The majority of people on HIV treatment in countries like Australia will have long-term suppression of symptoms and a reduced viral load. Without HIV treatment people with HIV may develop AIDS and die from infections, cancers and other illnesses the immune system can no longer fight.
In 2006, male circumcision was found to reduce the risk of female-to-male HIV transmission by 60%.81 Since then, the WHO and UNAIDS have emphasised that male circumcision should be considered in areas with high HIV and low male circumcision prevalence.82
The overall figures may give a false impression that the HIV epidemic is relatively homogeneous. In fact, the HIV epidemic is best viewed as numerous separate epidemics among distinct risk groups, although the various epidemics clearly have some level of overlap. In any given area, the infection may be most prevalent among users of intravenous drugs who share needles. In another, the main risk group may be men who have sex with other men. And in yet another, the main risk group may be female sex workers.
Modern HIV testing is extremely accurate. A single screening test is correct more than 99% of the time.[needs update] The chance of a false-positive result in standard two-step testing protocol is estimated to be about 1 in 250,000 in a low risk population. Testing post-exposure is recommended immediately and then at six weeks, three months, and six months.
AIDS is an acquired immunodeficiency syndrome defined by a severe depletion of T cells and over 20 conventional degenerative and neoplastic diseases. In the U.S. and Europe, AIDS correlates to 95% with risk factors, such as about 8 years of promiscuous male homosexuality, intravenous drug use, or hemophilia. Since AIDS also correlates with antibody to a retrovirus, confirmed in about 40% of American cases, it has been hypothesized that this virus causes AIDS by killing T cells. Consequently, the virus was termed human immunodeficiency virus (HIV), and antibody to HIV became part of the definition of AIDS. The hypothesis that HIV causes AIDS is examined in terms of Koch’s postulates and epidemiological, biochemical, genetic, and evolutionary conditions of viral pathology. HIV does not fulfill Koch’s postulates: (i) free virus is not detectable in most cases of AIDS; (ii) virus can only be isolated by reactivating virus in vitro from a few latently infected lymphocytes among millions of uninfected ones; (iii) pure HIV does not cause AIDS upon experimental infection of chimpanzees or accidental infection of healthy humans. Further, HIV violates classical conditions of viral pathology. (i) Epidemiological surveys indicate that the annual incidence of AIDS among antibody-positive persons varies from nearly 0 to over 10%, depending critically on nonviral risk factors. (ii) HIV is expressed in less than or equal to 1 of every 10(4) T cells it supposedly kills in AIDS, whereas about 5% of all T cells are regenerated during the 2 days it takes the virus to infect a cell. (iii) If HIV were the cause of AIDS, it would be the first virus to cause a disease only after the onset of antiviral immunity, as detected by a positive “AIDS test.” (iv) AIDS follows the onset of antiviral immunity only after long and unpredictable asymptomatic intervals averaging 8 years, although HIV replicates within 1 to 2 days and induces immunity within 1 to 2 months. (v) HIV supposedly causes AIDS by killing T cells, although retroviruses can only replicate in viable cells. In fact, infected T cells grown in culture continue to divide. (vi) HIV is isogenic with all other retroviruses and does not express a late, AIDS-specific gene. (vii) If HIV were to cause AIDS, it would have a paradoxical, country-specific pathology, causing over 90% Pneumocystis pneumonia and Kaposi sarcoma in the U.S. but over 90% slim disease, fever, and diarrhea in Africa.(viii) It is highly improbable that within the last few years two viruses (HIV-1 and HIV-2) that are only 40% sequence-related would have evolved that could both cause the newly defined syndrome AIDS. Also, viruses are improbable that kill their only natural host with efficiencies of 50-100%, as is claimed for HIVs. It is concluded that HIV is not sufficient for AIDS and that it may not even be necessary for AIDS because its activity is just as low in symptomatic carriers as in asymptomatic carriers. The correlation between antibody to HIV and AIDS does not prove causation, because otherwise indistinguishable diseases are now set apart only on the basis of this antibody. I propose that AIDS is not a contagious syndrome caused by one conventional virus or microbe. No such virus or microbe would require almost a decade to cause primary disease, nor could it cause the diverse collection of AIDS diseases. Neither would its host range be as selective as that of AIDS, nor could it survive if it were as inefficiently transmitted as AIDS. Since AIDS is defined by new combinations of conventional diseases, it may be caused by new combinations of conventional pathogens, including acute viral or microbial infections and chronic drug use and malnutrition. The long and unpredictable intervals between infection with HIV and AIDS would then reflect the thresholds for these pathogenic factors to cause AIDS diseases, instead of an unlikely mechanism of HIV pathogenesis.
