The HIV enzyme reverse transcriptase converts the viral RNA into DNA, which is compatible to human genetic material, when the virus is inside the cell. This DNA is transported to the cell’s nucleus, where it is spliced into human DNA by the HIV enzyme integrase. The HIV DNA is known as provirus after it is integrated.
Evidence for supplementation with selenium is mixed with some tentative evidence of benefit. For pregnant and lactating women with HIV, multivitamin supplement improves outcomes for both mothers and children. If the pregnant or lactating mother has been advised to take anti-retroviral medication to prevent mother-to-child HIV transmission, multivitamin supplements should not replace these treatments. There is some evidence that vitamin A supplementation in children with an HIV infection reduces mortality and improves growth.
Integrase strand transfer inhibitors (integrase inhibitors or integrases) stop HIV genes from becoming incorporated into the human cell’s DNA and are very well tolerated. Raltegravir (Isentress) was the first drug in this class. Elvitegravir is part of a fixed-dose combination (elvitegravir/cobicistat/tenofovir/emtricitabine) taken as one pill once daily, called Stribild. Dolutegravir (Tivicay) is also available in a once-daily combination pill with two NRTIs, abacavir and lamivudine, called Triumeq.
There is evidence that humans who participate in bushmeat activities, either as hunters or as bushmeat vendors, commonly acquire SIV. However, SIV is a weak virus which is typically suppressed by the human immune system within weeks of infection. It is thought that several transmissions of the virus from individual to individual in quick succession are necessary to allow it enough time to mutate into HIV. Furthermore, due to its relatively low person-to-person transmission rate, SIV can only spread throughout the population in the presence of one or more high-risk transmission channels, which are thought to have been absent in Africa before the 20th century.
Many opportunistic infections and conditions are used to mark when HIV infection has progressed to AIDS. The general frequency of these infections and conditions varies from rare to common, but all are uncommon or mild in immunocompetent persons. When one of these is unusually severe or frequent in a person infected with HIV and no other causes for immune suppression can be found, AIDS can be diagnosed. 
Franconi’s syndrome a form of anaemia associated with renal tubule dysfunction; adult Franconi’s syndrome shows synostosis with osteomalacia, and acquired Franconi’s syndrome is associated with multiple myeloma
Although most HIV-1 infected individuals have a detectable viral load and in the absence of treatment will eventually progress to AIDS, a small proportion (about 5%) retain high levels of CD4+ T cells (T helper cells) without antiretroviral therapy for more than 5 years. These individuals are classified as HIV controllers or long-term nonprogressors (LTNP). Another group consists of those who maintain a low or undetectable viral load without anti-retroviral treatment, known as “elite controllers” or “elite suppressors”. They represent approximately 1 in 300 infected persons.
^ Jump up to: a b Plantier JC, Leoz M, Dickerson JE, De Oliveira F, Cordonnier F, Lemée V, Damond F, Robertson DL, Simon F (August 2009). “A new human immunodeficiency virus derived from gorillas”. Nature Medicine. 15 (8): 871–2. doi:10.1038/nm.2016. PMID 19648927. Lay summary.
Sax PE, DeJesus E, Mills A, et al. Co-formulated elvitegravir, cobicistat, emtricitabine, and tenofovir versus co-formulated efavirenz, emtricitabine, and tenofovir for initial treatment of HIV-1 infection: a randomised, double-blind, phase 3 trial, analysis of results after 48 weeks. Lancet. 2012 Jun 30. 379(9835):2439-48. [Medline].
HIV is a very small virus that contains ribonucleic acid (RNA) as its genetic material. When HIV infects animal cells, it uses a special enzyme, reverse transcriptase, to turn (transcribe) its RNA into DNA. (Viruses that use reverse transcriptase are sometimes referred to as “retroviruses.”) When HIV reproduces, it is prone to making small genetic mistakes or mutations, resulting in viruses that vary slightly from each other. This ability to create minor variations allows HIV to evade the body’s immunologic defenses, essentially leading to lifelong infection, and has made it difficult to make an effective vaccine. The mutations also allow HIV to become resistant to antiretroviral medications.
On a late, lazy Sunday afternoon in early April, Sturdevant, in cutoff fatigues and a white tank top stained with barbecue sauce stretched over his generous belly, was flipping chicken and rib tips on his grill. He had gathered his family — nearly two dozen sons and daughters, some related by blood, most not — to his house in South Jackson for a family barbecue. His daughter Tenisha, who had moved in with her two children in November, handed off 6-month-old Kory Cedric to her father. Sturdevant nuzzled his grandson’s chubby cheek before passing him to one of his unrelated “sons,” Cord, who lifted the laughing baby high over his head.
HIV continues to be a major public health crisis both in the United States and around the world. While major scientific advances have made it easier than ever to prevent and treat HIV, there remains no vaccine or cure, and tens of thousands of people continue to contract HIV every year. Insufficient funding for public health programs, ideological opposition to common sense prevention policies, and societal barriers like stigma and discrimination, have made it especially difficult for us to turn the tide against the epidemic. Together, HRC and the HRC Foundation are committed to working with our friends, partners, members, and supporters to end the dual epidemics of HIV and HIV-related stigma.
Jump up ^ “Quick Reference Guide—Laboratory Testing for the Diagnosis of HIV Infection: Updated Recommendations” (PDF). cdc.gov. New York State Department of Health. June 27, 2014. pp. 1–2. Retrieved April 13, 2017.
At this point, the viral load is typically very high, and the CD4+ T-cell count drops precipitously. With the appearance of anti-HIV antibodies and CD8+ T-cell responses, the viral load drops to a steady state and the CD4+ T-cell count returns to levels within the reference range, although slightly lower than before infection.
Painful rash at the injection site and allergic (hypersensitivity) reactions (including rash, fever, chills, nausea, and low blood pressure), numbness and tingling in the hands and feet (peripheral neuropathy), insomnia, and loss of appetite
The ability of HIV to enter particular types of cell, known as the cellular tropism of the virus, is determined by the expression of specific receptors for the virus on the surface of those cells. HIV enters cells by means of a complex of two noncovalently associated viral glycoproteins, gp120 and gp41, in the viral envelope. The gp120 portion of the glycoprotein complex binds with high affinity to the cell-surface molecule CD4. This glycoprotein thereby draws the virus to CD4 T cells and to dendritic cells and macrophages, which also express some CD4. Before fusion and entry of the virus, gp120 must also bind to a co-receptor in the membrane of the host cell. Several different molecules may serve as a co-receptor for HIV entry, but in each case they have been identified as chemokine receptors. The chemokine receptors (see Chapters 2 and 10) are a closely related family of G protein-coupled receptors with seven transmembrane-spanning domains. Two chemokine receptors, known as CCR5, which is predominantly expressed on dendritic cells, macrophages, and CD4 T cells, and CXCR4, expressed on activated T cells, are the major co-receptors for HIV. After binding of gp120 to the receptor and co-receptor, the then causes fusion of the viral envelope and the plasma membrane of the cell, allowing the viral genome and associated viral proteins to enter the cytoplasm. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]