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Entry (fusion) inhibitors prevent HIV from entering cells. To enter a human cell, HIV must bind to a CD4 receptor and one other receptor, such as the CCR-5 receptor. One type of entry inhibitor, CCR-5 inhibitors, blocks the CCR-5 receptor, preventing HIV from entering human cells.

Spanish SIDA – síndrome de inmunodeficiencia adquirida, síndrome de inmunodeficiencia adquirida (SIDA), Síndrome de autoinmunodeficiencia, Síndrome de inmunodeficiencia adquirida no especificado, Síndrome de inmunodeficiencia adquirida NEOM, SIDA (trastorno), SINDROME INMUNODEFICIENCIA ADQUIR, síndrome de infección por el VIH, síndrome infección por el virus de la inmunodeficiencia humana adquirida, SAI (trastorno), síndrome de infección por el HIV, síndrome infección por el virus de la inmunodeficiencia humana adquirida, SAI, Síndrome de la Inmunodeficiencia Adquirida, síndrome de inmunodeficiencia adquirida (trastorno), síndrome de inmunodeficiencia adquirida (SIDA) (trastorno), SIDA, síndrome de inmunodeficiencia adquirida, Síndrome de inmunodeficiencia adquirida, Síndromes de inmunodeficiencia adquirida, Síndrome de Deficiencia Inmunológica Adquirida, Síndrome de Inmunodeficiencia Adquirida

In light of the limited ability of counseling and testing to curb the spread of the HIV pandemic, many researchers have moved toward other biologic strategies for preventing HIV that do not rely solely on people changing their behavior. It is in this area where there has been some success. During the last 10 years, there were several large studies showing that male circumcision along with behavioral counseling reduced the risk of heterosexual men acquiring HIV infection. This provides a novel prevention strategy for at-risk, HIV-uninfected heterosexual men. Another major advance on the prevention front came from the HPTN 052 study in which HIV-infected individuals with CD4 cells between 350 cells/mm3 and 550 cells/mm3 who had uninfected partners were randomly assigned to initiate antiviral therapy or wait until their CD4 cells declined to less than 250 cells/mm3 or they developed symptoms consistent with disease progression. All enrolled individuals were aggressively counseled about continued safe sex practices, provided condoms, and were monitored for sexual activities. The study ultimately showed that those treated early were more than 96% less likely to transmit to their partner than those who had antiviral treatment deferred. Subsequent cohort studies have shown that those who are virologically suppressed on antiretroviral therapy for at least six months have a very low risk of transmitting to uninfected partners, even when not using condoms. In fact, many groups have suggested that the risk in this setting of HIV transmission may be virtually zero based upon the existing data.

Since the first case was identified in 1981, acquired immune deficiency syndrome (AIDS) has grown into an epidemic that has taken approximately 500,000 lives in the United States alone. The Joint United Nations Programme on HIV/AIDS estimates that at the end of 2002 there were 42 million people living with HIV/AIDS worldwide. During 2002, AIDS caused the deaths of an estimated 3.1 million people. At this time, women were increasingly affected by AIDS; it was estimated that women comprised approximately 50 percent or 19.2 million of the 38.6 million adults living with HIV or AIDS worldwide. No cure has been found, although existing treatment employing multiple drugs has made some gains in prolonging life and reducing pain. Despite the limits of medical science, however, much is known about the disease. It is caused by the human immunodeficiency virus (HIV). Transmitted by bodily fluids from person to person, HIV invades certain key blood cells that are needed to fight off infections. HIV replicates, spreads, and destroys these host cells. When the body’s immune system becomes deficient, the person becomes AIDS-symptomatic, which means the person develops infections that the body can no longer ward off. Ultimately, a person with AIDS dies from diseases caused by other infections. The leading killer is a form of pneumonia.

The clinician providing care for a woman who is infected with HIV has important responsibilities concerning disclosure of the patient’s serostatus. Clinicians providing health care should be aware of and respect legal requirements regarding confidentiality and disclosure of HIV-related clinical information.

For people infected with HIV, the risk of progression to AIDS increases with the number of years the person has been infected. The risk of progression to AIDS is decreased by using highly effective antiretroviral therapy (ART) regimens.

Mycobacteria. AIDS patients may develop tuberculosis or mycobacterium avium complex (MAC) infections. MAC infections are caused by Mycobacterium avium-intracellulare and occur in about 40% of AIDS patients. This infection rarely develops until the CD4+ counts falls below 50 cells/mm3.

US Food and Drug Administration. FDA approves first rapid diagnostic test to detect both HIV-1 antigen and HIV-1/2 antibodies. US Department of Health and Human Services, US Food and Drug Administration. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm364480.htm. Accessed: August 12, 2013.

