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J Infect Dis. 2001 Nov 1;184(9):1127-33. Epub 2001 Sep 25.

Anatomically compartmentalized human immunodeficiency virus replication in HLA-DR+ cells and CD14+ macrophages at the site of pleural tuberculosis coinfection.

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Tuberculosis and Mycobacteriology Branch, Division of AIDS, STD, and TB Laboratory Research, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.


This study examined the impact of the host inflammatory microenvironment associated with localized tuberculosis (TB) on human immunodeficiency virus type 1 (HIV-1) replication within lymphocytes and macrophages in vivo. Paired plasma and pleural fluid samples from HIV-1-infected individuals with pleural TB (n=9) were analyzed. Detection of host proteins incorporated into the HIV-1 envelope by immunomagnetic capture analysis provided insight into the phenotype of cells supporting HIV-1 replication. The results indicated that the 4.0-fold greater median HIV-1 load in pleural fluid, compared with median load in plasma (P<.01), was derived in part from viral replication within HLA-DR+ cells, CD26+ lymphocytes, and, importantly, CD14+ macrophages. Greatly increased local concentrations of proinflammatory cytokines and immune activation markers in the pleural space correlated with the virologic findings. In summary, HIV-1 replication was increased at sites of Mycobacterium tuberculosis coinfection within activated cells, including lymphocytes and CD14+ macrophages.

[Indexed for MEDLINE]

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