Research overview: spike gene mutations and FIP cell tropism

Research into the molecular basis of the enteric-to-FIP transition has focused heavily on the coronavirus spike gene, which governs receptor binding and membrane fusion. Specific mutations in the spike protein, including changes affecting fusion activation, have been associated with the shift to systemic macrophage tropism characteristic of the virulent biotype. While candidate markers have been proposed as diagnostic aids, their sensitivity and specificity remain debated. This overview compiles the molecular-virology literature rather than one source, describing how spike alterations may redirect the virus from gut epithelium to macrophages, why no single mutation perfectly defines FIPV across all cases, and how ongoing genomic work seeks reliable markers to distinguish benign infection from impending disease.