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 feli ne fibroblast cell line, Crandell feline kidney cell, (CrFK), while th e progeny of the molecular clone pPPR was not. However, pPPR, after tr ansfection of CrFK cells, did produce virions which were able to produ ctively infect feline lymphocytes. To analyze the mechanisms responsib le for such differences in tropism and particularly the role of the en velope glycoproteins (Env), Env expression vectors were constructed by deletion of gag and pol genes from 34TF10 and PPR proviral clones. En v expression and function were studied by using a syncytium-formation assay and a quantitative ELISA. After transfection or CrFK, both 34TF1 0 and PPR Env precursors were correctly processed and Env surface glyc oprotein, gp100, was released in culture supernatants. However, the En v of 34TF10 caused a dramatic syncytial effect in CrFK cells, while PP R Env did not induce any syncytium formation. The Env of 34TF10 placed under the control of the long terminal repeal of PPR maintained its a bility 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. (C) 1995 Academic Press, I nc.