Date Published: July 31, 2011
Publisher: Hindawi Publishing Corporation
Author(s): Sophie Le Poder.
A new human coronavirus responsible for severe acute respiratory syndrome (SARS) was identified in 2003, which raised concern about coronaviruses as agents of serious infectious disease. Nevertheless, coronaviruses have been known for about 50 years to be major agents of respiratory, enteric, or systemic infections of domestic and companion animals. Feline and canine coronaviruses are widespread among dog and cat populations, sometimes leading to the fatal diseases known as feline infectious peritonitis (FIP) and pantropic canine coronavirus infection in cats and dogs, respectively. In this paper, different aspects of the genetics, host cell tropism, and pathogenesis of the feline and canine coronaviruses (FCoV and CCoV) will be discussed, with a view to illustrating how study of FCoVs and CCoVs can improve our general understanding of the pathobiology of coronaviruses.
Coronaviruses are enveloped viruses with a large (27–32 kb) single-stranded, positive-sense RNA . The genome includes at least 6 open reading frames (ORFs) flanked by 5′ and 3′ untranslated regions. The viral RNA is packaged by the nucleocapsid protein (N), which are themselves enclosed in an envelope containing at least three virally-encoded membrane proteins: the spike (S) glycoprotein, transmembrane protein (M), and small membrane protein (E) [2, 3]. Some coronaviruses have an additional membrane glycoprotein, hemagglutinin esterase .
The molecular determinants that may account for the dramatic difference in pathogenesis between FECV and FIPV have been extensively investigated. Today, FIPV is considered to be a genetic variant of enteric FECV and I shall focus in this chapter on the mutations probably implicated in virulence. It is likely, however, that host immunity also plays a role in the development of FIP. The pantropic CCoV has been described only recently, and there is little information about the molecular determinants its increased virulence.
Coronaviruses are characterized by a significant capacity for genetic change that enables them to adapt to new hosts and ecological niches, sometimes causing zoonotic outbreaks with disastrous consequences like the SARS epidemic in 2003 . In this chapter, I shall discuss the possibility of heterospecific coronavirus infections in cats or dogs.
Coronaviruses display unique molecular mechanisms of transcription and recombination. One of the most important insights gained over the past several years is that coronaviruses have crossed and in all likelihood will continue to cross between species, thus causing emerging disease in new host species, as was the case with the SARS epidemic in 2003. Coronaviruses of companion animal species were described long before the emergence of SARS-CoV. They exemplify the distinctive features of coronaviruses; that is, the presence of different biotypes and genotypes within each species, the critical role of accessory proteins in virulence and the possibility of interspecies transmission. FCoVs and CCoVs are common pathogens and readily evolve. It is necessary to pursue epidemiological surveillance of these viruses, so as to detect the emergence of new variants, which may have increased pathogenicity and/or a new host range, as early as possible. The knowledge accumulated about FCoVs and CCoVs, summarized in this paper, has made a substantial contribution to the understanding of the genetic evolution and pathobiology of coronaviruses. Observations that the spike protein and the accessory proteins contribute to pathogenesis and to host range have greatly benefited molecular investigation of the SARS-CoV. The next major goal will be to define the molecular determinants of virulence and tropism. Progress in these fields will require a better comprehension of the interactions between viral and host proteins and to what extent they are coronavirus- and organ-specific. In this context, study of FCoVs and CCoVs, as representative members of the Coronaviridae family, will again be helpful.