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.