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Retrovirology. 2009 May 15;6:46. doi: 10.1186/1742-4690-6-46.

Proteasome-independent degradation of HIV-1 in naturally non-permissive human placental trophoblast cells.

Author information

  • 1Institut Pasteur, Unit of Regulation of Retroviral Infections, Department of Virology, 25 rue du Docteur Roux, Paris, France. anna-laura.ross@pasteur.fr

Abstract

BACKGROUND:

The human placenta-derived cell line BeWo has been demonstrated to be restrictive to cell-free HIV-1 infection. BeWo cells are however permissive to infection by VSV-G pseudotyped HIV-1, which enters cells by a receptor-independent mechanism, and to infection by HIV-1 via a cell-to-cell route.

RESULTS:

Here we analysed viral entry in wild type BeWo (CCR5+, CXCR4+) and BeWo-CD4+ (CD4+, CCR5+, CXCR4+) cells. We report that HIV-1 internalisation is not restricted in either cell line. Levels of internalised p24 antigen between VSV-G HIV-1 pseudotypes and R5 or X4 virions were comparable. We next analysed the fate of internalised virions; X4 and R5 HIV-1 virions were less stable over time in BeWo cells than VSV-G HIV-1 pseudotypes. We then investigated the role of the proteasome in restricting cell-free HIV-1 infection in BeWo cells using proteasome inhibitors. We observed an increase in the levels of VSV-G pseudotyped HIV-1 infection in proteasome-inhibitor treated cells, but the infection by R5-Env or X4-Env pseudotyped virions remains restricted.

CONCLUSION:

Collectively these results suggest that cell-free HIV-1 infection encounters a surface block leading to a non-productive entry route, which either actively targets incoming virions for non-proteasomal degradation, and impedes their release into the cytoplasm, or causes the inactivation of mechanisms essential for viral replication.

PMID:
19445667
[PubMed - indexed for MEDLINE]
PMCID:
PMC2689159
Free PMC Article
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