, spread to cells of the central nervous system, producing disease, for example, acute or chronic demyelination in the case of MHV.
Coronavirus replication and disease are not necessarily restricted to a single host species. Canine enteric CoV and feline CoV can replicate and cause disease in pigs; these two viruses have proteins with very high amino acid identity to those of porcine TGEV. Canine respiratory CoV has proteins, including the S protein (which is the attachment protein and a determinant of host range), with very high amino acid identity (>95%) to other group 2 viruses Hu CoV-OC43 and BCoV. This raises the possibility of co-infection in these hosts. Bovine CoV causes enteritis in turkeys following experimental oral infection. There is evidence that pheasant CoV can infect chickens, and 1BV infect teal (a duck), though without causing disease. The most dramatic demonstration that corona-viruses can have a wide host range was provided by SARS-CoV. This may have had its origin in bats, was transferred to various other species (e.g., civet cat) that were captured for trade, and then caused lethal disease in humans.
Persistent infections in vivo are well known for MHV, and less well known for other coronaviruses (e.g., 1BV). Following infection of very young chickens, 1BV is re-excreted when hens start to lay eggs. The trigger for release is probably the stress of coming into lay
The S protein is a determinant of both tissue tropism within a host and host range. This has been elegantly demonstrated by genetic manipulation of the genome of MHV, which is unable to attach to feline cells. Replacement of the MHV S protein gene with that of CoV from feline coronavirus resulted in a recombinant virus that was able to attach, and subsequently replicate in, feline cells. However, other proteins can also affect pathogenicity. Research with genetically modified coronaviruses, using targeted recombination or 'infectious clones', has shown that modifications to proteins encoded in ORF1 and the small genes interspersed among the structural protein genes, result in attenuation of pathogenicity. Although the roles of these 'accessory proteins' are not known, this may offer a route to the development of a new generation of live vaccines. Currently, the most widely used prophylactics for control of 1BV in chickens include killed vaccines and live vaccines attenuated by passage in embryonated eggs. However, disease control is complicated by extensive variation in the S1 protein which is the inducer of protective immunity.
See also: Nidovirales.
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