Given the conservation of these sites in field strains, we predicted that one or both of these mutations may contribute to the process of cell culture adaptation which previous studies have shown to result in an increase in charge of the FIV Env V3-loop homologue and utilisation of CXCR4 alone as a viral receptor (CD134-independent infection) [27,33,34,89,90]. This evidence concerns the gene ERVW-1 and infection.