AIDS

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Posted by sonny 04/06/2009 @ 00:14

Tags : aids, sexually transmitted diseases, diseases, health

News headlines
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AIDS

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Acquired immune deficiency syndrome or acquired immunodeficiency syndrome (AIDS) is a disease of the human immune system caused by the human immunodeficiency virus (HIV).

This condition progressively reduces the effectiveness of the immune system and leaves individuals susceptible to opportunistic infections and tumors. HIV is transmitted through direct contact of a mucous membrane or the bloodstream with a bodily fluid containing HIV, such as blood, semen, vaginal fluid, preseminal fluid, and breast milk.

This transmission can involve anal, vaginal or oral sex, blood transfusion, contaminated hypodermic needles, exchange between mother and baby during pregnancy, childbirth, or breastfeeding, or other exposure to one of the above bodily fluids.

AIDS is now a pandemic. In 2007, an estimated 33.2 million people lived with the disease worldwide, and it killed an estimated 2.1 million people, including 330,000 children. Over three-quarters of these deaths occurred in sub-Saharan Africa, retarding economic growth and destroying human capital.

Genetic research indicates that HIV originated in west-central Africa during the late nineteenth or early twentieth century. AIDS was first recognized by the U.S. Centers for Disease Control and Prevention in 1981 and its cause, HIV, identified in the early 1980s.

Although treatments for AIDS and HIV can slow the course of the disease, there is currently no vaccine or cure. Antiretroviral treatment reduces both the mortality and the morbidity of HIV infection, but these drugs are expensive and routine access to antiretroviral medication is not available in all countries. Due to the difficulty in treating HIV infection, preventing infection is a key aim in controlling the AIDS epidemic, with health organizations promoting safe sex and needle-exchange programmes in attempts to slow the spread of the virus.

The symptoms of AIDS are primarily the result of conditions that do not normally develop in individuals with healthy immune systems. Most of these conditions are infections caused by bacteria, viruses, fungi and parasites that are normally controlled by the elements of the immune system that HIV damages.

Opportunistic infections are common in people with AIDS. HIV affects nearly every organ system.

People with AIDS also have an increased risk of developing various cancers such as Kaposi's sarcoma, cervical cancer and cancers of the immune system known as lymphomas. Additionally, people with AIDS often have systemic symptoms of infection like fevers, sweats (particularly at night), swollen glands, chills, weakness, and weight loss. The specific opportunistic infections that AIDS patients develop depend in part on the prevalence of these infections in the geographic area in which the patient lives.

Pneumocystis pneumonia (originally known as Pneumocystis carinii pneumonia, and still abbreviated as PCP, which now stands for Pneumocystis pneumonia) is relatively rare in healthy, immunocompetent people, but common among HIV-infected individuals. It is caused by Pneumocystis jirovecii.

Before the advent of effective diagnosis, treatment and routine prophylaxis in Western countries, it was a common immediate cause of death. In developing countries, it is still one of the first indications of AIDS in untested individuals, although it does not generally occur unless the CD4 count is less than 200 cells per µL of blood.

Tuberculosis (TB) is unique among infections associated with HIV because it is transmissible to immunocompetent people via the respiratory route, is easily treatable once identified, may occur in early-stage HIV disease, and is preventable with drug therapy. However, multidrug resistance is a potentially serious problem.

Even though its incidence has declined because of the use of directly observed therapy and other improved practices in Western countries, this is not the case in developing countries where HIV is most prevalent. In early-stage HIV infection (CD4 count >300 cells per µL), TB typically presents as a pulmonary disease. In advanced HIV infection, TB often presents atypically with extrapulmonary (systemic) disease a common feature. Symptoms are usually constitutional and are not localized to one particular site, often affecting bone marrow, bone, urinary and gastrointestinal tracts, liver, regional lymph nodes, and the central nervous system.

Esophagitis is an inflammation of the lining of the lower end of the esophagus (gullet or swallowing tube leading to the stomach). In HIV infected individuals, this is normally due to fungal (candidiasis) or viral (herpes simplex-1 or cytomegalovirus) infections. In rare cases, it could be due to mycobacteria.

Unexplained chronic diarrhea in HIV infection is due to many possible causes, including common bacterial (Salmonella, Shigella, Listeria or Campylobacter) and parasitic infections; and uncommon opportunistic infections such as cryptosporidiosis, microsporidiosis, Mycobacterium avium complex (MAC) and viruses, astrovirus, adenovirus, rotavirus and cytomegalovirus, (the latter as a course of colitis).

In some cases, diarrhea may be a side effect of several drugs used to treat HIV, or it may simply accompany HIV infection, particularly during primary HIV infection. It may also be a side effect of antibiotics used to treat bacterial causes of diarrhea (common for Clostridium difficile). In the later stages of HIV infection, diarrhea is thought to be a reflection of changes in the way the intestinal tract absorbs nutrients, and may be an important component of HIV-related wasting.

HIV infection may lead to a variety of neuropsychiatric sequelae, either by infection of the now susceptible nervous system by organisms, or as a direct consequence of the illness itself.

Toxoplasmosis is a disease caused by the single-celled parasite called Toxoplasma gondii; it usually infects the brain, causing toxoplasma encephalitis, but it can also infect and cause disease in the eyes and lungs. Cryptococcal meningitis is an infection of the meninx (the membrane covering the brain and spinal cord) by the fungus Cryptococcus neoformans. It can cause fevers, headache, fatigue, nausea, and vomiting. Patients may also develop seizures and confusion; left untreated, it can be lethal.

Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease, in which the gradual destruction of the myelin sheath covering the axons of nerve cells impairs the transmission of nerve impulses. It is caused by a virus called JC virus which occurs in 70% of the population in latent form, causing disease only when the immune system has been severely weakened, as is the case for AIDS patients. It progresses rapidly, usually causing death within months of diagnosis.

AIDS dementia complex (ADC) is a metabolic encephalopathy induced by HIV infection and fueled by immune activation of HIV infected brain macrophages and microglia. These cells are productively infected by HIV and secrete neurotoxins of both host and viral origin. Specific neurological impairments are manifested by cognitive, behavioral, and motor abnormalities that occur after years of HIV infection and are associated with low CD4+ T cell levels and high plasma viral loads.

