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Wednesday, June 6, 2007

HIV ( AIDS )

HIV

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Human immunodeficiency virus

Stylized rendering of a cross section
of the human immunodeficiency virus
Virus classification
Group: Group VI (ssRNA-RT)
Family: Retroviridae
Genus: Lentivirus
Species
  • Human immunodeficiency virus 1
  • Human immunodeficiency virus 2
International Statistical Classification of Diseases and Related Health Problems Codes
Classification & external resources
ICD-10 B20-B24
ICD-9 042-044

Human immunodeficiency virus (HIV) is a retrovirus that causes acquired immunodeficiency syndrome (AIDS, a condition in humans in which the immune system begins to fail, leading to life-threatening opportunistic infections). Previous names for the virus include human T-lymphotropic virus-III (HTLV-III), lymphadenopathy-associated virus (LAV), or AIDS-associated retrovirus (ARV).[1][2]

Infection with HIV occurs by the transfer of blood, semen, vaginal fluid, pre-ejaculate, or breast milk. Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells. The three major routes of transmission are unprotected sexual intercourse, contaminated needles, and transmission from an infected mother to her baby at birth, or through breast milk. Screening of blood products for HIV in the developed world has largely eliminated transmission through blood transfusions or infected blood products in these countries.

HIV infection in humans is now pandemic. As of January 2006, the Joint United Nations Programme on HIV/AIDS (UNAIDS) and the World Health Organization (WHO) estimate that AIDS has killed more than 25 million people since it was first recognized on December 1, 1981, making it one of the most destructive pandemics in recorded history. In 2005 alone, AIDS claimed an estimated 2.4–3.3 million lives, of which more than 570,000 were children. It is estimated that about 0.6% of the world's living population is infected with HIV.[3] A third of these deaths are occurring in sub-Saharan Africa, retarding economic growth and increasing poverty.[4] According to current estimates, HIV is set to infect 90 million people in Africa, resulting in a minimum estimate of 18 million orphans.[5] Antiretroviral treatment reduces both the mortality and the morbidity of HIV infection, but routine access to antiretroviral medication is not available in all countries.[6]

HIV primarily infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells), macrophages and dendritic cells. HIV infection leads to low levels of CD4+ T cells through three main mechanisms: firstly, direct viral killing of infected cells; secondly, increased rates of apoptosis in infected cells; and thirdly, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes that recognize infected cells. When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections. If untreated, eventually most HIV-infected individuals develop AIDS (Acquired Immunodeficiency Syndrome) and die; however about one in ten remains healthy for many years, with no noticeable symptoms.[7] Treatment with anti-retrovirals, where available, increases the life expectancy of people infected with HIV. It is hoped that current and future treatments may allow HIV-infected individuals to achieve a life expectancy approaching that of the general public (see Treatment).

Origin and discovery

Main article: AIDS origin

The AIDS epidemic was discovered June 5, 1981, when the U.S. Centers for Disease Control and Prevention reported a cluster 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.[8] The disease was originally dubbed GRID, or Gay-Related Immune Deficiency, but health authorities soon realized that nearly half of the people identified with the syndrome were not homosexual men. In 1982, the CDC introduced the term AIDS to describe the newly recognized syndrome, though it was still casually referred to as GRID.

In 1983, scientists led by Luc Montagnier at the Pasteur Institute in France first discovered the virus that causes AIDS.[9] They called it lymphadenopathy-associated virus (LAV). A year later 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).[10] The dual discovery led to considerable scientific disagreement, and it was not until President Mitterrand of France and President Reagan of the USA met that the major issues were resolved. In 1986, both the French and the U.S. names for the virus itself were dropped in favour of the new term, human immunodeficiency virus (HIV).[2]

HIV was classified as a member of the genus Lentivirus,[11] part of the family of Retroviridae.[12] Lentiviruses have many common morphologies and biological properties. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period.[13] Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry of the target cell, the viral RNA genome is converted to double-stranded DNA by a virally encoded reverse transcriptase that is present in the virus particle. This viral DNA is then integrated into the cellular DNA by a virally encoded integrase so that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latent and the infected cell continues to function, or the virus becomes active and replicates, and a large number of virus particles are liberated that can then infect other cells.

Two species of HIV infect humans: HIV-1 and HIV-2. HIV-1 is thought to have originated in southern Cameroon after jumping from wild chimpanzees (Pan troglodytes troglodytes) to humans during the twentieth century.[14][15] HIV-2 may have originated from the Sooty Mangabey (Cercocebus atys), an Old World monkey of Guinea-Bissau, Gabon, and Cameroon.[16] HIV-1 is more virulent. It is easily transmitted and is the cause of the majority of HIV infections globally. HIV-2 is less transmittable and is largely confined to West Africa.[16] HIV-1 is the virus that was initially discovered and termed LAV.

