Open AccessIncreased Replication of HIV-1 at Sites of Mycobacterium tuberculosis Infection: Potential Mechanisms of Viral Activation
Author(s) -
Zahra Toossi,
John L. Johnson,
Richard A. Kanost,
Mianda Wu,
Henry Luzze,
Pierre Peters,
Alphonse Okwera,
Moses Joloba,
Peter Mugyenyi,
Roy D. Mugerwa,
Htin Aung,
Jerrold J. Ellner,
Christina S. Hirsch
Publication year - 2001
Publication title -
journal of acquired immune deficiency syndromes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.162
H-Index - 157
eISSN - 1944-7884
pISSN - 1525-4135
DOI - 10.1097/00042560-200109010-00001
Subject(s) - peripheral blood mononuclear cell , mycobacterium tuberculosis , tuberculosis , chemokine , virology , immunology , viral replication , tumor necrosis factor alpha , biology , coinfection , lentivirus , medicine , human immunodeficiency virus (hiv) , inflammation , virus , viral disease , in vitro , pathology , biochemistry
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)-alpha and the HIV-1 noninhibitory beta-chemokine (MCP-1), low presence of HIV-1 inhibitory beta-chemokines (MIP-1 alpha, MIP-1 beta, 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.