The roles of endogenous retroviruses as cofactors of pathogenic retroviral infections

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T-lymphotropic feline leukemia virus (FeLV-T) is a highly pathogenic variants of FeLVs, and induces feline AIDS (FAIDS) in cats. FeLV-T is fusion- defective because its PHQ motif, gammaretroviral consensus motif in the N-terminal regions of envelope protein, has substitution of histidine to aspartate. Infection of FeLV-T requires FeLIX, a truncated envelope protein encoded by an endogenous FeLV (enFeLV) for transactivation its infectivity and Pit1 for FeLIX-binding. Although Pit1 distributes in many cells, the expression of FeLIX is expressed only in some lymphoid organs. Therefore, it has been thought that the host cell range of FeLV-T is restricted to cells expressing FeLIX. However, because FeLIX is a soluble factor and expressed constantly, we presumed that FeLIX is present in blood and evaluated FeLIX activities in sera of various mammalian species by LacZ pseudotype assay. Here, we demonstrated that cat serum has FeLIX activity at functional level, suggesting that FeLIX is present abundantly in the internal environment of a cat and FeLV-T may be able to infect cells expressing Pit1 regardless FeLIX expression in vivo. We also confirmed that FeLIX did not inhibit FeLV-B infection despite FeLIX and FeLV-B exhibit the same receptor usage. These results implies that FeLIX may work just negatively for the host defence against the infection of exogenous viruses.