Differences in feline immunodeficiency virus host cell range correlate with envelope fusogenic properties.

Feline immunodeficiency virus (FIV) establishes persistent infections in cats inducing an acquired immunodeficiency syndrome. Differences in cell tropism have been observed among isolates of FIV (T. R. Phillips et al., J. Virol. 64, 4605-4613, 1990). The progeny of the infectious molecular clone of FIV p34TF10 was able to productively infect a feline fibroblast cell line, Crandell feline kidney cell, (CrFK), while the progeny of the molecular clone pPPR was not. However, pPPR, after transfection of CrFK cells, did produce virions which were able to productively infect feline lymphocytes. To analyze the mechanisms responsible for such differences in tropism and particularly the role of the envelope glycoproteins (Env), Env expression vectors were constructed by deletion of gag and pol genes from 34TF10 and PPR proviral clones. Env expression and function were studied by using a syncytium-formation assay and a quantitative ELISA. After transfection of CrFK, both 34TF10 and PPR Env precursors were correctly processed and Env surface glycoprotein, gp100, was released in culture supernatants. However, the Env of 34TF10 caused a dramatic syncytial effect in CrFK cells, while PPR Env did not induce any syncytium formation. The Env of 34TF10 placed under the control of the long terminal repeat of PPR maintained its ability to induce CrFK fusion. These results suggest that the inability of FIV PPR to infect CrFK fibroblasts is related to a restriction of virus entry mediated by the viral envelope.