Mechanism
After the virus enters the body there is a period of rapid viral replication, leading to an abundance of virus in the peripheral blood. During primary infection, the level of HIV may reach several million virus particles per milliliter of blood. This response is accompanied by a marked drop in the number of circulating CD4+ T cells. The acute viremia is almost invariably associated with activation of CD8+ T cells, which kill HIV-infected cells, and subsequently with antibody production, or seroconversion. The CD8+ T cell response is thought to be important in controlling virus levels, which peak and then decline, as the CD4+ T cell counts recover. A good CD8+ T cell response has been linked to slower disease progression and a better prognosis, though it does not eliminate the virus.
Ultimately, HIV causes AIDS by depleting CD4+ T cells. This weakens the immune system and allows opportunistic infections. T cells are essential to the immune response and without them, the body cannot fight infections or kill cancerous cells. The mechanism of CD4+ T cell depletion differs in the acute and chronic phases. During the acute phase, HIV-induced cell lysis and killing of infected cells by cytotoxic T cells accounts for CD4+ T cell depletion, although apoptosis may also be a factor. During the chronic phase, the consequences of generalized immune activation coupled with the gradual loss of the ability of the immune system to generate new T cells appear to account for the slow decline in CD4+ T cell numbers.
Although the symptoms of immune deficiency characteristic of AIDS do not appear for years after a person is infected, the bulk of CD4+ T cell loss occurs during the first weeks of infection, especially in the intestinal mucosa, which harbors the majority of the lymphocytes found in the body. The reason for the preferential loss of mucosal CD4+ T cells is that the majority of mucosal CD4+ T cells express the CCR5 protein which HIV uses as a co-receptor to gain access to the cells, whereas only a small fraction of CD4+ T cells in the bloodstream do so.A specific genetic change that alters the CCR5 protein when present in both chromosomes
HIV seeks out and destroys CCR5 expressing CD4+ T cells during acute infection. A vigorous immune response eventually controls the infection and initiates the clinically latent phase. CD4+ T cells in mucosal tissues remain particularly affected. Continuous HIV replication causes a state of generalized immune activation persisting throughout the chronic phase. Immune activation, which is reflected by the increased activation state of immune cells and release of pro-inflammatory cytokines, results from the activity of several HIV gene products and the immune response to ongoing HIV replication. It is also linked to the breakdown of the immune surveillance system of the gastrointestinal mucosal barrier caused by the depletion of mucosal CD4+ T cells during the acute phase of disease
Scientists believe a virus similar to HIV first occurred in some populations of chimps and monkeys in Africa, where they're hunted for food. Contact with an infected monkey's blood during butchering or cooking may have allowed the virus to cross into humans and become HIV.
AIDS!!!!!!!!!!!!
HIV destroys CD4 cells — a specific type of white blood cell that plays a large role in helping your body fight disease. Your immune system weakens as more CD4 cells are killed. You can have an HIV infection for years before it progresses to AIDS.People infected with HIV progress to AIDS when their CD4 count falls below 200 or they experience an AIDS-defining complication, such as:
- Pneumocystis pneumonia
- Cytomegalovirus
- Tuberculosis
- Toxoplasmosis
- Cryptosporidiosis
HIV is transmitted...........How!!!!!!!!!!!!
To become infected with HIV, infected blood, semen or vaginal secretions must enter your body. You can't become infected through ordinary contact — hugging, kissing, dancing or shaking hands — with someone who has HIV or AIDS. HIV can't be transmitted through the air, water or via insect bites.You can become infected with HIV in several ways, including:
1-By having sex. You may become infected if you have vaginal, anal or oral sex with an infected partner whose blood, semen or vaginal secretions enter your body. The virus can enter your body through mouth sores or small tears that sometimes develop in the rectum or vagina during sexual activity.
2-From blood transfusions. In some cases, the virus may be transmitted through blood transfusions. American hospitals and blood banks now screen the blood supply for HIV antibodies, so this risk is very small.
