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 cf 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.
Address correspondence and reprint requests to Zahra Toossi, Division of Infectious Diseases, Department of Medicine, Case Western Reserve University, 10900 Euclid Ave, Cleveland, OH, 44106 U.S.A.; e-mail: firstname.lastname@example.org.
Manuscript received March 29, 2001; accepted July 6, 2001.
© 2001 Lippincott Williams & Wilkins, Inc.