| Summary: | Feline leukemia viruses (FeLVs) are pathogenic retroviruses of the domestic cat. FeLV transmission and emergence of pathogenic variants show striking similarity to HIV pathogenesis. The emergence of pathogenic subgroup-C FeLV from the transmitted subgroup-A FeLV coincides with a switch in host receptor used for infection as a result of mutations in the viral envelope protein (Env). I have characterized a novel FeLV Env that may represent an evolutionary intermediate between FeLV-A and FeLV-C.
I have also reported evidence suggesting that FeLVs may use co-factors/co-receptors for infection. I have found that FeLVs inefficiently infect murine NIH3T3 cells overexpressing FeLV receptors (NIH3T3/Receptor). I have provided evidence that the low infection is caused by a block at a post-binding but pre-entry stage of FeLV infection. Furthermore, fusion of NIH3T3/Receptor cells with highly susceptible cells rescues inhibition to infection suggesting that FeLVs, like HIV, may also use co-receptors for infection.
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