Prevalence is 10–20% in Western countries but only 1–2% of HIV infections in India. This difference is possibly due to the HIV subtype in India. AIDS related mania is sometimes seen in patients with advanced HIV illness; it presents with more irritability and cognitive impairment and less euphoria than a manic episode associated with true bipolar disorder. Unlike the latter condition, it may have a more chronic course. This syndrome is less often seen with the advent of multi-drug therapy.

Patients with HIV infection have substantially increased incidence of several cancers. This is primarily due to co-infection with an oncogenic DNA virus, especially Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV), and human papillomavirus (HPV).

Kaposi's sarcoma (KS) is the most common tumor in HIV-infected patients. The appearance of this tumor in young homosexual men in 1981 was one of the first signals of the AIDS epidemic. Caused by a gammaherpes virus called Kaposi's sarcoma-associated herpes virus (KSHV), it often appears as purplish nodules on the skin, but can affect other organs, especially the mouth, gastrointestinal tract, and lungs.

High-grade B cell lymphomas such as Burkitt's lymphoma, Burkitt's-like lymphoma, diffuse large B-cell lymphoma (DLBCL), and primary central nervous system lymphoma present more often in HIV-infected patients. These particular cancers often foreshadow a poor prognosis. In some cases these lymphomas are AIDS-defining. Epstein-Barr virus (EBV) or KSHV cause many of these lymphomas.

Cervical cancer in HIV-infected women is considered AIDS-defining. It is caused by human papillomavirus (HPV).

In addition to the AIDS-defining tumors listed above, HIV-infected patients are at increased risk of certain other tumors, such as Hodgkin's disease and anal and rectal carcinomas. However, the incidence of many common tumors, such as breast cancer or colon cancer, does not increase in HIV-infected patients. In areas where HAART is extensively used to treat AIDS, the incidence of many AIDS-related malignancies has decreased, but at the same time malignant cancers overall have become the most common cause of death of HIV-infected patients.

AIDS patients often develop opportunistic infections that present with non-specific symptoms, especially low-grade fevers and weight loss. These include infection with Mycobacterium avium-intracellulare and cytomegalovirus (CMV). CMV can cause colitis, as described above, and CMV retinitis can cause blindness.

Penicilliosis due to Penicillium marneffei is now the third most common opportunistic infection (after extrapulmonary tuberculosis and cryptococcosis) in HIV-positive individuals within the endemic area of Southeast Asia.

AIDS is the most severe acceleration of infection with HIV. HIV is a retrovirus that primarily infects vital organs of the human immune system such as CD4+ T cells (a subset of T cells), macrophages and dendritic cells. It directly and indirectly destroys CD4+ T cells.

Once HIV has killed so many CD4+ T cells that there are fewer than 200 of these cells per microliter (µL) of blood, cellular immunity is lost. Acute HIV infection progresses over time to clinical latent HIV infection and then to early symptomatic HIV infection and later to AIDS, which is identified either on the basis of the amount of CD4+ T cells remaining in the blood, and/or the presence of certain infections, as noted above.

In the absence of antiretroviral therapy, the median time of progression from HIV infection to AIDS is nine to ten years, and the median survival time after developing AIDS is only 9.2 months. However, the rate of clinical disease progression varies widely between individuals, from two weeks up to 20 years.

Many factors affect the rate of progression. These include factors that influence the body's ability to defend against HIV such as the infected person's general immune function. Older people have weaker immune systems, and therefore have a greater risk of rapid disease progression than younger people.

Poor access to health care and the existence of coexisting infections such as tuberculosis also may predispose people to faster disease progression. The infected person's genetic inheritance plays an important role and some people are resistant to certain strains of HIV. An example of this is people with the homozygous CCR5-Δ32 variation are resistant to infection with certain strains of HIV. HIV is genetically variable and exists as different strains, which cause different rates of clinical disease progression.

Sexual transmission occurs with the contact between sexual secretions of one person with the rectal, genital or oral mucous membranes of another. Unprotected receptive sexual acts are riskier than unprotected insertive sexual acts, and the risk for transmitting HIV through unprotected anal intercourse is greater than the risk from vaginal intercourse or oral sex.

However, oral sex is not entirely safe, as HIV can be transmitted through both insertive and receptive oral sex. Sexual assault greatly increases the risk of HIV transmission as condoms are rarely employed and physical trauma to the vagina occurs frequently, facilitating the transmission of HIV.

Other sexually transmitted infections (STI) increase the risk of HIV transmission and infection, because they cause the disruption of the normal epithelial barrier by genital ulceration and/or microulceration; and by accumulation of pools of HIV-susceptible or HIV-infected cells (lymphocytes and macrophages) in semen and vaginal secretions. Epidemiological studies from sub-Saharan Africa, Europe and North America suggest that genital ulcers, such as those caused by syphilis and/or chancroid, increase the risk of becoming infected with HIV by about fourfold. There is also a significant although lesser increase in risk from STIs such as gonorrhea, chlamydia and trichomoniasis, which all cause local accumulations of lymphocytes and macrophages.

Transmission of HIV depends on the infectiousness of the index case and the susceptibility of the uninfected partner. Infectivity seems to vary during the course of illness and is not constant between individuals. An undetectable plasma viral load does not necessarily indicate a low viral load in the seminal liquid or genital secretions.

However, each 10-fold increase in the level of HIV in the blood is associated with an 81% increased rate of HIV transmission. Women are more susceptible to HIV-1 infection due to hormonal changes, vaginal microbial ecology and physiology, and a higher prevalence of sexually transmitted diseases.

People who have been infected with one strain of HIV can still be infected later on in their lives by other, more virulent strains.

Infection is unlikely in a single encounter. High rates of infection have been linked to a pattern of overlapping long-term sexual relationships. This allows the virus to quickly spread to multiple partners who in turn infect their partners. A pattern of serial monogamy or occasional casual encounters is associated with lower rates of infection.

HIV spreads readily through heterosexual sex in Africa, but less so elsewhere. One possibility being researched is that schistosomiasis, which affects up to 50 per cent of women in parts of Africa, damages the lining of the vagina.

This transmission route is particularly relevant to intravenous drug users, hemophiliacs and recipients of blood transfusions and blood products. Sharing and reusing syringes contaminated with HIV-infected blood represents a major risk for infection with HIV.

