Hiv Induced Suppression Of Host Immunity: Relevance To Mycobacterium Tuberculosis Infections

Compromised immunity among human immunodeficiency virus (HIV) infection attracts some of the most notorious opportunistic infections (OIs) like Mycobacterium tuberculosis etc. The increased burden of HIV tuberculosis (HIV-TB) cases also increases their transmission rate in the community. Chemotherapy presumably brings down the viral number below certain threshold number, which can be successfully contained by the host immune response. An impaired immunity, not only facilitates the dissemination of virus, but also fails to mount sufficient level of effector immune response to inhibit the OIs. In general, the outcome of the infection is decided by the equilibrium between the host's effector immune response and extent of immune suppression, which facilitates immune evasion strategies evolved by the virus. During HIV infection, perturbation of immune homeostasis results from alteration in the representation of various fine T cell subsets, performing highly selective immune functions. This appears to have critical impact on effector T cell responses that keep the viral load under check and maintain latency of M. tuberculosis infection including other OIs. However, the precise role of these suppressor cells on the immune response among HIV infected individuals remains far from conclusive. Any alteration in frequency and function of these fine T cells that regulates the terminal effector response against latent M. tuberculosis infection, plausibly results in perturbation of immunity ending in reactivation of M. tuberculosis infection. The present review focuses the immunopathogenesis, immune suppression, and reactivation of M. tuberculosis among HIV infected patients.