Although many effective medications are on the market, the virus can become resistant to any drug. This can be a serious complication if it means that a less effective medicine must be used. To reduce the risk of resistance, patients should take their medications as prescribed and call their physician immediately if they feel they need to stop one or more drugs.

HIV-1 originated in Central Africa in the first half of the 20th century, when a closely related chimpanzee virus first infected humans. Epidemic global spread began in the late 1970s, and AIDS was recognized in 1981.

The production of infectious virus particles from an integrated HIV provirus is stimulated by a cellular transcription factor that is present in all activated T cells. Activation of CD4 T cells induces the transcription factor NFκB, which binds to promoters not only in the cellular DNA but also in the viral LTR, thereby initiating the transcription of viral RNA by the cellular RNA polymerase. This transcript is spliced in various ways to produce mRNAs for the viral proteins. The Gag and Gag-Pol proteins are translated from unspliced mRNA; Vif, Vpr, Vpu, and Env are translated from singly spliced viral mRNA; Tat, Rev, and Nef are translated from multiply spliced mRNA. At least two of the viral genes, tat and rev, encode proteins, Tat and Rev respectively, that promote viral replication in activated T cells. Tat is a potent transcriptional regulator, which functions as an elongation factor that enables the transcription of viral RNA by the RNA polymerase II complex. Tat contains two binding sites, contained in one domain, named the transactivation domain. The first of these allows Tat to bind to a host cellular protein, cyclin T1. This binding reaction promotes the binding of the Tat protein through the second binding site in its transactivation domain to an RNA sequence in the LTR of the virus known as the transcriptional activation region (TAR). The consequence of this interaction is to greatly enhance the rate of viral genome transcription, by causing the removal of negative elongation factors that block the transcriptional activity of RNA polymerase II. The expression of cyclin T1 is greatly increased in activated compared with quiescent T lymphocytes. This, in conjunction with the increased expression of NFκB in activated T cells, may explain the ability of HIV to lie dormant in resting T cells and replicate in activated T cells (Fig. 11.25).

Jump up ^ Larke, N (May 27, 2010). “Male circumcision, HIV and sexually transmitted infections: a review”. British journal of nursing (Mark Allen Publishing). 19 (10): 629–34. doi:10.12968/bjon.2010.19.10.48201. PMID 20622758.

6. Centers for Disease Control and Prevention (CDC) (1982) ‘A Cluster of Kaposi’s Sarcoma and Pneumocystis carinii Pneumonia among Homosexual Male Residents of Los Angeles and range Counties, California’ MMWR 31(23):305-307

The first few weeks after infection is called the acute infection stage. During this time the virus rapidly reproduces. Your immune system responds by producing HIV antibodies. Many people experience temporary flu-like symptoms during this stage. Even without symptoms, HIV is highly contagious during this time.

Antiviral therapy suppresses the replication of the HIV virus in the body. A combination of several antiretroviral agents, termed Highly Active Anti-Retroviral Therapy (HAART), has been highly effective in reducing the number of HIV particles in the blood stream (as measured by a blood test called the viral load). This can help the immune system bounce back for a while and improve T-cell counts.

The best time to start drug treatment is as soon as possible, even if people are not sick and their CD4 count is still above 500 (normal is 500 to 1,000). Doctors used to wait until the CD4 count was below 500 to start drug treatment. However, research has shown that people who are promptly treated with antiretroviral drugs are less likely to develop AIDS-related complications and to die of them.

HIV is probably directly responsible for a substantial loss of weight (AIDS wasting) in some people. Wasting in people with AIDS may also be caused by a series of infections or by an untreated, persistent digestive tract infection.

Fungi. The most common fungal disease associated with AIDS is Pneumocystis carinii pneumonia (PCP). PCP is the immediate cause of death in 15-20% of AIDS patients. It is an important measure of a patient’s prognosis. Other fungal infections include a yeast infection of the mouth (candidiasis or thrush) and cryptococcal meningitis.

From a legal, ethical, and moral standpoint, they should warn any prospective sexual partner of their HIV positive status. They should not exchange body fluids during sexual activity and must use whatever preventative measures (such as a latex condom) will afford the partner the most protection.

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The prevalence of women with HIV in the United States is low compared to the rate in many countries in the developing world. Worldwide about half the people living with HIV are women. According to the United Nations, in 2005 about 59% of women living in sub-Saharan Africa are infected with HIV. The vast majority of them were infected through sex with an infected male partner.

