Initially, some researchers referred to the syndrome as gay-related immune deficiency (GRID), since it appeared to be limited to homosexuals. In the media the disease commonly was referred to as the “gay plague.” But the disease had also been detected in intravenous drug users, who became infected mainly by sharing contaminated hypodermic needles. It also had been observed in women with male sexual partners. As a result, the term acquired immunodeficiency syndrome, or AIDS, was introduced to describe the disease; the CDC published its first report using the term in 1982.
Jump up ^ Hymes KB, Cheung T, Greene JB, et al. (September 1981). “Kaposi’s sarcoma in homosexual men-a report of eight cases”. Lancet. 2 (8247): 598–600. doi:10.1016/S0140-6736(81)92740-9. PMID 6116083.
HIV testing should be voluntary and the right to decline testing should be recognized. Mandatory or coerced testing by a health care provider, authority, or by a partner or family member is not acceptable as it undermines good public health practice and infringes on human rights.
Once infection has progressed to AIDS, the survival period is usually less than 2 years in untreated patients. Persons in whom the infection does not progress long-term may not develop AIDS for 15 years or longer, although many still exhibit laboratory evidence of CD4 T-cell decline or dysfunction. [79, 80, 81, 82]
The CDC reported that, at the end of 2014, the most recent year for which national prevalence statistics are available, there were 955,081 adults and adolescents living with HIV infection in the United States, 521,002 of whom had infection classified as stage 3 (AIDS). 
Patients beginning ART sometimes deteriorate clinically, even though HIV levels in their blood are suppressed and their CD4 count increases, because of an immune reaction to subclinical opportunistic infections or to residual microbial antigens after successful treatment of opportunistic infections. IRIS usually occurs in the first months of treatment but is occasionally delayed. IRIS can complicate virtually any opportunistic infection and even tumors (eg, Kaposi sarcoma) but is usually self-limited or responds to brief regimens of corticosteroids.
Human immunodeficiency virus infection and acquired immune deficiency syndrome (HIV/AIDS) is a spectrum of conditions caused by infection with the human immunodeficiency virus (HIV). Following initial infection, a person may not notice any symptoms or may experience a brief period of influenza-like illness. Typically, this is followed by a prolonged period with no symptoms. As the infection progresses, it interferes more with the immune system, increasing the risk of common infections like tuberculosis, as well as other opportunistic infections, and tumors that rarely affect people who have working immune systems. These late symptoms of infection are referred to as acquired immunodeficiency syndrome (AIDS). This stage is often also associated with weight loss.
Some enveloped RNA viruses can be produced in infected cells that continue growing and dividing without being killed. This probably involves some sort of intracellular regulation of viral growth. It is also possible for the DNA of some viruses to be incorporated into the host cell DNA, producing a carrier state. These are almost always retroviruses, which are called proviruses before and after integration of viral DNA into the host genome.
Data from NHBS were used to determine the percentage of persons at increased risk for infection who were tested in the past 12 months and the percentage who missed opportunities for testing.* NHBS monitors HIV-associated behaviors and HIV prevalence in cities† with high acquired immunodeficiency syndrome (AIDS) prevalence among three populations with HIV risk behaviors: MSM, persons who inject drugs, and heterosexual persons at increased risk for HIV infection.
When HIV infection is advanced, either through treatment failure or in untreated infection, and has caused immune system destruction, secondary infections (opportunistic infections) can occur. Using other antiviral drugs and antibiotics to prevent secondary infection may prevent severe illness and premature (early) death.
Jump up ^ Schindler M, Münch J, Kutsch O, Li H, Santiago ML, Bibollet-Ruche F, Müller-Trutwin MC, Novembre FJ, Peeters M, Courgnaud V, Bailes E, Roques P, Sodora DL, Silvestri G, Sharp PM, Hahn BH, Kirchhoff F (2006). “Nef-mediated suppression of T cell activation was lost in a lentiviral lineage that gave rise to HIV-1”. Cell. 125 (6): 1055–67. doi:10.1016/j.cell.2006.04.033. PMID 16777597.
