Opposite effects of SDF-1 on human immunodeficiency virus type 1 replication. - Institut Pasteur Accéder directement au contenu
Article Dans Une Revue Journal of Virology Année : 1999

Opposite effects of SDF-1 on human immunodeficiency virus type 1 replication.

Résumé

The alpha-chemokine SDF-1 binds CXCR4, a coreceptor for human immunodeficiency virus type 1 (HIV-1), and inhibits viral entry mediated by this receptor. Since chemokines are potent chemoattractants and activators of leukocytes, we examined whether the stimulation of HIV target cells by SDF-1 affects the replication of virus with different tropisms. We observed that SDF-1 inhibited the entry of X4 strains and increased the infectivity of particles bearing either a CCR5-tropic HIV-1 envelope or a vesicular stomatitis virus G envelope. In contrast to the inhibitory effect of SDF-1 on X4 strains, which is at the level of entry, the stimulatory effect does not involve envelope-receptor interactions or proviral DNA synthesis. Rather, we observed an increased ability of Tat to transactivate the HIV-1 long terminal repeat in the presence of the chemokine. Therefore, the effects of SDF-1 on the HIV-1 life cycle can be multiple and opposite, including both an inhibition of viral entry and a stimulation of proviral gene expression.

Dates et versions

pasteur-01372747 , version 1 (27-09-2016)

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Valérie Maréchal, F Arenzana-Seisdedos, J M Heard, O Schwartz. Opposite effects of SDF-1 on human immunodeficiency virus type 1 replication.. Journal of Virology, 1999, 73 (5), pp.3608-15. ⟨pasteur-01372747⟩

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