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Created on: December 18, 2008 Last Updated: May 22, 2010
The virus Human Immunodeficiency Virus (HIV) produces the epidemiologic disease AIDS (Acquired immunodeficiency disease). In the following article the mechanism by which the HIV virus disables the host's immune system is discussed, along with other aspects of the disease.
HIV virus disables the immune system by disabling the conductor of all acquired immune reactions - the CD4+ T lymphocytes. The CD4+ lymphocytes are of central importance in acquired immunity because they secrete the various cytokines required to activate other immunologic cells, such as the CD8+ T lymphocytes, eosinophils, macrophages, etc. HIV virus have a cell-surface protein known as the gp 120 protein. This protein acts on the CD4, CCR5, CXCR4 receptors of the CD4+ T lymphocytes. The CCR5 and CXCR4 coreceptors function in the entry of the HIV virus into the CD4+ cytoplasm. Upon gaining entry, the disease now progresses to the latent stage. The duration of the latent stage depends on how long the host (patient) remains unexposed to potent immunologic antigens. Upon exposure, the CD4+ T lymphocytes are activated, and the proviral DNA of the HIV virus is retrotranscribed into the host's DNA, progressing the disease to the next stage. However, if the patient remains unexposed, the latent period can last to up to twenty years. Upon progression to the symptomatic stage, the patient may exhibit flu-like symptoms in the early phases, but later become susceptible to diseases such as mononucleosis, Kaposi sarcoma, etc. Such manifestation may be contributed by inactivation of the CD4+ T lymphocytes, which, as stated before, are of central importance in activation of other immunocompetent cells. The virus retrotranscribes more and more viral DNA into the host DNA, and the disease finally progresses to the fully blown AIDS. The progression of the disease may be measured serologically by the amount of retroviral genes such as gag, env, and pol. Levels of anitbodies gp 120 and p24 are also indicative of the progressions.
It is worth noting that in the blood stream, monocytes and macrophages, the supposedly immunologic cells, function as potent vehicles of transportation for the disease and can serve as reservoirs of viruses. Due to the fact that the HIV viruses by virtue of certain protective mechanisms, are able to evade the grave effects of phagocytosis, the viruses are phagocytosed but not fused in the lysosomes. The lack in the fusion results in intracellular viruses that can evade most of the other host defensive mechanisms, since the majority of them aim at cell-surface antigens. Due to the fact that the viral antigens are masked by those of the macrophages and monocytes, the former remains unseen and undetected. In later stages of the disease, these phagocytes migrate to the central nervous system by blood and further affects nervous cells. This results in the neural deformities observed in AIDS.
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