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McMahon DK, Zheng L, Hitti J, Chan ES, Halvas EK, Hong F, et al. Greater Suppression of Nevirapine Resistance With 21- vs 7-Day Antiretroviral Regimens After Intrapartum Single-Dose Nevirapine for Prevention of Mother-to-Child Transmission of HIV. Clin Infect Dis. 2013 Apr. 56(7):1044-51. [Medline]. [Full Text].

Sexual intercourse is the major mode of HIV transmission. Both X4 and R5 HIV are present in the seminal fluid, which enables the virus to be transmitte from a male to his sexual partner. The virions can then infect numerous cellular targets and disseminate into the whole organism. However, a selection process leads to a predominant transmission of the R5 virus through this pathway.[47][48][49] In patients infected with subtype B HIV-1, there is often a co-receptor switch in late-stage disease and T-tropic variants that can infect a variety of T cells through CXCR4.[50] These variants then replicate more aggressively with heightened virulence that causes rapid T cell depletion, immune system collapse, and opportunistic infections that mark the advent of AIDS.[51] Thus, during the course of infection, viral adaptation to the use of CXCR4 instead of CCR5 may be a key step in the progression to AIDS. A number of studies with subtype B-infected individuals have determined that between 40 and 50 percent of AIDS patients can harbour viruses of the SI and, it is presumed, the X4 phenotypes.[52][53]

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Not everyone who has HIV have AIDS. When people first get HIV, they can be healthy for years. A person is diagnosed as having AIDS when he or she gets specific types of illnesses or gets sick in certain ways due to their HIV. Once a person’s HIV progresses to (or turns into) AIDS, the person will continue to have AIDS for the rest of their life. While there are many treatments for HIV/AIDS, at this point there is no cure.

Isolates of HIV-1 and HIV-2 with resistance to antiretroviral drugs arise through natural selection and genetic mutations, which have been tracked and analyzed. The Stanford HIV Drug Resistance Database and the International AIDS Society publish lists of the most important of these; first year listing 80 common mutations, and the latest year 93 common mutations, and made available through the Stanford HIV RT and Protease Sequence Database.

Drug treatment guidelines for HIV/AIDS change frequently as new drugs are approved and new drug regimens developed. Two principles currently guide doctors in developing drug regimens for AIDS patients: using combinations of drugs rather than one medication alone; and basing treatment decisions on the results of the patient’s viral load tests. Current information on United States Food and Drug Administration-(FDA)approved drugs by class can be found at the United States Department of Health and Human Services Aids Info Website at . Individuals interested in participating in a trial of new HIV/AIDS drugs under development can find a list of clinical trials currently accepting volunteers at . There is not cost to volunteers to participate and some medical care and testing is provided.

In 1983, two separate research groups led by Robert Gallo and Luc Montagnier declared that a novel retrovirus may have been infecting people with AIDS, and published their findings in the same issue of the journal Science.[230][231] Gallo claimed that a virus his group had isolated from a person with AIDS 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 person 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).[221] As these two viruses turned out to be the same, in 1986, LAV and HTLV-III were renamed HIV.[232]

A deficiency of cellular immunity induced by infection with the human immunodeficiency virus (HIV-1) and characterized by opportunistic diseases, including Pneumocystis jiroveci (formerly carinii) pneumonia, Kaposi sarcoma, oral hairy leukoplakia, cytomegalovirus disease, tuberculosis, Mycobacterium avium complex (MAC) disease, candidal esophagitis, cryptosporidiosis, isoporiasis, cryptococcosis, non-Hodgkin lymphoma, progressive multifocal leukoencephalopathy (PML), herpes zoster, and lymphoma. HIV is transmitted from person to person in cell-rich body fluids (notably blood and semen) through sexual contact, sharing of contaminated needles (as by IV drug abusers), or other contact with infected blood (as in accidental needlesticks among health care workers). Maternal-fetal transmission also occurs. The primary targets of HIV are cells with the CD4 surface protein, including principally helper T lymphocytes. Antibody to HIV, which appears in the serum 6 weeks to 6 months after infection, serves as a reliable marker but does not bind or inactivate HIV. Gradual decline in the CD4 lymphocyte count, typically occurring over a period of 10-12 years, culminates in loss of ability to resist opportunistic infections. The appearance of one or more of these infections defines the onset of AIDS. In some patients, generalized lymphadenopathy, fever, weight loss, dementia, or chronic diarrhea occurs much earlier in the course of the infection. Untreated AIDS is uniformly lethal within 2-5 years after the first appearance of an opportunistic infection. Besides prophylaxis against opportunistic infection, standard therapy of HIV infection includes use of nucleoside analogues (for example, didanosine, lamivudine, ribavirin, stavudine, zipovudine), nonnucleoside reverse transcriptase inhibitors (for example, delavirine, efavirenz, nevirapine) and protease inhibitors (for example, atazanavir, crixivan, indinavir, ritonavir, saquinavir).

