Identification of a cellular cofactor required for infection by feline leukemia virus

Retroviral infection involves continued genetic variation, Leading to pheno typic and immunological selection for more fit virus variants in the host. For retroviruses that cause immunodeficiency, pathogenesis is linked to the emergence of T cell-tropic, cytopathic viruses. Here we show that an immun odeficiency-inducing, T cell-tropic feline Leukemia virus (FeLV) has evolve d such that it cannot infect cells unless both a classic multiple membrane- spanning receptor molecule (Pit1) and a second coreceptor or entry factor a re present. This second receptor component, which we call FeLIX, was identi fied as an endogenously expressed protein that is similar to a portion of t he FeLV envelope protein. This cellular protein can function either as a tr ansmembrane protein or as a soluble component to facilitate infection.