Needle sharing is the cause of one third of all new HIV-infections in North America, China, and Eastern Europe. The risk of being infected with HIV from a single prick with a needle that has been used on an HIV-infected person is thought to be about 1 in 150 (see table above). Post-exposure prophylaxis with anti-HIV drugs can further reduce this risk.

This route can also affect people who give and receive tattoos and piercings. Universal precautions are frequently not followed in both sub-Saharan Africa and much of Asia because of both a shortage of supplies and inadequate training.

The WHO estimates that approximately 2.5% of all HIV infections in sub-Saharan Africa are transmitted through unsafe healthcare injections. Because of this, the United Nations General Assembly has urged the nations of the world to implement precautions to prevent HIV transmission by health workers.

The risk of transmitting HIV to blood transfusion recipients is extremely low in developed countries where improved donor selection and HIV screening is performed. However, according to the WHO, the overwhelming majority of the world's population does not have access to safe blood and between 5% and 10% of the world's HIV infections come from transfusion of infected blood and blood products.

The transmission of the virus from the mother to the child can occur in utero during the last weeks of pregnancy and at childbirth. In the absence of treatment, the transmission rate between a mother and her child during pregnancy, labor and delivery is 25%.

However, when the mother takes antiretroviral therapy and gives birth by caesarean section, the rate of transmission is just 1%. The risk of infection is influenced by the viral load of the mother at birth, with the higher the viral load, the higher the risk. Breastfeeding also increases the risk of transmission by about 4 %.

A number of misconceptions have arisen surrounding HIV/AIDS. Three of the most common are that AIDS can spread through casual contact, that sexual intercourse with a virgin will cure AIDS, and that HIV can infect only homosexual men and drug users. Other misconceptions are that any act of anal intercourse between gay men can lead to AIDS infection, and that open discussion of homosexuality and HIV in schools will lead to increased rates of homosexuality and AIDS.

The pathophysiology of AIDS is complex, as is the case with all syndromes. Ultimately, HIV causes AIDS by depleting CD4+ T helper lymphocytes. This weakens the immune system and allows opportunistic infections. T lymphocytes 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 a majority of mucosal CD4+ T cells express the CCR5 coreceptor, whereas a small fraction of CD4+ T cells in the bloodstream do so.

HIV seeks out and destroys CCR5 expressing CD4+ cells during acute infection. A vigorous immune response eventually controls the infection and initiates the clinically latent phase. However, CD4+ T cells in mucosal tissues remain depleted throughout the infection, although enough remain to initially ward off life-threatening infections.

Continuous HIV replication results in 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 proinflammatory cytokines, results from the activity of several HIV gene products and the immune response to ongoing HIV replication. Another cause is the breakdown of the immune surveillance system of the mucosal barrier caused by the depletion of mucosal CD4+ T cells during the acute phase of disease.

This results in the systemic exposure of the immune system to microbial components of the gut’s normal flora, which in a healthy person is kept in check by the mucosal immune system. The activation and proliferation of T cells that results from immune activation provides fresh targets for HIV infection. However, direct killing by HIV alone cannot account for the observed depletion of CD4+ T cells since only 0.01-0.10% of CD4+ T cells in the blood are infected.

The virus has cytopathic effects but how it does it is still not quite clear. It can remain inactive in these cells for long periods, though. This effect is hypothesized to be due to the CD4-gp120 interaction.

The diagnosis of AIDS in a person infected with HIV is based on the presence of certain signs or symptoms. Since June 5, 1981, many definitions have been developed for epidemiological surveillance such as the Bangui definition and the 1994 expanded World Health Organization AIDS case definition. However, clinical staging of patients was not an intended use for these systems as they are neither sensitive, nor specific. In developing countries, the World Health Organization staging system for HIV infection and disease, using clinical and laboratory data, is used and in developed countries, the Centers for Disease Control (CDC) Classification System is used.

In 1990, the World Health Organization (WHO) grouped these infections and conditions together by introducing a staging system for patients infected with HIV-1. An update took place in September 2005. Most of these conditions are opportunistic infections that are easily treatable in healthy people.

There are two main definitions for AIDS, both produced by the Centers for Disease Control and Prevention (CDC). The older definition is to referring to AIDS using the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus. In 1993, the CDC expanded their definition of AIDS to include all HIV positive people with a CD4+ T cell count below 200 per µL of blood or 14% of all lymphocytes. The majority of new AIDS cases in developed countries use either this definition or the pre-1993 CDC definition. The AIDS diagnosis still stands even if, after treatment, the CD4+ T cell count rises to above 200 per µL of blood or other AIDS-defining illnesses are cured.

Many people are unaware that they are infected with HIV. Less than 1% of the sexually active urban population in Africa has been tested, and this proportion is even lower in rural populations. Furthermore, only 0.5% of pregnant women attending urban health facilities are counseled, tested or receive their test results. Again, this proportion is even lower in rural health facilities. Therefore, donor blood and blood products used in medicine and medical research are screened for HIV.

HIV tests are usually performed on venous blood. Many laboratories use fourth generation screening tests which detect anti-HIV antibody (IgG and IgM) and the HIV p24 antigen. The detection of HIV antibody or antigen in a patient previously known to be negative is evidence of HIV infection. Individuals whose first specimen indicates evidence of HIV infection will have a repeat test on a second blood sample to confirm the results.

The window period (the time between initial infection and the development of detectable antibodies against the infection) can vary since it can take 3–6 months to seroconvert and to test positive. Detection of the virus using polymerase chain reaction (PCR) during the window period is possible, and evidence suggests that an infection may often be detected earlier than when using a fourth generation EIA screening test.

Positive results obtained by PCR are confirmed by antibody tests. Routinely used HIV tests for infection in neonates, born to HIV-positive mothers, have no value because of the presence of maternal antibody to HIV in the child's blood. HIV infection can only be diagnosed by PCR, testing for HIV pro-viral DNA in the children's lymphocytes.

The three main transmission routes of HIV are sexual contact, exposure to infected body fluids or tissues, and from mother to fetus or child during perinatal period. It is possible to find HIV in the saliva, tears, and urine of infected individuals, but there are no recorded cases of infection by these secretions, and the risk of infection is negligible.

