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Short communication: Nitazoxanide inhibits HIV viral replication in monocyte-derived macrophages.

Abstract
We document the anti-HIV activity of nitazoxanide (NTZ), the first member of the thiazolide class of antiinfective drugs, originally effective against enteritis caused by Cryptosporidium parvum and Giardia lamblia. NTZ has been administered extensively worldwide, with no severe toxicities associated with its use. Here, we show for the first time that NTZ decreases HIV-1 replication in monocyte-derived macrophages (MDM) if present before or during HIV-1 infection. This NTZ effect is associated with downregulation of HIV-1 receptors CD4 and CCR5, and increasing gene expression of host cell anti-HIV resistance factors APOBEC3A/3G and tetherin. As NTZ is already in clinical use for other conditions, this newly described anti-HIV activity in MDM may facilitate innovative intensification strategies against HIV-1 when combined with current antiretroviral drug regimens.
AuthorsBethsebah Gekonge, Matthew C Bardin, Luis J Montaner
JournalAIDS research and human retroviruses (AIDS Res Hum Retroviruses) Vol. 31 Issue 2 Pg. 237-41 (Feb 2015) ISSN: 1931-8405 [Electronic] United States
PMID25303025 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)
Chemical References
  • Anti-HIV Agents
  • Antigens, CD
  • Antiprotozoal Agents
  • BST2 protein, human
  • CCR5 protein, human
  • CD4 Antigens
  • GPI-Linked Proteins
  • Nitro Compounds
  • Proteins
  • Receptors, CCR5
  • Thiazoles
  • APOBEC-3G Deaminase
  • APOBEC3A protein, human
  • APOBEC3G protein, human
  • Cytidine Deaminase
  • nitazoxanide
Topics
  • APOBEC-3G Deaminase
  • Anti-HIV Agents (pharmacology)
  • Antigens, CD (metabolism)
  • Antiprotozoal Agents (pharmacology)
  • CD4 Antigens (metabolism)
  • Cells, Cultured
  • Cytidine Deaminase (metabolism)
  • Down-Regulation
  • Drug Repositioning
  • GPI-Linked Proteins (metabolism)
  • HIV-1 (drug effects, physiology)
  • Humans
  • Macrophages (virology)
  • Nitro Compounds
  • Proteins (metabolism)
  • Receptors, CCR5 (metabolism)
  • Thiazoles (pharmacology)
  • Up-Regulation
  • Virus Replication (drug effects)

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