Abstract

Endogenous viruses of Old and New World monkeys are divided morphologically into type C isolates of baboons, macaques, and owl monkeys and type D isolates of squirrel monkeys and langurs. Mason-Pfizer monkey virus (MPMV), a type D virus, is horizontally transmitted in rhesus monkeys and is highly related to the langur isolate. Although these endogenous type C and D viruses possess little nucleic acid sequence homology and are antigenically distinct, they do possess cross-reactive determinants in their envelope gp70 antigen, as shown by sensitive interspecies radioimmunoassays. The ability of MPMV to induce syncytia in KC (Rous sarcoma virus-transformed human glioma) cells allowed for investigation of the role that these conserved determinants play in recognition of cellular receptors. The capacity of other viruses to bind to common cellular receptors and to inhibit MPMV-induced syncytia was measured in a quantitative assay using a high syncytia-inducing variant of MPMV. Pretreatment of KC cells with disrupted MPMV, baboon endogenous virus (BaEV), squirrel monkey retrovirus, and the BaEV-related endogenous cat virus RD114 blocked syncytia formation by MPMV. Partial competition was observed with endogenous macaque isolates MAC-1 and MMC-1. However, no inhibition was observed using feline leukemia, murine leukemia, equine infectious anemia, or murine mammary tumor viruses, none of which possess antigenic determinants which are cross-reactive with the endogenous primate retroviruses. Syncytia formation was also blocked by purified gp70s of MPMV and BaEV, demonstrating that inhibition was due to competition for viral gp70 cellular receptors.

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