Maréchal V, Arenzana-Seisdedos F, Heard J M, Schwartz O
Laboratoire Rétrovirus et Transfert Génétique, URA CNRS 1157, 75724 Paris Cedex 15, France.
J Virol. 1999 May;73(5):3608-15. doi: 10.1128/JVI.73.5.3608-3615.1999.
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.
α趋化因子SDF-1可与CXCR4（人类免疫缺陷病毒1型，即HIV-1的一种共受体）结合，并抑制由该受体介导的病毒进入。由于趋化因子是白细胞的强效化学引诱剂和激活剂，我们研究了SDF-1对HIV靶细胞的刺激是否会影响不同嗜性病毒的复制。我们观察到，SDF-1可抑制X4毒株的进入，并增加携带CCR5嗜性HIV-1包膜或水疱性口炎病毒G包膜的病毒颗粒的感染性。与SDF-1对X4毒株在进入水平的抑制作用相反，其刺激作用不涉及包膜-受体相互作用或前病毒DNA合成。相反，我们观察到在趋化因子存在的情况下，Tat反式激活HIV-1长末端重复序列的能力增强。因此，SDF-1对HIV-1生命周期的影响可能是多方面且相反的，包括对病毒进入的抑制和对前病毒基因表达的刺激。
