Research Article: The Paradox of Feline Coronavirus Pathogenesis: A Review

Date Published: August 21, 2011

Publisher: Hindawi Publishing Corporation

Author(s): Luciana Wanderley Myrrha, Fernanda Miquelitto Figueira Silva, Ethel Fernandes de Oliveira Peternelli, Abelardo Silva Junior, Maurício Resende, Márcia Rogéria de Almeida.


Feline coronavirus (FCoV) is an enveloped single-stranded RNA virus, of the family Coronaviridae and the order Nidovirales. FCoV is an important pathogen of wild and domestic cats and can cause a mild or apparently symptomless enteric infection, especially in kittens. FCoV is also associated with a lethal, systemic disease known as feline infectious peritonitis (FIP). Although the precise cause of FIP pathogenesis remains unclear, some hypotheses have been suggested. In this review we present results from different FCoV studies and attempt to elucidate existing theories on the pathogenesis of FCoV infection.

Partial Text

Feline coronavirus (FCoV) belongs to the family Coronaviridae and the order Nidovirales [1] and affects both wild and domestic cats [2]. FCoV contains a positive polarity RNA genome approximately 29 kb in length, consisting of 11 open reading frames (ORFs). Two major ORFs encode a replicase, four ORFs encode the structural proteins S (spike), E (envelope), M (membrane), and N (nucleocapsid), and five ORFs encode the nonstructural proteins 3a, 3b, 3c, 7a, and 7b [3].

The close similarity of FECV to FIPV, and the low incidence of FIP, despite the high proportion of FCoV seropositive cats, led to the hypothesis that FECV carriers are sources of FIPV, which is proposed to be generated by small mutations in FECV [5, 19]. After this hypothesis was first postulated in the literature, several studies have been conducted to test its validity.

Despite numerous efforts by the scientific community to understand FIP pathogenesis, this disease still remains an enigma. As demonstrated in this review, the causes underlying FIP pathogenesis are probably multifactorial, with both viral and host factors as well as viral genetic determinants playing important roles in FIP pathogenesis. The studies necessary to show this interaction will likely be complex. Because FCoV is an RNA virus, it is able to easily mutate, and thus there are many FCoV viral subpopulations with variations in different regions of its genome. In addition, individual cats may respond differently to FCoV infection, suggesting that the immune response to FIP is complex. Thus, by definition, both of the FIP pathogenesis theories presented in this review are too simplistic, and further studies are essential to elucidate FIP pathogenesis, and to obtain information that will assist in the development of more accurate diagnostic methods and effective vaccines.




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