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Immunopathogenesis of AIDS

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AIDS in Africa

Conclusion

The immunopathogenesis of AIDS is a product of host and viral genetics, immune activation, and environmental conditions. Exposed individuals either become infected or resist infection based on the interactions of these factors. Among those infected, their capacity to transmit the virus, their rate of disease progression, and their clinical prognosis also depend upon multiple factors. We have come to understand that HLA alleles and their cognate T-cell epitopes; cellular and humoral immune responses; and chemokine receptor polymorphisms and mutations each play a role in the immunopathogenesis of HIV-1 infection. The immune response within an individual and a population may select for the transmission, replication, and the relative success of certain viral subtypes and circulating recombinant forms (194). Immune responses, conditioned by HLA alleles inherited from each parent and chemokine receptor genes, exert negative and positive selection pressures on viruses for their expression of antigens and their susceptibility to various arms of the immune system. In Africa, these interactions between host and pathogen take place in individuals and populations who may be more vulnerable to infection due to nutritional deficiencies and chronic parasitic infections with concomitant immune hyperactivation.

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Zijenah, L.S., Katzenstein, D.A. (2002). Immunopathogenesis of AIDS. In: Essex, M., Mboup, S., Kanki, P.J., Marlink, R.G., Tlou, S.D., Holme, M. (eds) AIDS in Africa. Springer, Boston, MA. https://doi.org/10.1007/0-306-47817-X_3

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