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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.

Author information

1
Tuberculosis and Mycobacteriology Branch, Division of AIDS, STD, and TB Laboratory Research, Centers for Disease Control and Prevention, Atlanta, Georgia, USA. stevelawn@yahoo.co.uk

Abstract

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.

PMID:
11598835
DOI:
10.1086/323649
[Indexed for MEDLINE]

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