The majority of HIV infections are acquired through unprotected sexual relations between partners, one of whom has HIV. The primary mode of HIV infection worldwide is through sexual contact between members of the opposite sex.

During a sexual act, only male or female condoms can reduce the chances of infection with HIV and other STDs and the chances of becoming pregnant. The best evidence to date indicates that typical condom use reduces the risk of heterosexual HIV transmission by approximately 80% over the long-term, though the benefit is likely to be higher if condoms are used correctly on every occasion.

The male latex condom, if used correctly without oil-based lubricants, is the single most effective available technology to reduce the sexual transmission of HIV and other sexually transmitted infections. Manufacturers recommend that oil-based lubricants such as petroleum jelly, butter, and lard not be used with latex condoms, because they dissolve the latex, making the condoms porous. If necessary, manufacturers recommend using water-based lubricants.

Oil-based lubricants can however be used with polyurethane condoms.

The female condom is an alternative to the male condom and is made from polyurethane, which allows it to be used in the presence of oil-based lubricants. They are larger than male condoms and have a stiffened ring-shaped opening, and are designed to be inserted into the vagina.

The female condom contains an inner ring, which keeps the condom in place inside the vagina – inserting the female condom requires squeezing this ring. However, at present availability of female condoms is very low and the price remains prohibitive for many women.

Preliminary studies suggest that, where female condoms are available, overall protected sexual acts increase relative to unprotected sexual acts, making them an important HIV prevention strategy.

Studies on couples where one partner is infected show that with consistent condom use, HIV infection rates for the uninfected partner are below 1% per year. Prevention strategies are well-known in developed countries, but epidemiological and behavioral studies in Europe and North America suggest that a substantial minority of young people continue to engage in high-risk practices despite HIV/AIDS knowledge, underestimating their own risk of becoming infected with HIV.

Randomized controlled trials have shown that male circumcision lowers the risk of HIV infection among heterosexual men by up to 60%. It is expected that this procedure will be actively promoted in many of the countries affected by HIV, although doing so will involve confronting a number of practical, cultural and attitudinal issues.

Some experts fear that a lower perception of vulnerability among circumcised men may result in more sexual risk-taking behavior, thus negating its preventive effects. However, one randomized controlled trial indicated that adult male circumcision was not associated with increased HIV risk behavior.

Health care workers can reduce exposure to HIV by employing precautions to reduce the risk of exposure to contaminated blood. These precautions include barriers such as gloves, masks, protective eyeware or shields, and gowns or aprons which prevent exposure of the skin or mucous membranes to blood borne pathogens. Frequent and thorough washing of the skin immediately after being contaminated with blood or other bodily fluids can reduce the chance of infection. Finally, sharp objects like needles, scalpels and glass, are carefully disposed of to prevent needlestick injuries with contaminated items. Since intravenous drug use is an important factor in HIV transmission in developed countries, harm reduction strategies such as needle-exchange programmes are used in attempts to reduce the infections caused by drug abuse.

Current recommendations state that when replacement feeding is acceptable, feasible, affordable, sustainable and safe, HIV-infected mothers should avoid breast-feeding their infant. However, if this is not the case, exclusive breast-feeding is recommended during the first months of life and discontinued as soon as possible. It should be noted that women may breastfeed other children who are not their own; see wetnurse.

There is currently no vaccine or cure for HIV or AIDS. The only known methods of prevention are based on avoiding exposure to the virus or, failing that, an antiretroviral treatment directly after a highly significant exposure, called post-exposure prophylaxis (PEP). PEP has a very demanding four week schedule of dosage. It also has very unpleasant side effects including diarrhea, malaise, nausea and fatigue.

Current treatment for HIV infection consists of highly active antiretroviral therapy, or HAART. This has been highly beneficial to many HIV-infected individuals since its introduction in 1996 when the protease inhibitor-based HAART initially became available. Current optimal HAART options consist of combinations (or "cocktails") consisting of at least three drugs belonging to at least two types, or "classes," of antiretroviral agents. Typical regimens consist of two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). Because HIV disease progression in children is more rapid than in adults, and laboratory parameters are less predictive of risk for disease progression, particularly for young infants, treatment recommendations are more aggressive for children than for adults. In developed countries where HAART is available, doctors assess the viral load, rapidity in CD4 decline, and patient readiness while deciding when to recommend initiating treatment.

Standard goals of HAART include improvement in the patient’s quality of life, reduction in complications, and reduction of HIV viremia below the limit of detection, but it does not cure the patient of HIV nor does it prevent the return, once treatment is stopped, of high blood levels of HIV, often HAART resistant. Moreover, it would take more than the lifetime of an individual to be cleared of HIV infection using HAART. Despite this, many HIV-infected individuals have experienced remarkable improvements in their general health and quality of life, which has led to the plummeting of HIV-associated morbidity and mortality. In the absence of HAART, progression from HIV infection to AIDS occurs at a median of between nine to ten years and the median survival time after developing AIDS is only 9.2 months. HAART is thought to increase survival time by between 4 and 12 years.

For some patients, which can be more than fifty percent of patients, HAART achieves far less than optimal results, due to medication intolerance/side effects, prior ineffective antiretroviral therapy and infection with a drug-resistant strain of HIV. Non-adherence and non-persistence with therapy are the major reasons why some people do not benefit from HAART. The reasons for non-adherence and non-persistence are varied. Major psychosocial issues include poor access to medical care, inadequate social supports, psychiatric disease and drug abuse. HAART regimens can also be complex and thus hard to follow, with large numbers of pills taken frequently. Side effects can also deter people from persisting with HAART, these include lipodystrophy, dyslipidaemia, diarrhoea, insulin resistance, an increase in cardiovascular risks and birth defects. Anti-retroviral drugs are expensive, and the majority of the world's infected individuals do not have access to medications and treatments for HIV and AIDS.

It has been postulated that only a vaccine can halt the pandemic because a vaccine would possibly cost less, thus being affordable for developing countries, and would not require daily treatments. However, even after almost 30 years of research, HIV-1 remains a difficult target for a vaccine.