The Centers for Disease Control and Prevention (CDC) estimates that approximately 40,000–50,000 new human immunodeficiency virus (HIV) infections occurred annually in the United States from 2006 to 2009 (1). Almost 1 in 5 (18.1%) of all individuals infected with HIV are unaware of their HIV status (2). In order to identify individuals with undiagnosed HIV infection, the CDC recommends HIV screening for all patients aged 13–64 years in health care settings (3). Because obstetrician–gynecologists provide primary and preventive care for adolescents and women, they are ideally suited to play an important role in promoting HIV screening for their patients. The American College of Obstetricians and Gynecologists (the College) recommends routine HIV screening for females aged 13–64 years and older women with risk factors. Screening after age 64 years is indicated if there is ongoing risk of HIV infection, as indicated by risk assessment (eg, new sexual partners).

defective virus one that cannot be completely replicated or cannot form a protein coat; in some cases replication can proceed if missing gene functions are supplied by other viruses; see also helper virus.

The RNA genome consists of at least seven structural landmarks (LTR, TAR, RRE, PE, SLIP, CRS, and INS), and nine genes (gag, pol, and env, tat, rev, nef, vif, vpr, vpu, and sometimes a tenth tev, which is a fusion of tat, env and rev), encoding 19 proteins. Three of these genes, gag, pol, and env, contain information needed to make the structural proteins new virus particles.[21] For example, env codes for a protein called gp160 that is cut in two by a cellular protease to form gp120 and gp41. The six remaining genes, tat, rev, nef, vif, vpr, and vpu (or vpx in the case of HIV-2), are regulatory genes for proteins that control the ability of HIV to infect cells, produce new copies of virus (replicate), or cause disease.[21]

The US Centers for Disease Control and Prevention (CDC) estimates that about 1.3 million  people are living with HIV infection or AIDS; about 15% of them do not know they have it. About 73 percent of the 56,000 new infections each year are in men and about 27 percent are in women. About half of the new infections are in Blacks, even though they make up only 12 percent of the US population. In the mid-1990s, AIDS was a leading cause of death. However, newer treatments have cut the AIDS death rate significantly. For more information, see the US Government fact sheet at http://www.cdc.gov/hiv/topics/surveillance/index.htm.

Some people will wish to use herbal remedies and a Cochrane review was able to find a small number of trials, some of which seemed to have adequate methodology.[14]There was no significant clinical benefit and objective criteria such as CD4 count were unaffected. Since the review there have been a few studies in the literature suggesting some benefit from herbal remedies but larger trials are needed.[15, 16]

The number of new infections worldwide continues to rise, particularly in women, and effective drug treatments have not yet reached the vast majority of infected individuals in resource-limited countries.[13]In addition, patients require high adherence to the therapy to achieve viral suppression and prevent the development of a drug-resistant virus. Modern regimes are less onerous than older ones. They are simpler and involve fewer tablets, whereas it used to be necessary to take 16 to 20 tablets a day.

Health care workers are at risk on the job and should take special precautions. Some health care workers have become infected after being stuck with needles containing HIV-infected blood or less frequently, after infected blood comes into contact with an open cut or through splashes into the worker’s eyes or inside their nose.

It is important to remember that sometimes, for reasons not entirely understood, the viral load can briefly increase. Unexpected increases, therefore, necessitate repeated testing of the viral load before any clinical decisions are made. If, however, the viral load is continually detected despite proper adherence to the prescribed therapy, serious consideration must be given to the possibility that the virus has become resistant to one or more of the medications being given, especially if viral load is greater than 200 copies/mL. There is now an abundance of data showing that the use of drug-resistance tests can improve the response to a follow-up regimen. Testing can be used to determine if an individual’s HIV has become resistant to one or more of the drugs that are being taken. There are currently two main types of resistance tests available in the clinic: one that is called a genotype and the other a phenotype assay. The former looks for mutations in the virus and the latter the actual amount of drug it takes to block infection by the patient’s virus. The genotype test is very helpful in those being screened for the presence of resistant virus prior to initiating treatment and those experiencing viral rebound on one of their first treatment regimens. The phenotype test is particularly useful in those who are highly treatment experienced and have substantial amounts of drug resistance, especially to the protease class. The information derived from these tests, along with a tropism test will ultimately tell the provider which of the many approved drugs are likely to be fully active against the specific patient’s virus. Using this information, the goal is to include at least two and at times preferably three fully active drugs in the next regimen in order to optimize the chances of suppressing the viral load to undetectable levels. It is often useful to seek expert consultation in managing those with multidrug resistant virus.

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America [redirect url=’http://penetratearticles.info/bump’ sec=’7′]

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