An updated review of feline coronavirus: mind the two biotypes

Abstract

Feline coronavirus (FCoV) includes two biotypes: feline infectious peritonitis virus (FIPV) and feline enteric coronavirus (FECV). Although both biotypes can infect cats, their pathogenicities differ. The FIPV biotype is more virulent than the FECV biotype and can cause peritonitis or even death in cats, while most FECV biotypes do not cause lesions. Even pathogenic strains of the FECV biotype can cause only mild enteritis because of their very low virulence. This article reviews recent progress in FCoV research with regard to FCoV etiological characteristics; epidemiology; clinical symptoms and pathological changes; pathogenesis; and current diagnosis, prevention and treatment methods. It is hoped that this review will provide a reference for further research on FCoV and other coronaviruses.

Keywords: Etiological characteristics; Feline coronavirus; Feline enteric coronavirus; Feline infectious peritonitis virus; Pathogenicity.

Graphical abstract

Fig. 1

(a) Schematic representation of FCoV (Jaimes and Whittaker, 2018). (b) Schematic representation of the genomes of FCoV I and FCoV II (Gao et al., 2022; Le Poder, 2011). Note: The genomes of FCoV I and FCoV II (represented by FIPV-II-79–1146 in this article) are both approximately 29 kb in size and contain 11 ORFs encoding four structural proteins (S, M, E and N) and seven nonstructural proteins (replicase proteins 1a and 1b and accessory proteins 3a, 3b, 3c, 7a and 7b). Light blue indicates the genes from FCoV I, while dark blue indicates the genes from canine coronavirus (CCoV). The S protein consists of two subunits: S1 (the receptor binding domain, RBD) and S2 (the fusion domain, FD). The S1 subunit also includes two functional domains: the amino terminal domain (NTD) and the carboxyl terminal domain (CTD). The S2 subunit consists of a fusion peptide (FP), two heptad repeats (HR1 and HR2), a transmembrane (TM) domain and an internal domain (ID). The arrows indicate the two activation sites, S1/S2 and S2′, and the linker sequence (L) region between S1/S2 and S2′. The upper dotted line in each FCoV genome representation indicates the difference in the key amino acid 1058 of the S gene between FECV and FIPV, and the lower dotted line indicates the difference in the S1/S2 furin cleavage site between FECV and FIPV.

Fig. 2

Schematic representation of the internal mutation theory.

Fig. 3

Schematic representation of the pathogenesis of effusive and noneffusive FIP (Pedersen, 2009).