Discovery
AIDS was first clinically observed in 1981 in the United States. The initial cases were a cluster of injecting
drug users and homosexual men with no known cause of impaired immunity who
showed symptoms of Pneumocystis
carinii pneumonia (PCP), a rare
opportunistic infection that was known to occur in people with very compromised
immune systems. Soon thereafter, an
unexpected number of gay men developed a previously rare skin cancer called Kaposi's sarcoma (KS). Many more cases of PCP and KS emerged, alerting U.S. Centers for
Disease Control and Prevention (CDC) and a CDC task force was formed to monitor
the outbreak.
In the early days, the 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. At one point, the CDC coined the phrase "the 4H disease",
since the syndrome seemed to affect Haitians, homosexuals, hemophiliacs,
and heroin users. In the general press, the
term "GRID", which stood for gay-related immune deficiency, had been coined. However, after
determining that AIDS was not isolated to the gay community, it was realized that the term GRID was
misleading and the term AIDS was introduced at a meeting in July 1982. By September 1982 the CDC started referring to
the disease as AIDS. In 1983, two separate research groups led by Robert Gallo and Luc Montagnier independently declared that a novel retrovirus
may have been infecting AIDS patients, and published their findings in the same
issue of the journal Science. Gallo claimed that a
virus his group had isolated from an AIDS patient was strikingly similar in shape to other human T-lymphotropic viruses (HTLVs) his group had been the first to isolate. Gallo's group
called their newly isolated virus HTLV-III. At the same time, Montagnier's
group isolated a virus from a patient presenting with swelling of the lymph nodes of the neck and physical weakness, two characteristic symptoms of AIDS.
Contradicting the report from Gallo's group, Montagnier and his colleagues
showed that core proteins of this virus were immunologically different from
those of HTLV-I. Montagnier's group named their isolated virus
lymphadenopathy-associated virus (LAV). As these two viruses turned out to be
the same, in 1986, LAV and HTLV-III were renamed HIV.
Origins
Both HIV-1 and HIV-2 are believed to have originated in non-human primates in West-central Africa and were transferred to humans in the early 20th century. 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 SIVcpz endemic in the
chimpanzee subspeciesPan 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 litoral West Africa (from southern Senegal to western Côte d'Ivoire). New World monkeys such as theowl 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.[
There is evidence that humans who participate in bushmeat activities, either as hunters or as bushmeat
vendors, commonly acquire SIV. However, SIV is a weak
virus which is typically suppressed by the human immune system within weeks of
infection. It is thought that several transmissions of the virus from
individual to individual in quick succession are necessary to allow it enough
time to mutate into HIV. Furthermore, due to its relatively low
person-to-person transmission rate, SIV can only spread throughout the
population in the presence of one or more of high-risk transmission channels,
which are thought to have been absent in Africa prior to the 20th century.
Specific proposed high-risk transmission channels, allowing the
virus to adapt to humans and spread throughout the society, depend on the
proposed timing of the animal-to-human crossing. Genetic studies of the virus
suggest that the most recent common ancestor of the HIV-1 M group dates back to
circa 1910. Proponents of this
dating link the HIV epidemic with the emergence of colonialism and growth of large colonial African cities,
leading to social changes, including a higher degree of sexual promiscuity, the
spread ofprostitution,
and the accompanying high frequency of genital ulcer diseases (such as syphilis)
in nascent colonial cities. While transmission rates
of HIV during vaginal intercourse, are low under regular circumstances, they
are increased many fold if one of the partners suffers from an sexually transmitted infection resulting in genital ulcers. Early 1900s colonial cities were
notable due to their high prevalence of prostitution and genital ulcers, to the
degree that, as of 1928, as many as 45% of female residents of easternKinshasa were thought to have been prostitutes, and, as
of 1933, around 15% of all residents of the same city were infected by one of
the forms of syphilis.[
An alternative view holds that unsafe medical practices in Africa
during years following World War II, such as unsterile reuse of single use
syringes during mass vaccination, antibiotic and anti-malaria treatment
campaigns, were the initial vector that allowed the virus to adapt to humans
and spread.
The earliest well documented case of HIV in a human dates back to
1959 in the Congo. The virus may have been
present in the United States as early as 1966, but the vast majority of infections occurring outside sub-Saharan
Africa (including the U.S.) can be traced back to a single unknown individual
who got infected with HIV in Haiti and then brought the infection to the United
States some time around 1969. The epidemic then
rapidly spread among high-risk groups (initially, sexually promiscuous men who
have sex with men). By 1978, the prevalence of HIV-1 among gay male residents
of New York and San Francisco was estimated at 5%, suggesting that several
thousand individuals in the country had been infected.
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