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human immunodeficiency virus (part i)

What is HIV and what does it do?

Human Immunodeficiency Virus (HIV) targets the CD4+ T lymphocytes of the immune system^[14], designated as CD4+ due to their surface proteins. These cells are critical during an immune response, for they activate nearly all the other cascading systems that may need to be initiated for a complete and successful immune response. The significant downregulation of CD4+T cells by HIV leads to the Acquired Immune Deficiency Syndrome, commonly known as AIDS.

Human Immunodeficiency Virus Pathology.

HIV infection is most commonly transmitted through exchange of bodily fluids. However, HIV cannot reproduce and proliferate on its own; it requires a host cell, and usurps the replication mechanisms of the host cell for its own uses^[15]. For example, the HIV virus will attack the CD4+T cell by use of specific glycoproteins, gp120 and gp41, embedded in the lipoprotein envelope of the invasive virus^[16,17]. Entry into the cell relies on the sequential interaction of the gp120 of the virus with the CD4 receptor that is embedded in the T-lymphocyte^[17]. The binding of the gp120 with the CD4 receptor interferes also recruits the interaction of chemokines receptors. This creates a fusion between the viral envelope and the cellular envelope, generating a connection that allows the virus to inject its viral RNA into the lymphocyte, which in essence, "hijacks" the cell^[18].

Once inside the cell, the hardest task of survival is over for the HIV. The virus then uses reverse transcription to create a double stranded DNA molecule from its single stranded RNA genome. It has been hypothesised that this is the main selective advantage of the HIV. Because reverse transcriptase has no proof-reading mechanisms, high levels of mutations are observed. This increases difficulty of combating the virus through use of antiviral drugs, and also prevents the immune system from performing its normal task. The production of viral DNA is produced at an exponentially higher rate than that of the normal cell DNA. This causes the cell to have reduced basal function, and it will eventually burst. Normally, the CD4+ T cell survives for about one day before it is destroyed by the infection^[19]. It is worth noting that doctors are able to take advantage of this fact, and can determine the progression of the disease simply through a count of the CD4+ T cells, and/or the amount of HIV in the blood serum^[19].

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references

14) Rosenberg ES, Billingsley JM, Caliendo AM, Boswell SL, Sax PE, Kalams SA, Walker BD. Vigorous HIV -1-Specific CD4+T cell responses associated with control of Viremia. Science 1997, 21:1447-1450.
15) Hiroyuki S, Mariko N, Tsyuneya O, Yuzuru M, Yasikatsu Y, Yoshiaki N. Myosin-actin interaction plays an important role in immunodeficiency virus type 1 release from host cells. Medical Sciences 1995, 92: 2026-2030.
16) Wyatt R, Kwong P, Desjardins E, Sweet R, Robinsons J, Hendrickson W, Sodroski J. The antigenic structure of the HIV gp120 envelope glycoprotein. Nature 2000, 393: 705-711.
17) Ariyoshi, Koya, Jaffar, Shabbar, Alabi, Abraham S, Berry, Neil, Schim van der Loeff, Maarten, Sabally Sehu, N'Gom Pa Tamba, Corrah, Tumani, Tedder, Richard, Whittle, Hilton. Plasma RNA Viral load predicts the rate of CD4 T cell Decline and death in HIV-2-Infected patients in West Africa. AIDS 2000, 14: 339-344.
18) Mary Lou Clements-Mann, et al. Immune Responses to Human immunodeficiency Virus (HIV) Type 1 Induced by Caranypox Expressing HIV-1mn gp120, HIV-1SF2, Recombinant gp120, or Both Vaccines in Seronegative Adults. AIDS 1998, 7: 212-232.
19) Bianchi M, Robles AM Vitale R, Helou S, Arechavala A, Negroni R. The usefulness of blood culture in diagnosing HIV related systemic mycoses: evaluation of a manual lysis centrifugation method. Medical Mycology 2000, 38: 77-80.