Since 1981 cases were detected infection amazing Pneumocystis jiroveci (Pneumocystis carinii then designated), a fungus related to the original forms of Ascomycetes, known to infect severely immunocompromised patients. Initially there was a group of similar cases in which gay men were involved and where they appeared together cytomegalovirus infection and candidiasis. It was first thought that the cause should be linked to common practices among homosexual men.
He soon began appearing cases involving heterosexual male and female intravenous drug users and their children, and also between patients and healthy habits homosexuals who had received transfusions of whole blood or blood products for hemophiliacs his condition. Soon it was thought, by basically epidemiological criteria, the cause must be an infectious agent that is transmitted in a similar way as does the virus of hepatitis B. Several teams began searching for a virus associated with the acquired immunodeficiency known cases; perhaps a retrovirus such as that produced immunodeficiency knew cat or HTLV, producing a type of leukemia.
In 1983, at the Pasteur Institute in Paris, a team dedicated to the investigation of the relationship between retroviruses and cancer led by JC Chermann, F. Barre-Sinoussi and L. Montagnier found a candidate he called lymphadenopathy-associated virus (lymphadenopathy-associated virus, LAV). In 1984 the team of R. Gallo, discoverer of HTLV, then only known human retrovirus, confirmed the discovery, but calling the human T lymphotropic virus type III virus (human T-lymphotropic virus type III, with the initials HTLV-III).
There was a subsequent dispute over the priority in which it became clear that Gallo had described the virus only after receiving samples of the French. As part of the resolution of the conflict, the virus acquired its final name, human immunodeficiency virus (HIV) in Castilian is expressed as human immunodeficiency virus (HIV). In the same year, 1983, when the virus was identified, several teams began work on its genome sequence, published in early 1985, and also began the characterization of their proteins. Treatments Non-nucleoside reverse transcriptase inhibitors (NNRTIs). NNRTIs disable a protein needed by HIV to make copies of itself.
Examples include efavirenz (Sustiva), etravirine (Intelence) and nevirapine (Viramune). Nucleoside reverse transcriptase inhibitors (NRTIs). NRTIs are faulty versions of building blocks that HIV needs to make copies of itself. Examples include Abacavir (Ziagen), and the combination drugs emtricitabine and tenofovir (Truvada), and lamivudine and zidovudine (Combivir). Protease inhibitors (PIs). PIs disable protease, another protein that HIV needs to make copies of itself. Examples include atazanavir (Reyataz), darunavir (Prezista), fosamprenavir (Lexiva) and ritonavir (Norvir). Entry or fusion inhibitors.
These drugs block HIV’s entry into CD4 cells. Examples include enfuvirtide (Fuzeon) and maraviroc (Selzentry). Integrase inhibitors. Raltegravir (Isentress) works by disabling integrase, a protein that HIV uses to insert its genetic material into CD4 cells. Who discovered? Robert Charles Gallo (Waterbury, Connecticut, March 23, 1937) is an American original biomedical researcher best known for his role in identifying the Human Immunodeficiency Virus (HIV) as the agent responsible for the Acquired Immune Deficiency Syndrome (AIDS), although their contribution to this discovery remains controversial.