Research to improve current treatments includes decreasing side effects of current drugs, further simplifying drug regimens to improve adherence, and determining the best sequence of regimens to manage drug resistance. A number of studies have shown that measures to prevent opportunistic infections can be beneficial when treating patients with HIV infection or AIDS. Vaccination against hepatitis A and B is advised for patients who are not infected with these viruses and are at risk of becoming infected. Patients with substantial immunosuppression are also advised to receive prophylactic therapy for Pneumocystis jiroveci pneumonia (PCP), and many patients may benefit from prophylactic therapy for toxoplasmosis and Cryptococcus meningitis as well.

Researchers have discovered an abzyme that can destroy the protein gp120 CD4 binding site. This protein is common to all HIV variants as it is the attachment point for B lymphocytes and subsequent compromising of the immune system.

In Berlin, Germany, a 42-year-old leukemia patient infected with HIV for more than a decade was given an experimental transplant of bone marrow with cells that contained an unusual natural variant of the CCR5 cell-surface receptor. This CCR5-Δ32 variant has been shown to make some cells from people who are born with it resistant to infection with some strains of HIV. Almost two years after the transplant, and even after the patient reportedly stopped taking antiretroviral medications, HIV has not been detected in the patient's blood.

Various forms of alternative medicine have been used to treat symptoms or alter the course of the disease. Current studies indicate that alternative medicine therapies have little effect on the mortality or morbidity of the disease, but may improve the quality of life of individuals with AIDS. The psychological benefits of these therapies are the most important use. Acupuncture has been used to alleviate some symptoms with no success and cannot cure the HIV infection. Several randomized clinical trials testing the effect of herbal medicines have shown that there is no evidence that these herbs have any effect on the progression of the disease, but may instead produce serious side-effects.

Morbidity and mortality among HIV-infected adults with adequate dietary nutritional intake is unaffected by multivitamin supplementation. A large Tanzanian trial in immunologically- and nutritionally-compromised pregnant and lactating women showed a number of benefits to daily multivitamin supplementation for both mothers and children. Dietary intake of micronutrients at RDA levels by HIV-infected adults is recommended by the World Health Organization. There is some evidence that vitamin A supplementation in children reduces mortality and improves growth. Daily doses of selenium can suppress HIV viral burden with an associated improvement of the CD4 count. Selenium can be used as an adjunct therapy to standard antiviral treatments, but cannot itself reduce mortality and morbidity.

Without treatment, the net median survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype, and the median survival rate after diagnosis of AIDS in resource-limited settings where treatment is not available ranges between 6 and 19 months, depending on the study. In areas where it is widely available, the development of HAART as effective therapy for HIV infection and AIDS reduced the death rate from this disease by 80%, and raised the life expectancy for a newly diagnosed HIV-infected person to about 20 years.

As new treatments continue to be developed and because HIV continues to evolve resistance to treatments, estimates of survival time are likely to continue to change. Without antiretroviral therapy, death normally occurs within a year. Most patients die from opportunistic infections or malignancies associated with the progressive failure of the immune system. The rate of clinical disease progression varies widely between individuals and has been shown to be affected by many factors such as host susceptibility and immune function health care and co-infections, as well as which particular strain of the virus is involved.

The AIDS pandemic can also be seen as several epidemics of separate subtypes; the major factors in its spread are sexual transmission and vertical transmission from mother to child at birth and through breast milk. Despite recent, improved access to antiretroviral treatment and care in many regions of the world, the AIDS pandemic claimed an estimated 2.1 million (range 1.9–2.4 million) lives in 2007 of which an estimated 330,000 were children under 15 years. Globally, an estimated 33.2 million people lived with HIV in 2007, including 2.5 million children. An estimated 2.5 million (range 1.8–4.1 million) people were newly infected in 2007, including 420,000 children.

Sub-Saharan Africa remains by far the worst affected region. In 2007 it contained an estimated 68% of all people living with AIDS and 76% of all AIDS deaths, with 1.7 million new infections bringing the number of people living with HIV to 22.5 million, and with 11.4 million AIDS orphans living in the region. Unlike other regions, most people living with HIV in sub-Saharan Africa in 2007 (61%) were women. Adult prevalence in 2007 was an estimated 5.0%, and AIDS continued to be the single largest cause of mortality in this region. South Africa has the largest population of HIV patients in the world, followed by Nigeria and India. South & South East Asia are second worst affected; in 2007 this region contained an estimated 18% of all people living with AIDS, and an estimated 300,000 deaths from AIDS. India has an estimated 2.5 million infections and an estimated adult prevalence of 0.36%. Life expectancy has fallen dramatically in the worst-affected countries; for example, in 2006 it was estimated that it had dropped from 65 to 35 years in Botswana.

AIDS was first reported June 5, 1981, when the U.S. Centers for Disease Control and Prevention recorded a cluster of Pneumocystis carinii pneumonia (now still classified as PCP but known to be caused by Pneumocystis jirovecii) in five homosexual men in Los Angeles. In the beginning, the Centers for Disease Control and Prevention (CDC) did not have an official name for the disease, often referring to it by way of the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus. They also used Kaposi's Sarcoma and Opportunistic Infections, the name by which a task force had been set up in 1981. In the general press, the term GRID, which stood for Gay-related immune deficiency, had been coined. The CDC, in search of a name, and looking at the infected communities coined “the 4H disease,” as it seemed to single out Haitians, homosexuals, hemophiliacs, and heroin users. However, after determining that AIDS was not isolated to the homosexual community, the term GRID became misleading and AIDS was introduced at a meeting in July 1982. By September 1982 the CDC started using the name AIDS, and properly defined the illness.

A more controversial theory known as the OPV AIDS hypothesis suggests that the AIDS epidemic was inadvertently started in the late 1950s in the Belgian Congo by Hilary Koprowski's research into a poliomyelitis vaccine. According to scientific consensus, this scenario is not supported by the available evidence.

A recent study states that HIV probably moved from Africa to Haiti and then entered the United States around 1969.

AIDS stigma exists around the world in a variety of ways, including ostracism, rejection, discrimination and avoidance of HIV infected people; compulsory HIV testing without prior consent or protection of confidentiality; violence against HIV infected individuals or people who are perceived to be infected with HIV; and the quarantine of HIV infected individuals. Stigma-related violence or the fear of violence prevents many people from seeking HIV testing, returning for their results, or securing treatment, possibly turning what could be a manageable chronic illness into a death sentence and perpetuating the spread of HIV.

Often, AIDS stigma is expressed in conjunction with one or more other stigmas, particularly those associated with homosexuality, bisexuality, promiscuity, prostitution, and intravenous drug use.

