Anatomically compartmentalized human immunodeficiency virus replication inHLA-DR+ cells and CD14(+) macrophages at the site of pleural tuberculosis coinfection

This study examined the impact of the host inflammatory microenvironment as sociated with localized tuberculosis (TB) on human immunodeficiency virus t ype 1 (HIV-1) replication within lymphocytes and macrophages in vivo. Paire d plasma and pleural fluid samples from HIV-1-infected individuals with ple ural TB (n = 9) were analyzed. Detection of host proteins incorporated into the HIV-1 envelope by immunomagnetic capture analysis provided insight int o the phenotype of cells supporting HIV-1 replication. The results indicate d that the 4.0-fold greater median HIV-1 load in pleural fluid, compared wi th median load in plasma (P < .01), was derived in part from viral replicat ion within HLA-DR+ cells, CD26(+) lymphocytes, and, importantly, CD14(+) ma crophages. Greatly increased local concentrations of proinflammatory cytoki nes 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 l ymphocytes and CD14(+) macrophages.