3-By sharing needles. HIV can be transmitted through needles and syringes contaminated with infected blood. Sharing intravenous drug paraphernalia puts you at high risk of HIV and other infectious diseases, such as hepatitis.
4-During pregnancy or delivery or through breast-feeding. Infected mothers can infect their babies. But receiving treatment for HIV infection during pregnancy, mothers significantly lower the risk to their babies.
References
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- Malta, M; Strathdee, SA; Magnanini, MM; Bastos, FI (August 2008). "Adherence to antiretroviral therapy for human immunodeficiency virus/acquired immune deficiency syndrome among drug users: a systematic review". Addiction (Abingdon, England) 103 (8): 1242–57. doi:10.1111/j.1360-0443.2008.02269.x. PMID 18855813.
- Nachega, JB; Marconi, VC; van Zyl, GU; Gardner, EM; Preiser, W; Hong, SY; Mills, EJ; Gross, R (April 2011). "HIV treatment adherence, drug resistance, virologic failure: evolving concepts". Infectious disorders drug targets 11 (2): 167–74. doi:10.2174/187152611795589663. PMID 21406048.
- Orsi, F; d'almeida, C (May 2010). "Soaring antiretroviral prices, TRIPS and TRIPS flexibilities: a burning issue for antiretroviral treatment scale-up in developing countries". Current Opinion in HIV and AIDS 5 (3): 237–41. doi:10.1097/COH.0b013e32833860ba. PMID 20539080.
- Nachega, JB; Mills, EJ; Schechter, M (January 2010). "Antiretroviral therapy adherence and retention in care in middle-income and low-income countries: current status of knowledge and research priorities". Current Opinion in HIV and AIDS 5 (1): 70–7. doi:10.1097/COH.0b013e328333ad61. PMID 20046150.
- Montessori, V., Press, N., Harris, M., Akagi, L., Montaner, J. S. (2004). "Adverse effects of antiretroviral therapy for HIV infection". CMAJ 170 (2): 229–238. PMC 315530. PMID 14734438.
- Burgoyne RW, Tan DH (March 2008). "Prolongation and quality of life for HIV-infected adults treated with highly active antiretroviral therapy (HAART): a balancing act". J. Antimicrob. Chemother. 61 (3): 469–73. doi:10.1093/jac/dkm499. PMID 18174196.
- Barbaro, G; Barbarini, G (December 2011). "Human immunodeficiency virus & cardiovascular risk". The Indian journal of medical research 134 (6): 898–903. doi:10.4103/0971-5916.92634. PMC 3284097. PMID 22310821.
- "Summary of recommendations on when to start ART in children" (PDF). Consolidated ARV guidelines, June 2013. June 2013.
- "Guidelines for the Use of Antiretroviral Agents in Pediatric HIV Infection" (PDF). Department of Health and Human Services, February 2014. March 2014.
- "Guidelines for intensified tuberculosis case-finding and isoniazid preventive therapy for people living with HIV in resource-constrained settings" (PDF). Department of HIV/AIDS, World Health Organization 2011. 2011.
- Laurence J (2006). "Hepatitis A and B virus immunization in HIV-infected persons". AIDS Reader 16 (1): 15–17. PMID 16433468.
- UNAIDS 2011 pg. 150–160
- Huang, L; Cattamanchi, A; Davis, JL; den Boon, S; Kovacs, J; Meshnick, S; Miller, RF; Walzer, PD; Worodria, W; Masur, H; International HIV-associated Opportunistic Pneumonias (IHOP), Study; Lung HIV, Study (June 2011). "HIV-associated Pneumocystis pneumonia". Proceedings of the American Thoracic Society 8 (3): 294–300. doi:10.1513/pats.201009-062WR. PMC 3132788. PMID 21653531.
- "Treating opportunistic infections among HIV-infected adults and adolescents. Recommendations from CDC, the National Institutes of Health, and the HIV Medicine Association/Infectious Diseases Society of America.". Department of Health and Human Services. February 2, 2007.
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