In many developed countries, there is an association between AIDS and homosexuality or bisexuality, and this association is correlated with higher levels of sexual prejudice such as anti-homosexual attitudes. There is also a perceived association between AIDS and all male-male sexual behavior, including sex between uninfected men.

HIV and AIDS affects economic growth by reducing the availability of human capital. Without proper nutrition, health care and medicine that is available in developed countries, large numbers of people suffer and die from AIDS-related complications. They will not only be unable to work, but will also require significant medical care. The forecast is that this will likely cause a collapse of economies and societies in countries with a significant AIDS population. In some heavily infected areas, the epidemic has left behind many orphans cared for by elderly grandparents.

The increased mortality in this region will result in a smaller skilled population and labor force. This smaller labor force will be predominantly young people, with reduced knowledge and work experience leading to reduced productivity. An increase in workers’ time off to look after sick family members or for sick leave will also lower productivity. Increased mortality will also weaken the mechanisms that generate human capital and investment in people, through loss of income and the death of parents. By killing off mainly young adults, AIDS seriously weakens the taxable population, reducing the resources available for public expenditures such as education and health services not related to AIDS resulting in increasing pressure for the state's finances and slower growth of the economy. This results in a slower growth of the tax base, an effect that will be reinforced if there are growing expenditures on treating the sick, training (to replace sick workers), sick pay and caring for AIDS orphans. This is especially true if the sharp increase in adult mortality shifts the responsibility and blame from the family to the government in caring for these orphans.

On the level of the household, AIDS results in both the loss of income and increased spending on healthcare by the household. The income effects of this lead to spending reduction as well as a substitution effect away from education and towards healthcare and funeral spending. A study in Côte d'Ivoire showed that households with an HIV/AIDS patient spent twice as much on medical expenses as other households.

A small number of activists question the connection between HIV and AIDS, the existence of HIV, or the validity of current treatment methods (even going so far as to claim that the drug therapy itself was the cause of AIDS deaths). Though these claims have been examined and thoroughly rejected by the scientific community, they continue to be promulgated through the Internet and have had a significant political impact. In South Africa, former President Thabo Mbeki's embrace of AIDS denialism resulted in an ineffective governmental response to the AIDS epidemic that has been blamed for hundreds of thousands of AIDS-related deaths.

A subculture of homosexual men desire and actively pursue HIV infection by seeking partners who are HIV-positive and voluntarily having unprotected intercourse with them. In slang terms, those who seek infection are called bugchasers and those who infect them are called giftgivers. This phenomenon should be distinguished from barebacking, which is the preference for unprotected intercourse without the active desire for HIV infection.

The exact extent of practice remains largely unknown. Not all those who self-identify as part of this subculture are actually intent on spreading HIV. Some bugchasers try to connect with giftgivers via the Internet. Other bugchasers organize and participate in "bug parties" or "conversion parties," sex parties where HIV positive and negative men engage in unprotected sex, in hopes of acquiring HIV ("getting the gift").

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Origin of AIDS

Scanning electron micrograph of HIV-1 budding from cultured lymphocyte.

HIV, the virus that causes AIDS, probably originated in non-human primates in sub-Saharan Africa and was transferred to humans during the late 19th or early 20th century.

Two types of HIV infect humans: HIV-1 and HIV-2. HIV-1 is more virulent, is easily transmitted and is the cause of the majority of HIV infections globally. HIV-1 is closely related to a virus found in chimpanzees, and molecular phylogenetics indicates that the HIV-1 virus appeared sometime between 1884 and 1924 in equatorial Africa. HIV-2 is less transmittable and is largely confined to West Africa, along with its closest relative, a virus of the Sooty Mangabey (Cercocebus atys), an Old World monkey of Guinea-Bissau, Gabon, and Cameroon.

Most HIV researchers agree that HIV evolved from the closely related Simian Immunodeficiency Virus (SIV), and that HIV was transferred from non-human primates to humans in the recent past (as a type of zoonosis). Research in this area is conducted using molecular phylogenetics, comparing viral genomic sequences to determine relatedness.

Because HIV-1 is closely related to a strain of the simian immunodeficiency virus that infects the chimpanzee subspecies Pan troglodytes troglodytes (SIVcpz), scientists generally accept that the virus originated in populations of wild chimpanzees in West-Central Africa. Exactly where this occurred—in the southeastern rain forests of Cameroon (modern East Province) near the Sanaga River, or further south near Kinshasa in the Democratic Republic of the Congo—has been a matter of scientific discussion.

Using HIV-1 sequences preserved in human biological samples along with estimates of viral mutation rates, scientists calculate that the jump from chimpanzee to human probably happened during the late 19th or early 20th century, a time of rapid urbanisation and colonialisation in equatorial Africa. Exactly when the zoonosis occurred is not known. Some estimates suggest that HIV-1 (group M) entered the human population in the early 20th century, probably between 1915 and 1941. A study published in 2008, analyzing viral sequences recovered from a recently-discovered 1960 biopsy along with previously-known sequences, suggested a common ancestor between 1884 and 1924.

Genetic recombination had earlier been thought to "seriously confound" such phylogenetic analysis, but later "work has suggested that recombination is not likely to systematically bias ", although recombination is "expected to increase variance". The results of the study supported the later work and indicated that HIV evolves "fairly reliably".

According to the 'Hunter Theory', the "simplest and most plausible explanation for the cross-species transmission", the virus was transmitted from a chimpanzee to a human when a bushmeat hunter was bitten or cut while hunting or butchering an animal. The resulting exposure of the hunter to blood or other bodily fluids of the chimpanzee could have resulted in infection.

Such requirements existed for smallpox and for the 20th century Spanish flu at Fort Riley, Kansas, where the animal reservoir seems to have been two species, chickens and pigs.

Conditions introduced by colonialisation may have been conducive to the spread of the virus. The hardships of forced labour could have suppressed the immune system of the initial hunter, allowing the virus to infect and take hold in a new host. Rapid urbanisation brought infected people into close contact with others, and colonial commerce provided opportunities for further geographical spread. Vaccination campaigns against illnesses such as sleeping sickness may have sped the initial spread of HIV-1 when immunisation needles were re-used. Other technological and social disruptions, especially those that affected the food supply and the hunting of bushmeat, may also have promoted the cross-over from chimpanzees and the spread amongst humans.

