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Journal of Virology, May 1999, p. 3608-3615, Vol. 73, No. 5
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Opposite Effects of SDF-1 on Human Immunodeficiency Virus Type 1 Replication

Valérie Maréchal,1 Fernando Arenzana-Seisdedos,2 Jean-Michel Heard,1 and Olivier Schwartz1,*

Laboratoire Rétrovirus et Transfert Génétique, URA CNRS 1157,1 and Unité d'Immunologie Virale, Institut Pasteur,2 75724 Paris Cedex 15, France

Received 7 October 1998/Accepted 19 January 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.

* Corresponding author. Mailing address: Laboratoire Rétrovirus et Transfert Génétique, URA CNRS 1157, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris Cedex 15, France. Phone: 33 (1) 45 68 83 53. Fax: 33 (1) 45 68 89 40. E-mail: schwartz{at}pasteur.fr.

Journal of Virology, May 1999, p. 3608-3615, Vol. 73, No. 5
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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