Persistent infection with primate foamy virus type 1 increases human immunodeficiency virus type 1 cell binding via a Bet-independent mechanism.

نویسندگان

  • Cecile Schiffer
  • Charles-Henri Lecellier
  • Abdelkrim Mannioui
  • Nathalie Felix
  • Elisabeth Nelson
  • Jacqueline Lehmann-Che
  • Marie-Louise Giron
  • Jean Claude Gluckman
  • Ali Saib
  • Bruno Canque
چکیده

We report that human T cells persistently infected with primate foamy virus type 1 (PFV-1) display an increased capacity to bind human immunodeficiency virus type 1 (HIV-1), resulting in increased cell permissiveness to HIV-1 infection and enhanced cell-to-cell virus transmission. This phenomenon is independent of HIV-1 receptor, CD4, and it is not related to PFV-1 Bet protein expression. Increased virus attachment is specifically inhibited by heparin, indicating that it should be mediated by interactions with heparan sulfate glycosaminoglycans expressed on the target cells. Given that both viruses infect similar animal species, the issue of whether coinfection with primate foamy viruses interferes with the natural course of lentivirus infections in nonhuman primates should be considered.

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عنوان ژورنال:
  • Journal of virology

دوره 78 20  شماره 

صفحات  -

تاریخ انتشار 2004