KEYWORDS
feline coronavirus, detection; S gene; NTD; recombination
INTRODUCTION
Feline coronavirus (FCoV) is a Coronaviridae family member (genusAlphacoronavirus ), first identified in America in 1968. This identification was followed by outbreaks of the disease in many countries, severely endangering kitten health (Chang, Egberink, Halpin, Spiro, & Rottier, 2012; Pedersen, 2009; Ward, Munn, Gribble, & Dungworth, 1968). FCoV includes two pathogenic biotypes: feline enteric coronavirus (FECV) and feline infectious peritonitis virus (FIPV). FECV infection is characterized by mild diarrhea. In contrast, FIPV efficiently replicates in macrophages/monocytes and can lead to feline infectious peritonitis (FIP), a highly lethal systemic granulomatous disease (Ehmann et al., 2018; Oguma, Ohno, Yoshida, & Sentsui, 2018).
FCoV is an enveloped, single-stranded, positive-sense RNA virus of approximately 29 kb in size, containing 11 open reading frames encoding four structural proteins: spike (S), envelope (E), membrane (M), nucleocapsid (N), and seven nonstructural proteins (Dye & Siddell, 2005; Pedersen, 2009). The S protein of FCoV is a membrane glycoprotein thought to be a viral regulator of binding and entry to the cells (Bosch, van der Zee, de Haan, & Rottier, 2003; Jaimes & Whittaker, 2018; Millet & Whittaker, 2015). This protein is also involved in FCoV tropism and virulence and is the switch from enteric disease to FIP (Belouzard, Millet, Licitra, & Whittaker, 2012; Jaimes & Whittaker, 2018; B. N. Licitra et al., 2013). The S protein comprises two amino acid (aa) subunits, S1 and S2, with the S1 being more genetically diverse than S2 (Yang et al., 2020). S1 contains a receptor-binding domain and is responsible for the initial attachment of the virus to the surface of host cells (Belouzard et al., 2012; Jaimes & Whittaker, 2018; Wu, Li, Peng, & Li, 2009). Based on the amino acid sequence of the S protein, FCoV is classified into two genotypes, types I and II (Motokawa, Hohdatsu, Hashimoto, & Koyama, 1996; Takano, Satomi, Oyama, Doki, & Hohdatsu, 2016). Type II FCoV emerged via double recombination between type I FCoV and type II canine coronavirus (CCoV) (Herrewegh, Smeenk, Horzinek, Rottier, & de Groot, 1998). As a result of this recombination, the spike (S) gene and adjacent regions of type I FCoV were replaced by the corresponding part of the CCoV genome (Herrewegh et al., 1998; Lin, Chang, Su, & Chueh, 2013; Terada et al., 2014).
FCoV has a worldwide distribution (Amer et al., 2012; An et al., 2011; Klein-Richers et al., 2020; Li et al., 2019; Luo, Liu, Chen, & Chen, 2020; McKay et al., 2020; Soma, Wada, Taharaguchi, & Tajima, 2013). Infections with FCoV are mostly type I FCoV, while type II FCoV occurs primarily in southeast Asia (An et al., 2011; Li et al., 2019; Luo et al., 2020). With a gradual increase in the number of cats raised in China, coronavirus-related diseases have become more and more complex and diverse in cats. Nevertheless, the prevalence and genetic diversity of FCoV in southwest China remain unclear. Therefore, in this study, we recorded the current infection status of FCoV in southwest China and analyzed the sequences of currently circulating FCov strains.