SIV in non-human primates tends to cause a non-fatal disease. Comparison of the gene sequence of SIV with HIV should therefore give us information about the factors necessary to cause disease in humans. The factors that determine the virulence of HIV as compared to most SIVs are only now being elucidated. Non-human SIVs contain a nef gene that down-regulates CD3, CD4, and MHC class I expression; most non-human SIVs therefore do not induce immunodeficiency; the HIV nef gene however has lost its ability to down-regulate CD3, which results in the immune activation and apoptosis that is characteristic of chronic HIV infection.

The new data may not convince the hardened conspiracy theorist who thinks that contamination of OPV by chimpanzee virus was subsequently and deliberately covered up. But those of us who were formerly willing to give some credence to the OPV hypothesis will now consider that the matter has been laid to rest.

Phylogenetic DNA analysis of HIV suggests that the virus established itself in the human population decades before the introduction of the polio vaccine.

The oldest documented possible case of the then-unknown syndrome was thought to have been detected in 1959, when a 25-year-old British printer (usually referred to, mistakenly, as a sailor) who had travelled in the navy between 1955 and 1957 (but apparently not to Africa) sought help at the Royal Infirmary of Manchester, England. He reported to have been suffering from puzzling symptoms, among them purplish skin lesions, for nearly two years. His condition had taken a turn for worse during Christmas 1958, when he started suffering from shortness of breath, extreme fatigue, rapid weight loss, night sweats and high fever. The doctors thought he might be suffering from tuberculosis and, even though they found no evidence of bacterial infection, they treated him for tuberculosis just to be safe, to no avail. The printer continued to weaken and he died shortly after in August 1959. His autopsy revealed evidence of two unusual infections, cytomegalovirus and Pneumocystis carinii pneumonia (PCP, later, when redetermined as P. jirovecii, renamed Pneumocystis pneumonia), very rare at the time but now commonly associated with AIDS patients. His case had puzzled his doctors, who preserved tissue samples from him and for years retained some interest in solving the mystery.

One of the earliest documented HIV-1 infections was discovered in a preserved blood sample taken in 1959 from a man from Leopoldville, Belgian Congo (now Kinshasa, Democratic Republic of the Congo). However, it is unknown whether this anonymous person ever developed AIDS and died of its complications.

A second early documented HIV-1 infection was discovered in a preserved lymph node biopsy sample taken in 1960 from a woman from Leopoldville, Belgian Congo.

In 1969, a 15-year-old African-American male known to medicine as Robert R. died at the St. Louis City Hospital from aggressive Kaposi's sarcoma. AIDS was suspected as early as 1984, and in 1987, researchers at Tulane University School of Medicine confirmed this, finding HIV-1 in his preserved blood and tissues. The doctors who worked on his case at the time suspected he was a prostitute, though the patient did not discuss his sexual history with them in detail.

In 1976, a Norwegian sailor named Arvid Noe, his wife, and his nine-year-old daughter died of AIDS. The sailor had first presented symptoms in 1969, eight years after he first spent time in ports along the West African coastline. A gonorrhoea infection during his first African voyage shows he was sexually active at this time. Tissue samples from the sailor and his wife were tested in 1988 and found to contain the HIV-1 virus (Group O).

HIV-1 strains are thought to have arrived in the United States from Haiti in the late 1960s or early 1970s. HIV-1 is believed to have arrived in Haiti from central Africa, possibly through professional contacts with the Democratic Republic of the Congo.

Because of the long incubation period of HIV (up to a decade or longer) before symptoms of AIDS appear, and because of the initially low incidence, AIDS was not noticed at first. By the time the first reported cases of AIDS were found in large United States cities, the prevalence of HIV infection in some communities had passed 5%. Worldwide, HIV infection has spread from urban to rural areas, and has appeared in regions such as China and India.

A Canadian airline steward named Gaëtan Dugas was referred to as "Patient 0" in an early AIDS study by Dr. William Darrow of the Centers for Disease Control. Many people consider Dugas to be responsible for bringing HIV to North America. This is considered inaccurate, as HIV had spread long before Dugas began his career. This rumor may have started with Randy Shilts' 1987 book And the Band Played On (and the movie based on it, in which Dugas is referred to as AIDS' Patient Zero), but neither the book nor the movie state him to have been the first to bring the virus to North America. He was called "Patient Zero" because at least 40 of the 248 people known to be infected by AIDS in 1983 had had sexual intercourse with him, or with someone who had sexual intercourse with him.

The current consensus is that HIV was introduced to North America by a Haitian immigrant who contracted it while working in the Democratic Republic of the Congo in the early 1960s, or from another person who worked there during that time.

The AIDS epidemic officially began on June 5, 1981, when the U.S. Centers for Disease Control and Prevention in its Morbidity and Mortality Weekly Report newsletter reported unusual clusters of Pneumocystis pneumonia (PCP) caused by a form of Pneumocystis carinii (now recognized as a distinct species Pneumocystis jirovecii) in five homosexual men in Los Angeles.

Over the next 18 months, more PCP clusters were discovered among otherwise healthy men in cities throughout the country, along with other opportunistic diseases (such as Kaposi's sarcoma and persistent, generalized lymphadenopathy), common in immunosuppressed patients.

In June 1982, a report of a group of cases amongst gay men in Southern California suggested that a sexually transmitted infectious agent might be the etiological agent, and the syndrome was initially termed "GRID", or gay-related immune deficiency.

Health authorities soon realized that nearly half of the people identified with the syndrome were not homosexual men. The same opportunistic infections were also reported among hemophiliacs, heterosexual intravenous drug users, and Haitian immigrants.

By August 1982, the disease was being referred to by its new CDC-coined name: Acquired Immune Deficiency Syndrome (AIDS).

In May 1983, doctors from Dr. Luc Montagnier's team at the Pasteur Institute in France, reported that they had isolated a new retrovirus from lymphoid ganglions that they believed was the cause of AIDS. The virus was later named lymphadenopathy-associated virus (LAV) and a sample was sent to the U.S. Centers for Disease Control, which was later passed to the National Cancer Institute (NCI).

