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|Title:||Immune response and possible causes of CD4 + T-cell depletion in human immunodeficiency virus (HIV)-1 infection||Authors:||Oguntibeju, Oluwafemi Omoniyi
Van den Heever, W.M.J.
Van Schalkwyk, F.E.
|Keywords:||Immune response;T cells;HIV (Viruses);HIV infections;HIV antibodies||Issue Date:||2009||Publisher:||Academic Journals||Source:||Oguntibeju, O.O, van den Heever, W.M.J & Van Schalkwyk, F.E. (2009). Immune response and possible causes of CD4 + T-cell depletion in human immunodeficiency virus (HIV)-1 infection. African Journal of Microbiology Research, 3(7):344-352, [http://www.academicjournals.org/ajmr]||Journal:||African Journal of Microbiology Research||Abstract:||This review work examines immune response and possible causes of depletion of CD4 + T-cells in patients with human immunodeficiency (HIV)-1 infection. HIV has been accepted as a global problem however, the developing countries are the most affected by the epidemic. Countries in the sub-Saharan Africa seem to bear the bulk of the HIV burden among the developing countries with about 24.7 million (almost 63%) of all people living with HIV globally in 2006 live in sub-Saharan Africa. The major factor obstructing progress towards an effective vaccine to prevent or modulate HIV-1 infection is that the critical features needed for a protective immune response are not fully understood. Although, it has been found that potent neutralizing antibodies can protect against experimentally acquired HIV infection in animal models, they are scarcely generated in vivo in the infected person and neutralization resistant viral variants have been noticed to develop rapidly in chronic infection. It is generally believed that cellular immune responses, particularly specific cytotoxic T lymphocytes (CTL), are important in the host response to HIV-1 infection. Scientists have observed that CTL develop very early in acute HIV-1 infection, coincident with a rapid fall in plasma vireamia, whereas in chronic infection their levels are inversely related to viral load. However, the powerful HIV-specific CTL response ultimately fails to control HIV replication. This could be due to the emergence of viral variants that escape CTL recognition or impairment of CTL function.||Description:||Article||URI:||http://www.academicjournals.org/ajmr
|Appears in Collections:||HWSci - Journal Articles (DHET subsidised)|
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