Tuberculosis results in activation of T cells and macrophages that may harbor latent human immunodeficiency virus (HIV-1). Although such activation is beneficial to the host in terms of mycobacterial disease, it may be deleterious in terms of HIV-1. In Ugandan HIV-1-seropositive patients with pulmonary tuberculosis, antigen-induced blastogenesis and production of tumor necrosis factor-α (a cytokine that induces expression of HIV-1 in latently infected cells) were 3-10 times greater than in controls. The mean serum β2-microglobulin level was 5.22 mg/L in recently diagnosed patients, significantly greater than levels in HIV-negative patients with tuberculosis or asymptomatic HIV-1-seropositive subjects. β2-microglobulin was significantly lower in subjects who had completed at least 2 months of antituberculous therapy. These observations suggest that HIV-1-associated tuberculosis is accompanied by immune activation that may result in increased HIV expression and accelerated progression to AIDS.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Infectious Diseases|
|State||Published - Jan 1993|
ASJC Scopus subject areas
- Public Health, Environmental and Occupational Health