Immunopathogenesis of HIV infection.

Progression of HIV infection is largely dependent on the interaction between the viral factors and host factors. HIV primarily infects the CD4 lymphocytes in the body. It brings about the destruction of CD4 cells through multiple mechanisms including apoptosis. The loss of CD4 cell population ultimately leads to the inability of infected person to deal with opportunistic organisms. Host genetic factors such as HLA polymorphism and HIV co-receptor polymorphism may influence either susceptibility to infection or disease progression. Innate immune mechanisms may play a role in disease progression. However, adaptive immune response is the most critical component of immune system for control of HIV infection. HIV-specific CD4 helper response and HIV-specific CTL responses have clearly emerged as the most important host factors that may decide the rate of disease progression. However, the role of neutralizing antibodies still remains to be understood in context with the disease progression. One of the gray areas is the role of mucosal immune response in HIV infection. However, it is clear that it is not a single component but orchestrated action of different immune mechanisms will decide the outcome of HIV infection. The studies in persons exposed to HIV infection but who are uninfected and the long term non-progressors will be critical for understanding the immunopathogenesis of HIV infection.

Incident HIV infection among men attending STD clinics in Pune, India: pathways to disparity and interventions to enhance equity.

Systematic disparities in rates of HIV incidence by socioeconomic status were assessed among men attending three sexually transmitted disease (STD) clinics in Pune, India, to identify key policy-intervention points to increase health equity. Measures of socioeconomic status included level of education, family income, and occupation. From 1993 to 2000, 2,260 HIV-uninfected men who consented to participate in the study were followed on a quarterly basis. Proportional hazards regression analysis of incident HIV infection identified a statistically significant interaction between level of education and genital ulcer disease. Compared to the lowest-risk men without genital ulcer disease who completed high school, the relative risk (RR) for acquisition of HIV was 7.02 (p < 0.001) for illiterate men with genital ulcer disease, 3.62 (p < 0.001) for men with some education and genital ulcer disease, and 3.02 (p < 0.001) for men who completed high school and had genital ulcer disease. For men with no genital ulcer disease and those with no education RR was 1.09 (p = 0.84), and for men with primary/middle school it was 1.70 (p = 0.03). The study provides evidence that by enhancing access to treatment and interventions that include counselling, education, and provision of condoms for prevention of STDs, especially genital ulcer disease, among disadvantaged men, the disparity in rates of HIV incidence could be lessened considerably. Nevertheless, given the same level of knowledge on AIDS, the same level of risk behaviour, and the same level of biological co-factors, the most disadvantaged men still have higher rates of HIV incidence.