HIV infection increases susceptibility to Chlamydia trachomatis pelvic inflammatory disease

Reduced interferon-gamma production by T cells in HIV-1 infected women appears to increase their susceptibility to Chlamydia trachomatis pelvic inflammatory disease (PID), researchers report in the December issue of the Journal of Infectious Diseases. Dr Robert C. Brunham and associates from the University of British Columbia Centre for Disease Control in Vancouver stimulated peripheral blood mononuclear cells with C trachomatis antigens of native serovars.

Included were samples from 22 HIV-1 infected women and 73 uninfected women seen at a clinic in Nairobi, Kenya. All of the subjects reported low abdominal pain and were considered to be at high risk of C trachomatis acute PID.

Secretion of interferon-gamma stimulated by C trachomatis antigens was impaired in HIV-1 iinfected women compared with the HIV-1 negative women. The investigators observed similar results when limiting analysis to the 5 HIV-1 infected and 12 HIV-1 uninfected women with confirmed C trachomatis infection. In HIV-1 infected women only, production of interferon-gamma was significantly correlated with reduced CD4+ cell count, but not CD8+ cell count.

Stimulation with unrelated mitogens did not alter interferon-gamma secretion, suggesting that “decreased interferon-gamma secretion in chlamydial antigen-stimulated peripheral blood mononuclear cells was not due to an overall depressed T-cell response.” The authors deduce that “HIV-1 causes depletion of CD4+ T cells preferentially from the effector and/or memory compartment, rather than from the naive T-cell compartment.”

These findings support the hypothesis that reduced interferon-gamma secretion from peripheral blood mononuclear cells after C trachomatis antigen stimulation contributes to the higher incidence of PID in HIV-1 infected women.