In May 1984 a team led by Robert Gallo of the United States confirmed the discovery of the virus, but they renamed it human T lymphotropic virus type III (HTLV-III).

In January 1985 a number of more detailed reports were published concerning LAV and HTLV-III, and by March it was clear that the viruses were the same, were from the same source, and were the etiological agent of AIDS.

In May 1986, the International Committee on Taxonomy of Viruses ruled that both names should be dropped and a new name, HIV (Human Immunodeficiency Virus), be used.

According to a 2008 Proceedings of the National Academy of Sciences study, a team lead by Robert Shafer at Stanford University School of Medicine has discovered that the Gray Mouse Lemur has an endogenous lentivirus (the genus to which HIV belongs) in its genetic makeup. This suggests that lentiviruses have existed for at least 14 million years, much longer than the currently known existence of HIV. In addition, the time frame falls into place when Madagascar was still yet connected to what is now the African continent; the said Lemurs later developed immunity to the virus strain and survived an era when the lentivirus was widespread among other mammalia. The study is being hailed as crucial, because it fills the blanks in the origin of the virus, as well as in its evolution, and may be important in the development of new antiviral drugs.

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AIDS (journal)

Image:AIDS cover 2007.gif

AIDS is a peer-reviewed academic journal, published by Lippincott Williams & Wilkins in London, UK. Founded in 1987, it is the official journal of the International AIDS Society. It covers all aspects of HIV/AIDS, including basic science, clinical trials, epidemiology and social science. The Editor-in-Chief is Jay A. Levy and the Editors are Brigitte Autran, Roel A. Coutinho and John P. Phair.

Eighteen issues are published annually. AIDS was the first journal in the field to operate a fast-track service to facilitate rapid publication of important short papers. Articles over a year old are available freely online in PDF and HTML formats.

The journal had a 2007 impact factor of 5.842, making it the most highly cited journal in the HIV/AIDS area; it was ranked second of 25 journals in the virology category and fourth of 50 journals in the infectious diseases category. Indexing includes Chemical Abstracts Service, EMBASE, Index Medicus, Medline and Science Citation Index.

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World AIDS Day

World AIDS Day banner, European Commission building, Brussels

World AIDS Day, observed December 1 each year, is dedicated to raising awareness of the AIDS pandemic caused by the spread of HIV infection. It is common to hold memorials to honor persons who have died from HIV/AIDS on this day. Government and health officials also observe the event, often with speeches or forums on the AIDS topics. Since 1995, the President of the United States has made an official proclamation on World AIDS Day. Governments of other nations have followed suit and issued similar announcements.

AIDS has killed more than 25 million people between 1981 and 2007, and an estimated 33.2 million people worldwide live with HIV as of 2007, making it one of the most destructive epidemics in recorded history. Despite recent, improved access to antiretroviral treatment and care in many regions of the world, the AIDS epidemic claimed an estimated 2 million lives in 2007, of which about 270,000 were children.

World AIDS Day was first conceived in 1987 by James W. Bunn and Thomas Netter, two public information officers for the Global Programme on AIDS at the World Health Organization in Geneva, Switzerland. Bunn and Netter took their idea to Dr. Jonathan Mann, Director of the Global Programme on AIDS (now known as UNAIDS). Dr. Mann liked the concept and agreed that the first observance of World AIDS Day should be December 1, 1988.

Bunn suggested the date of December 1st to ensure coverage by western news media, something he believed was vital to the success of World AIDS Day. He felt that because 1988 was an election year in the U.S. media outlets would be weary of their post-election coverage and eager to find a fresh story to cover. Bunn and Netter felt that December 1st was long enough after the election and soon enough before the Christmas holidays that it was, in effect, a dead spot in the news calendar and thus perfect timing for World AIDS Day.

Bunn, originally a reporter covering the epidemic for KPIX-TV in San Francisco, along with producer Nancy Saslow, also conceived and initiated “AIDS Lifeline” - a public awareness and health education campaign that was syndicated to television stations in the U.S. "AIDS Lifeline" was honored with a Peabody Award, a local Emmy, and the first National Emmy ever awarded to a local station.

On June 18, 1986 the “AIDS Lifeline” project was honored with a Presidential Citation for Private Sector Initiatives, presented by President Ronald Reagan. Bunn was then asked by Dr. Mann, on behalf of the U.S. government, to take a two-year leave-of-absence from his reporting duties to join Dr. Mann (an epidemiologist for the Centers for Disease Control) in the creation of the Global Programme on AIDS. Mr. Bunn accepted and was named the first Public Information Officer for the Global Programme on AIDS. Along with Mr. Netter he created, designed, and implemented the inaugural World AIDS Day observance – now the longest-running disease awareness and prevention initiative of its kind in the history of public health.

The Joint United Nations Programme on HIV/AIDS (UNAIDS) became operational in 1996, and it took over the planning and promotion of World AIDS Day. Rather than focus on a single day, UNAIDS created the World AIDS Campaign in 1997 to focus on year-round communications, prevention and education.

In its first two years, the theme of World AIDS Day focused on children and young people. These themes were strongly criticized at the time for ignoring the fact that people of all ages may become infected with HIV and suffer from AIDS. But the themes drew attention to the HIV/AIDS epidemic, helped alleviate some of the stigma surrounding the disease, and helped boost recognition of the problem as a family disease.

In 2004, the World AIDS Campaign became an independent organization.

From its inception until 2004, UNAIDS spearheaded the World AIDS Day campaign, choosing annual themes in consultation with other global health organizations.

As of 2008, each year's World AIDS Day theme is chosen by the World AIDS Campaign's Global Steering Committee after extensive consultation with people, organizations and government agencies involved in the prevention and treatment of HIV/AIDS. For each World AIDS Day from 2005 through 2010, the theme will be "Stop AIDS. Keep the Promise.", with a yearly sub-theme. This overarching theme is designed to encourage political leaders to keep their commitment to achieve universal access to HIV/AIDS prevention, treatment, care, and support by the year 2010.

This theme is not specific to World AIDS Day, but is used year-round in WAC's efforts to highlight HIV/AIDS awareness within the context of other major global events including the G8 Summit. World AIDS Campaign also conducts "in-country" campaigns throughout the world, like the Student Stop AIDS Campaign, an infection-awareness campaign targeting young people throughout the UK.

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Source : Wikipedia