[Guideline] World Health Organization. Scaling up antiretroviral therapy in resource-limited settings: Treatment guidelines for a public health approach: 2003 revision. World Health Organization, Geneva 2004. Available at http://www.who.int/hiv/pub/prev_care/en/arvrevision2003en.pdf.
There are six additional known HIV-2 groups, each having been found in just one person. They all seem to derive from independent transmissions from sooty mangabeys to humans. Groups C and D have been found in two people from Liberia, groups E and F have been discovered in two people from Sierra Leone, and groups G and H have been detected in two people from the Ivory Coast. Each of these HIV-2 strains, for which humans are probably dead-end hosts, is most closely related to SIVsmm strains from sooty mangabeys living in the same country where the human infection was found.
HIV/AIDS has become a chronic rather than an acutely fatal disease in many areas of the world. Prognosis varies between people, and both the CD4 count and viral load are useful for predicted outcomes. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype. After the diagnosis of AIDS, if treatment is not available, survival ranges between 6 and 19 months. HAART and appropriate prevention of opportunistic infections reduces the death rate by 80%, and raises the life expectancy for a newly diagnosed young adult to 20–50 years. This is between two thirds and nearly that of the general population. If treatment is started late in the infection, prognosis is not as good: for example, if treatment is begun following the diagnosis of AIDS, life expectancy is ~10–40 years. Half of infants born with HIV die before two years of age without treatment.
There are various reasons which can contribute to the failure of the immune system to control HIV infection and prevent AIDS development. By infecting CD4+ T cells, HIV is able to replicate predominantly in activated T cells and paralyse one of the main components of adaptive immune system. HIV can also establish latent infection in CD4+ T cells and remain invisible to CD8+ T cells and therefore replication can occur later in the infection and generate new virions. Antigenic mutation within the T-cell epitopes can affect the binding capacity of MHC molecules to the viral peptides, resulting in the inability of the TCRs to recognise the MHC-peptide complex. Finally, HIV is able to hide from anti-HIV antibodies by expressing non-immunogenic glycans on key antibody epitopes.
As soon as you’re infected with HIV, it starts to reproduce in your body. Your immune system reacts to the antigens by producing antibodies. The time between exposure to HIV and when it becomes detectable in your blood is called the HIV window period.
The impact of AIDS in southern Africa has been devastating. Some communities have been very hard hit with many deaths and economic hardship related to loss of the workforce of young adults. However, significant progress has been made in the last decade. South Africa has the largest antiviral roll-out programme in the world. Campaigns to reduce homophobia are encouraging MSM to declare their sexuality and come forward for testing and treatment. Innovative work with sex workers and injectable drug users, antiretroviral treatment of children, condom distribution programmes and mother-to-child transmission prevention services are all beginning to bear fruit. Life expectancy has increased by five years since the height of the epidemic.With a prevalence of 17.9% and a population of 6.1 million, South Africa has the largest HIV epidemic of any country. In neighbouring countries in southern Africa, the prevalance ranges from 10-15%.
In addition, 1 in 3 people living with HIV present to care with advanced disease, at low CD4 counts and at high risk of serious illness and death. To reduce this risk, WHO recommends that these patients receive a “package of care” that includes testing for and prevention of the most common serious infections that can cause death, such as tuberculosis and cryptococcal meningitis, in addition to ART.
Jump up ^ Robinson, Rachel; Okpo, Emmanuel; Mngoma, Nomusa (2015). “Interventions for improving employment outcomes for workers with HIV”. The Cochrane Database of Systematic Reviews. 5: CD010090. doi:10.1002/14651858.CD010090.pub2. ISSN 1469-493X. PMID 26022149.