Three of the earliest known instances of HIV-1 infection are as follows:

  1. A plasma sample taken in 1959 from an adult male living in what is now the Democratic Republic of Congo.[17]
  2. HIV found in tissue samples from a 15-year-old African-American teenager who died in St. Louis in 1969.[18]
  3. HIV found in tissue samples from a Norwegian sailor who died around 1976.[19]

Although a variety of theories exist explaining the transfer of HIV to humans, no single hypothesis is unanimously accepted, and the topic remains controversial. The most widely accepted theory is so called 'Hunter' Theory according to which transference from simian to human most likely occurred when a human was bitten by a monkey or was cut while butchering one, and the human became infected.[20] The Times published an article in 1987 stating that WHO suspected some kind of connection with its vaccine program and AIDS-epidemic. The story was almost entirely based on statements given by one unnamed WHO advisor. The theory was supported only by weak circumstantial evidence and is now disproven by unraveling the genetic code of the virus and finding out that the virus dates back to the 1930s.[21]

Freelance journalist Tom Curtis discussed one controversial possibility for the origin of HIV/AIDS in a 1992 Rolling Stone magazine article. He put forward what is now known as the OPV AIDS hypothesis, which suggests that AIDS was inadvertently caused in the late 1950s in the Belgian Congo by Hilary Koprowski's research into a polio vaccine.[22] Although subsequently retracted due to libel issues surrounding its claims, the Rolling Stone article motivated another freelance journalist, Edward Hooper, to probe more deeply into this subject. Hooper's research resulted in his publishing a 1999 book, The River, in which he alleged that an experimental oral polio vaccine prepared using chimpanzee kidney tissue was the route through which simian immunodeficiency virus (SIV) crossed into humans to become HIV, thus starting the human AIDS pandemic.[23] This theory is contradicted by an analysis of genetic mutation in primate lentivirus strains that estimates the origin of the HIV-1 strain to be around 1930, with 95% certainty of it lying between 1910 and 1950.[24]

Furthermore in February 2000 one of the original developers of the polio vaccine, Philadelphia based Wistar Institute found from its stores a vial of the original vaccine used in the vaccination program. It was analyzed in April 2001 and no traces of either HIV-1 or SIV were found in the sample.[25] A second analysis showed that only macaque monkey kidney cells, which cannot be infected with SIV or HIV, were used to produce the vaccine.[26] While the analysis was done on only one vial of vaccine, most scientists have concluded that the polio vaccine theory of the origins of HIV is not possible.[20]

Transmission

For more details on this topic, see AIDS transmission and prevention
Estimated per act risk for acquisition of HIV-1
by exposure route[27]
Exposure Route Estimated infections per 10,000 exposures to an infected source
Blood Transfusion 9,000[28]
Childbirth 2,500[29]
Needle-sharing injection drug use 67[30]
Receptive anal intercourse* 50[31][32]
Percutaneous needle stick 30[33]
Receptive penile-vaginal intercourse* 10[31][32][34]
Insertive anal intercourse* 6.5[31][32]
Insertive penile-vaginal intercourse* 5[31][32]
Receptive fellatio* 1[32]
Insertive fellatio* 0.5[32]
* assuming no condom use

Since the beginning of the pandemic, three main transmission routes for HIV have been identified:

  • Sexual route. The majority of HIV infections are acquired through unprotected sexual relations. Sexual transmission can occur when infected sexual secretions of one partner come into contact with the genital, oral, or rectal mucous membranes of another.
  • Blood or blood product route. This transmission route can account for infections in intravenous drug users, hemophiliacs and recipients of blood transfusions (though most transfusions are checked for HIV in the developed world) and blood products. It is also of concern for persons receiving medical care in regions where there is prevalent substandard hygiene in the use of injection equipment, such as the reuse of needles in Third World countries. HIV can also be spread through the sharing of leeches. Health care workers such as nurses, laboratory workers, and doctors, have also been infected, although this occurs more rarely. People who give and receive tattoos, piercings, and scarification procedures can also be at risk of infection.
  • Mother-to-child transmission (MTCT). 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 the mother and child is 25%.[29] However, where drug treatment and Cesarian section are available, this can be reduced to 1%.[29] Breast feeding also presents a risk of infection for the baby.

HIV-2 is transmitted much less frequently by the MTCT and sexual route than HIV-1.

