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

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