Increased replication of HIV-1 at sites of Mycobacterium tuberculosis infection: Potential mechanisms of viral activation

Zahra Toossi, John L. Johnson, Richard A. Kanost, Mianda Wu, Herry Luzze, Pierre Peters, Alphonse Okwera, Moses Joloba, Peter Mugyenyi, Roy D. Mugerwa, Htin Aung, Jerrold J. Ellner, Christina S. Hirsch

Research output: Contribution to journalArticlepeer-review

Abstract

Tuberculosis (TB) enhances HIV-1 replication and the progression to AIDS in dually infected patients. We employed pleural TB as a model to understand the interaction of the host with HIV-1 during active TB, at sites of Mycobacterium tuberculosis (MTB) infection. HIV-1 replication was enhanced both in the cellular (pleural compared with blood mononuclear cells) and acellular (pleural fluid compared with plasma) compartments of the pleural space. Several potential mechanisms for expansion of HIV-1 in situ were found, including augmentation in expression of tumor necrosis factor (TNF)-α and the HIV-1 noninhibitory β-chemokine (MCP-1), low presence of HIV-1 inhibitory β-chemokines (MIP-1α, MIP-1β, and RANTES [regulated on activation, normal T expressed and secreted]), and upregulation in expression of the HIV-1 coreceptor, CCR5, by pleural fluid mononuclear cells. Thus, at sites of MTB infection, conditions are propitious both for transcriptional activation of HIV-1 in latently infected mononuclear cells, and facilitation of viral infection of newly recruited cells. These mechanisms may contribute to enhanced viral burden and dissemination during TB infection.

Original languageEnglish (US)
Pages (from-to)1-8
Number of pages8
JournalJournal of Acquired Immune Deficiency Syndromes
Volume28
Issue number1
StatePublished - Sep 1 2001
Externally publishedYes

Keywords

  • CCR5
  • HIV
  • MCP-1
  • TNF-α
  • Tuberculosis

ASJC Scopus subject areas

  • Virology
  • Immunology

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