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A tale of two cat viruses

Jaimes JA et al. A tale of two viruses: The distinct spike glycoproteins of feline coronaviruses. Viruses, 2020; 12: 83.

Feline coronavirus (FCoV) is a complex virus causing a variety of clinical manifestations in cats, including the lethal feline infectious peritonitis (FIP). The currently accepted model of the virus’ behaviour, is that it either causes sub-clinical disease (when referred to as feline enteric coronavirus (FECV)), or a more aggressive and severe disease known as FIP. To date, there is still no definitive evidence to elucidate viral transition between the two clinical forms. It is also widely accepted that FCoV occurs in two serotypes:  serotype I and serotype II. While both serotypes are characterized in FECV and FIP forms, serotype I is much more prevalent in cat populations, and thus is the leading biotype causing FIP.

The authors of the present study previously provided evidence for serotype classification based on surface spike (S) protein, thus distinguishing serotype I and serotype II as separate biological entities. The authors propose that, as such, each serotype should also be considered as a distinct virus type, likely to result in distinct biological outcomes. Furthermore, the authors propose that the currently accepted model of FCoV pathogenesis, while describing many of the key elements of the disease, fails to capture the complexity and diversity of FCoV infection and the subsequent clinical outcomes.

To support this proposition, the authors of the present experimental study compared genetic, structural and functional characteristics of FCoV and the FCoV S protein among the two serotypes. Documented differences in cell culture between serotypes I and II (including interferon responses and activity of antiviral drugs) suggest that there are different mechanisms utilized by each serotype to gain entry into cells. Phylogenetic analyses also revealed distinct origins of S protein genes, translating to significant functional differences between serotypes I and II. Moreover, distinct structural differences identified in the present study imply different cell fusion techniques and receptor binding of FCoV to cellular receptors for each serotype.

In conclusion, the authors suggest that our understanding of FIP should consider the existence of two distinct viruses, in order to determine whether it has implications in clinical settings. The realization that systemic forms of FCoV may exist beyond the FECV-FIP paradigm should be more fully considered and explored. Without this consideration, the current understanding of FCoV transmission, pathogenesis and its clinical impact remains incomplete. (HM)

See also:

Shirato K et al. Differential susceptibility of macrophages to serotype II feline coronaviruses correlates with differences in the viral spike protein. Virus Res. 2018; 255:14-23.