HIV has been found at low concentrations in the saliva, tears and urine of infected individuals, but there are no recorded cases of infection by these secretions and the potential risk of transmission is negligible. The use of physical barriers such as the latex condom is widely advocated to reduce the sexual transmission of HIV. Spermicide, when used alone or with vaginal contraceptives like a diaphragm, actually increases the male to female transmission rate due to inflammation of the vagina; it should not be considered a barrier to infection.[35] Research is clarifying the relationship between male circumcision and HIV in differing social and cultural contexts, however critics point out that any correlation between circumcision and HIV is likely to come from cultural factors (which govern not only whether someone is circumcised, but also their sexual practices and beliefs).[36] Even though male circumcision may lead to a reduction of infection risk in heterosexual men by up to 60%,[37] UNAIDS believes that it is premature to recommend male circumcision as part of HIV prevention programs.[38] Trials, in which some uncircumcised men were randomly assigned to be circumcised in presumably sterile conditions and other men were not circumcised, have been conducted in Kenya[39] and Uganda.[40] South African medical experts are concerned that the repeated use of unsterilized blades in the ritual circumcision of adolescent boys may be spreading HIV.[41]

Treatment

See also AIDS Treatment and Antiretroviral drug.

There is currently no vaccine or cure for HIV or AIDS. The only known method of prevention is avoiding exposure to the virus. However, an antiretroviral treatment, known as post-exposure prophylaxis is believed to reduce the risk of infection if begun directly after exposure.[85] Current treatment for HIV infection consists of highly active antiretroviral therapy, or HAART.[86] This has been highly beneficial to many HIV-infected individuals since its introduction in 1996, when the protease inhibitor-based HAART initially became available.[87] Current HAART options are combinations (or "cocktails") consisting of at least three drugs belonging to at least two types, or "classes," of anti-retroviral agents. Typically, these classes are two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). Because AIDS progression in children is more rapid and less predictable than in adults, particularly in young infants, more aggressive treatment is recommended for children than adults.[88] In developed countries where HAART is available, doctors assess their patients thoroughly: measuring the viral load, how fast CD4 declines, and patient readiness. They then decide when to recommend starting treatment.[89]

HAART allows the stabilisation of the patient’s symptoms and viremia, but it neither cures the patient, nor alleviates the symptoms, and high levels of HIV-1, often HAART resistant, return once treatment is stopped.[90][91] Moreover, it would take more than a lifetime for HIV infection to be cleared using HAART.[92] Despite this, many HIV-infected individuals have experienced remarkable improvements in their general health and quality of life, which has led to a large reduction in HIV-associated morbidity and mortality in the developed world.[87][93][94] A computer based study in 2006 projected that following the 2004 United States treatment guidelines gave an average life expectancy of an HIV infected individual to be 32.1 years from the time of infection if treatment was started when the CD4 count was 350/µL.[95] This study was limited as it did not take into account possible future treatments and the projection has not been confirmed within a clinical cohort setting. In the absence of HAART, progression from HIV infection to AIDS has been observed to occur at a median of between nine to ten years and the median survival time after developing AIDS is only 9.2 months.[96] However, HAART sometimes achieves far less than optimal results, in some circumstances being effective in less than fifty percent of patients. This is due to a variety of reasons such as medication intolerance/side effects, prior ineffective antiretroviral therapy and infection with a drug-resistant strain of HIV. However, non-adherence and non-persistence with antiretroviral therapy is the major reason most individuals fail to benefit from HAART.[97] The reasons for non-adherence and non-persistence with HAART are varied and overlapping. Major psychosocial issues, such as poor access to medical care, inadequate social supports, psychiatric disease and drug abuse contribute to non-adherence. The complexity of these HAART regimens, whether due to pill number, dosing frequency, meal restrictions or other issues along with side effects that create intentional non-adherence also contribute to this problem.[98][99][100] The side effects include lipodystrophy, dyslipidaemia, insulin resistance, an increase in cardiovascular risks and birth defects.[101][102]

The timing for starting HIV treatment is still debated. There is no question that treatment should be started before the patient's CD4 count falls below 200, and most national guidelines say to start treatment once the CD4 count falls below 350; but there is some evidence from cohort studies that treatment should be started before the CD4 count falls below 350.[103][93] There is also evidence to say that treatment should be started before CD4 percentage falls below 15%.[104] In those countries where CD4 counts are not available, patients with WHO stage III or IV disease[105] should be offered treatment.

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.[106] 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. Unfortunately, only a vaccine is thought to be able to halt the pandemic. This is because a vaccine would cost less, thus being affordable for developing countries, and would not require daily treatment.[106] However, after over 20 years of research, HIV-1 remains a difficult target for a vaccine.[106]In February 2007, The National Institute of Allergy and Infectious Diseases published a report that gave details of a potential region on HIV's surface that is a potential target for a vaccine.[107]

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