Jump up ^ “Making Headway Under Hellacious Circumstances” (PDF). American Association for the Advancement of Science. July 28, 2006. Archived (PDF) from the original on June 24, 2008. Retrieved June 23, 2008.

HIV infects T cells via high-affinity interaction between the virion envelope glycoprotein (gp120) and the CD4 molecule. The infection of T cells is assisted by the T-cell co-receptor called CXCR4 while HIV infects monocytes by interacting with CCR5 co-receptor (Figure 1). As illustrated in Figure 2, after gp120 binds to CD4 on the T cell (1). Nucleocapsids containing viral genome and enzymes enters the target cell (2). Following the release of viral genome and enzymes from the core protein, viral reverse transcriptase catalyses reverse transcription of ssRNA to form RNA-DNA hybrids (3). To yield HIV dsDNA the viral RNA template is partially degraded by ribonuclease H and the second DNA strand is synthesized (4). The viral dsDNA is translocated into the nucleus and integrated into the host genome by the viral integrase enzyme (5). Transcription factors transcribe the proviral DNA into genomic ssRNA (6), which is exported to cytoplasm (7). In the cytoplasm, host-cell ribosomes catalyse synthesis of viral precursor proteins (8). The viral precursor proteins are cleaved into viral proteins by viral proteases (9). HIV ssRNA and proteins assemble beneath the host-cell plasma membrane (10) forming virion buds from it (11). Maturation occurs either in the forming buds or after budding from the host cell (12). During maturation, HIV proteases cleave the poly-proteins into individual functional HIV proteins. The mature virions are able to infect another host cell.

By 1984 researchers working in Africa had provided clear evidence for heterosexual transmission of the causative agent, HIV. The virus had been isolated the year before by a team of French researchers led by virologist Luc Montagnier. Montagnier and his colleagues identified the virus as a new type of human retrovirus, and they suspected that it was the cause of AIDS. But more-detailed characterization was needed to confirm the connection, so Montagnier sent samples to American virologist Robert C. Gallo, who had contributed to the discovery of the first known human retrovirus (human T-lymphotropic virus) several years earlier. Gallo helped establish that HIV caused AIDS, and he contributed to the subsequent development of a blood test for its detection. Montagnier initially called the new infectious agent lymphadenopathy-associated virus (LAV), but in 1986 the International Committee on Taxonomy of Viruses renamed it HIV. Montagnier and French virologist Françoise Barré-Sinoussi were awarded the 2008 Nobel Prize for Physiology or Medicine for their discovery of HIV; despite Gallo’s role in confirming HIV as the cause of AIDS, Montagnier and colleagues were the first to isolate the virus.

AHF Federation is a consortium of AIDS Service Organizations (ASOs) and community groups committed to HIV/AIDS education, prevention, advocacy, medical treatment and support for underserved populations across the nation. Through the collective, organizations work to build upon their regional knowledge, experience and operations within AHF’s innovative network of support to expand their capacity to meet the growing needs of people in the communities they serve.

AIDS is caused by a virus called the Human Immunodeficiency Virus (HIV). If you get infected with HIV, your body will try to fight the infection. It will make “antibodies,” special immune molecules the body makes to fight HIV. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]

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