Mutation of amino acids within the gibbon ape leukemia virus (GALV) receptor differentially affects feline leukemia virus subgroup B, simian sarcoma-associated virus, and GALV infections.

摘要: The three type C retroviruses, gibbon ape leukemia virus (GALV), simian sarcoma-associated (SSAV), and feline subgroup B (FeLV-B), infect human cells by interacting with the same cell surface receptor, GLVR1. Using LacZ retroviral pseudotypes murine transfected mutant GLVR1 expression vectors, we show that 9-amino-acid region of is critical for infection viruses. Rat were not susceptible to (FeLV-B) because a block at receptor level. We found multiple amino acid differences from in rat Expression human-rat chimeric demonstrated could function as GALV SSAV but FeLV-B. Substitution acids identified responsible resistance FeLV-B infection; two these affect infection, none affects infection.