FECV and FIPV: What biotype labels can, and cannot, tell us about feline coronavirus biology.

The distinction between feline enteric coronavirus (FECV) and feline infectious peritonitis virus (FIPV) has long provided a practical framework for understanding how common feline coronavirus (FCoV) infection can give rise to feline infectious peritonitis (FIP). The internal mutation hypothesis remains central to explaining many cases. However, the two biotype labels are often used to imply genetic, anatomical, cellular, clinical, and epidemiological properties simultaneously, although these properties are neither synonymous nor invariably linked. Longitudinal observations made possible by effective antiviral treatment and the emergence of the recombinant lineage FCoV-23 have made these interpretive limitations particularly apparent. Clinical remission after treatment does not necessarily coincide with clearance of viral RNA, cessation of faecal shedding, or normalisation of all host-response measures, and post-treatment RNA detection does not by itself establish persistence of replication-competent virus or treatment failure. FCoV-23 combines between-cat transmission of a viral lineage with heterogeneous, cat-specific spike domain 0 deletions consistent with within-host emergence or selection. In this review, we reassess the FECV/FIPV dichotomy by separating five levels of description: genetic background, anatomical compartment, cell tropism, host clinical state, and transmissibility. These levels are analytically distinct but biologically interconnected, and experimentally measurable viral properties can provide mechanistic links between genetic variation and downstream biological outcomes. We examine how molecular markers, PCR findings, faecal shedding, experimental phenotypes, and post-antiviral observations should be interpreted in relation to the biological processes they directly reflect. We argue that FECV and FIPV remain useful terms, but should not be treated as fixed viral entities or used as substitutes for direct evidence. Matching the level of inference to the level of observation will improve interpretation of FCoV studies, diagnostic reporting, and the design of future work on within-host evolution, transmission, and treatment response.