177-M. Incorporation of Host CD80 (B7.1) and CD86 (B7.2) Glycoproteins into HIV-1 Increases Viral Infectivity in Primary Human Mononuclear Cells

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Session 38 Poster Session
Viral and Cellular Proteins on the Virion Surface
Session Time: 4:30-6:30 pm
Room 4E-F

177-M.

Incorporation of Host CD80 (B7.1) and CD86 (B7.2) Glycoproteins into HIV-1 Increases Viral Infectivity in Primary Human Mononuclear Cells
S. Bounou*, J. F. Giguère, and M. J. Tremblay
Univ. of Laval, Ste-Foy, QC, Canada

Background: Human immunodeficiency virus type 1 (HIV-1) acquires several host cell membrane proteins during the budding process. It was demonstrated that the attachment process is accentuated by supplementary interactions between virion-anchored host molecules and their cognate ligands. Furthermore the enhancement of the viral attachment process was found to lead to an increase in virus infectivity in primary human mononuclear cells, as well as in established lymphoid cell lines. Given that previous work indicates that HIV-1 is budding at the site of cell-to-cell contact, a location rich in the costimulatory glycoproteins CD80 and CD86, we investigated if these molecules could be efficiently acquired by HIV-1 and whether virion-anchored CD80 and CD86 can influence the process of virus infection.
Methods: We have produced progeny viruses bearing or not on their surfaces host-derived CD80 or CD86 using our previously described transient transfection-and-expression system or by propagation of HIV-1 strains in primary human mononuclear cells. Human lymphoid cell lines and PBMCs were then infected with isogenic virions bearing or not bearing host-encoded CD80 and CD86 proteins. Virus-encoded luciferase activity and p24 antigen were next evaluated.
Results: Our data indicate that host-encoded CD80 and CD86 proteins are found embedded on viruses produced by human lymphoid tissue following a normal infection with HIV-1. The physical presence of CD80 and CD86 within the virus envelope was found to markedly increase virus infectivity in a CD28/B7-dependent manner following infection of several human lymphoid cell lines. The physiological significance of CD80 and CD86 incorporation was provided by the observation that an anti-CD80 and anti-CD86 antibody decreased replication in primary human cells infected with HIV-1 isolates.
Conclusions: These findings further support the concept that virally incorporated host cell surface proteins modulates virus-host dynamics and AIDS pathogenesis.