Jump up ^ Friedman-Kien AE (October 1981). “Disseminated Kaposi’s sarcoma syndrome in young homosexual men”. Journal of the American Academy of Dermatology. 5 (4): 468–71. doi:10.1016/S0190-9622(81)80010-2. PMID 7287964.
During successful treatment, the viral load decreases to very low or undetectable levels (less than about 20 to 40 copies per microliter of blood). However, inactive (latent) HIV is still present within cells, and if treatment is stopped, HIV starts replicating and the viral load increases.
In a too brightly lit wood-paneled back room, Sturdevant and the younger men set up a table, displaying brochures, condoms, lube and a few lollipops. Stevenson and Watson, both open, friendly and handsome, attracted a few guys to the table, but mainly ones who had already heard the protect-yourself-against-H.I.V. spiel. Stevenson pointed out that the crowd was sparse — maybe 50 men and a few transgender women — because so many Jackson residents were attending the annual state fair. “Anyway, it’s always hard to make contact in the club,” he said. “I prefer one on one. That way it’s not, ‘I’m trying to educate you’; we’re just talking and having fun. I tell them what I do, and they feel comfortable asking questions.”
Sexual contact. In adults and adolescents, HIV is spread most commonly by sexual contact with an infected partner. The virus enters the body through the lining of the vagina, vulva, penis, rectum, or mouth through sexual activity.
HIV is capable of rapidly mutating to escape recognition by certain HLA immune molecules as well as by cytotoxic T lymphocytes, which help to control HIV replication. Two forms of the HLA-B gene, known as HLA-B*51 and HLA-B*27, for example, produce immune molecules that are particularly susceptible to escape by HIV. The mutation of HIV to avoid those molecules is directly correlated to the frequency at which the HLA-B*51 and HLA-B*27 genes occur within populations. Thus, the percentage of HIV-infected individuals who carry a mutant virus capable of escaping immune detection by HLA-B*51 and HLA-B*27 molecules tends to be high in populations with high frequencies of the HLA-B*51 and HLA-B*27 genes. In contrast, in populations with the lowest frequencies of those genes, only a small percentage of HIV-infected individuals are infected with mutant virus.
HIV for Human Immunodeficiency Virus. It’s a virus that breaks down certain cells in your immune system (your body’s defense against diseases that helps you stay healthy). When HIV damages your immune system, it’s easier to get really sick and even die from infections that your body could normally fight off.
Screening antibody tests or newer combination antigen/antibody tests should be offered routinely to adults and adolescents, particularly pregnant women, regardless of their perceived risk. For people at highest risk, especially sexually active people who have multiple partners and who do not practice safe sex, testing should be repeated every 6 to 12 mo. Such testing is confidential and available, often free of charge, in many public and private facilities throughout the world.
Black America, however, never got a Pepfar. Though the raw numbers were much lower than in Africa, parts of our country looked like the continent the program was created to save. Yet while buckets of money went overseas, domestic funding for H.I.V./AIDS remained flat, and efforts to fight the disease here were reduced to a poorly coordinated patchwork affair. “When we saw that the epidemic was out of proportion in the black community, we started calling for a domestic Pepfar that would bring new resources to the effort, create clear and ambitious objectives and rebuild health care infrastructure around the country,” Lee said. “But we just couldn’t get the administration to focus on a domestic plan.”
And having herpes can also be a risk factor for contracting HIV. This is because genital herpes can cause ulcers that make it easier for HIV to enter the body during sex. And people who have HIV tend to have more severe herpes outbreaks more often because HIV weakens the immune system.
Jump up ^ Israël N, Gougerot-Pocidalo MA (1997). “Oxidative stress in human immunodeficiency virus infection”. Cellular and Molecular Life Sciences. 53 (11–12): 864–70. doi:10.1007/s000180050106. PMID 9447238. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]