Mortality from HIV disease has not been among the 15 leading causes of death in the US since 1997. The age-adjusted death rate for HIV disease peaked in 1995 at 16.3 per 100,000 population, decreased 69.9% through 1998, then further decreased 30.2% from 1999 through 2007, to 3.7 per 100,000 population. In 2007, a total of 11,295 persons died from HIV disease. However, HIV disease has remained among the 5 leading causes of death for specific age groups for females, and in the black population. 
Most individuals infected with HIV will progress to AIDS, if not treated. However, there is a tiny group of patients who develop AIDS very slowly or never at all. These patients are called non-progressors and many seem to have a genetic difference which prevents the virus from attaching to certain immune receptors.
Abnormal elevation of immune activation may be caused in part by absorption of components of bowel bacteria. Immune activation contributes to CD4+ depletion and immunosuppression by mechanisms that remain unclear.
The latest recommendations of the CDC show that HIV testing must start with an immunoassay combination test for HIV-1 and HIV-2 antibodies and p24 antigen. A negative result rules out HIV exposure, while a positive one must be followed by an HIV-1/2 antibody differentiation immunoassay to detect which antibodies are present. This gives rise to four possible scenarios:
Protease inhibitors (PIs) interrupt virus replication at a later step in the HIV life cycle, preventing cells from producing new viruses. Currently, these include ritonavir (Norvir), darunavir (Prezista), and atazanavir (Reyataz). Using PIs with NRTIs reduces the chances that the virus will become resistant to medications. Atazanavir and darunavir are available in combination with cobicistat as atazanavir/cobicistat (Evotaz) and darunavir/cobicistat (Prezcobix). Cobicistat and ritonavir inhibit the breakdown of other drugs, so they are used as boosters to reduce the number of pills needed.
Jump up ^ Klein, Joshua S.; Bjorkman, Pamela J.; Rall, Glenn F. (27 May 2010). “Few and Far Between: How HIV May Be Evading Antibody Avidity”. PLOS Pathogens. 6 (5): e1000908. doi:10.1371/journal.ppat.1000908. PMC 2877745 . PMID 20523901.
In April 1984, the National Cancer Institute announced they had found the cause of AIDS, the retrovirus HTLV-III. In a joint conference with the Pasteur Institute they announced that LAV and HTLV-III are identical and the likely cause of AIDS.22 A blood test was created to screen for the virus with the hope that a vaccine would be developed in two years.23
The closely related simian immunodeficiency virus (SIV) has evolved into many strains, classified by the natural host species. SIV strains of the African green monkey (SIVagm) and sooty mangabey (SIVsmm) are thought to have a long evolutionary history with their hosts. These hosts have to the presence of the virus, which is present at high levels in the host’s blood, but evokes only a mild immune response, does not cause the development of simian AIDS, and does not undergo the extensive mutation and recombination typical of HIV infection in humans.
HIV-1 appears to have originated in southern Cameroon through the evolution of SIV(cpz), a simian immunodeficiency virus (SIV) that infects wild chimpanzees (HIV-1 descends from the SIV(cpz) endemic in the chimpanzee subspecies Pan troglodytes troglodytes). The closest relative of HIV-2 is SIV (smm), a virus of the sooty mangabey (Cercocebus atys atys), an Old World monkey living in littoral West Africa (from southern Senegal to western Côte d’Ivoire). New World monkeys such as the owl monkey are resistant to HIV-1 infection, possibly because of a genomic fusion of two viral resistance genes. HIV-1 is thought to have jumped the species barrier on at least three separate occasions, giving rise to the three groups of the virus, M, N, and O.
Acquired immunodeficiency syndrome A condition defined by CDC criteria, which is intimately linked to infection by a retrovirus, human immunodeficiency virus–HIV-1; long-term survival after HIV infection is possible; once clinical AIDS develops, it is fatal, despite temporary response to various therapies. See ARC, ‘Dominant dozen. ‘, gp120, gp160, Hairy leukoplakia, HIV-1, HIV-2, Isospora belli, Nonprogressive HIV infection Patient zero, Pneumocystis carinii, VLIA–virus-like infectious agent, Walter Reed classification. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]