Nitric oxide modulates HIV-1 replication.


Journal Article

Although nitric oxide (NO) production is increased in HIV-1-infected patients, and NO is known to inhibit the replication of several viruses, very little is known about the effects of NO on HIV-1 replication. In the present studies, we find that S-nitrosothiols (RSNOs), a class of NO donor compounds present in the human circulatory system, inhibit HIV-1 replication in acutely infected human peripheral blood mononuclear cells (PBMCs) and have an additive inhibitory effect on HIV-1 replication in combination with 3'-azido-3'-deoxythymidylate (AZT). RSNOs inhibit HIV-1 replication in acutely infected PBMCs at a step in the viral replicative cycle after reverse transcription, but before or during viral protein expression through a cGMP-independent mechanism. In the latently infected U1 cell line, NO donor compounds and intracellular NO production stimulate HIV-1 reactivation. These studies suggest that NO both inhibits HIV-1 replication in acutely infected cells and stimulates HIV-1 reactivation in chronically infected cells. Thus, NO may have a physiologic role in HIV-1 replication, and NO donor compounds, which have been used for decades in the treatment of coronary artery disease with limited toxicity, might be useful in the treatment of HIV-1 disease by inhibiting acute infection, reactivating latent virus, or both.

Full Text

Duke Authors

Cited Authors

  • Mannick, JB; Stamler, JS; Teng, E; Simpson, N; Lawrence, J; Jordan, J; Finberg, RW

Published Date

  • September 1, 1999

Published In

Volume / Issue

  • 22 / 1

Start / End Page

  • 1 - 9

PubMed ID

  • 10534141

Pubmed Central ID

  • 10534141

International Standard Serial Number (ISSN)

  • 1525-4135

Digital Object Identifier (DOI)

  • 10.1097/00042560-199909010-00001


  • eng

Conference Location

  • United States