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Doctors and the person who was exposed typically decide together whether to use these preventive drugs. They base the decision on the estimated risk of infection and the possible side effects of the drugs. If they do not know whether the source is infected with HIV, they consider how likely the source is to be infected. However, even when the source of the exposure is known to be infected with HIV, the risk of infection after exposure varies, depending on the type of exposure. For example, risk from a blood splash is less than that from a needlestick.
Historically, the greatest success in preventing viral transmission has resulted from the development of preventative vaccines. Unfortunately, decades of research to develop an HIV vaccine has led to little hope for success. In 2007, a major setback in this area occurred when the STEP study investigating a promising vaccine candidate was prematurely stopped due to the lack of evidence that it produced any protection from HIV infection. In contrast, a glimmer of hope did emerge with the report in 2009 of the results of the RV 144 Thai HIV vaccine trial, which demonstrated borderline effectiveness in the more than 16,000 recipients. While this vaccine demonstrated only limited evidence of protection, research is under way to further explore what can be learned for future vaccine development from this modest success.
The time from HIV infection to the development of AIDS varies. Rarely, some individuals develop complications of HIV that define AIDS within one year, while others remain completely asymptomatic after as many as 20 years from the time of infection. However, in the absence of antiretroviral therapy, the time for progression from initial infection to AIDS is approximately eight to 10 years. The reason why people experience clinical progression of HIV at different rates remains an area of active research.
HIV is a very small virus that contains ribonucleic acid (RNA) as its genetic material. When HIV infects animal cells, it uses a special enzyme, reverse transcriptase, to turn (transcribe) its RNA into DNA. (Viruses that use reverse transcriptase are sometimes referred to as “retroviruses.”) When HIV reproduces, it is prone to making small genetic mistakes or mutations, resulting in viruses that vary slightly from each other. This ability to create minor variations allows HIV to evade the body’s immunologic defenses, essentially leading to lifelong infection, and has made it difficult to make an effective vaccine. The mutations also allow HIV to become resistant to antiretroviral medications.
Guidelines for starting antiviral therapy have been proposed by panels of experts from several groups, including the DHHS (https://aidsinfo.nih.gov/) and IAS-USA. There are similar guidelines for treatment throughout Europe and by the World Health Organization for treatment in resource-limited countries. Until recently a recommendation supporting the start of therapy in those with CD4 cells greater than 500 cells was based upon evidence that ongoing viral replication, even in the setting of high CD4 cell counts, may be associated with damage to the brain, kidneys, heart, and possibly even liver. Along with this rationale, it was clear that newer regimens were easy to take, including a growing number of one-pill-per-day options, with minimal side effects. Another compelling argument that can be made for early therapy is the ability to reduce the risk of transmission to uninfected partners. A study called HPTN 052 demonstrated that amongst couples where one person is HIV-infected and the other is not, those who were on antiretroviral therapy were 96% less likely to transmit HIV to their uninfected partner than those not on treatment. Finally, a large study was recently reported that demonstrated unequivocally that starting therapy even with a CD4 cell count of greater than 500 cells/mm3 was associated with less risk of disease progression than waiting until CD4 cells were less than 350 cells/mm3. This study was called the START study and demonstrated a major reduction in disease progression with early therapy with virtually no increased risk for side effects. Based upon START, HPTN 052 and other accumulated data, currently all major guidelines around the world, including those of the World Health Organization recommend that antiretroviral therapy be initiated in all HIV-infected patients at the time of diagnosis. It is worth noting that these recommendations for universal treatment of HIV-infected patients will be limited by resources available for antiviral treatment in resource-limited countries.
Definition (MSHFRE) Immunodéficience cellulaire acquise, associée à l’infection par le virus de l’immunodéficience humaine (VIH). Selon les critères du CDC définis en 1993, le sida correspond à un nombre de lymphocytes T CD4 inférieur à 200 cellules/microlitre ou inférieur à 14% des lymphocytes totaux, à une augmentation de la susceptibilité aux infections opportunistes et à l’apparition de néoplasies. Les manifestations cliniques incluent des pertes de poids (diarrhée) et une démence.
Seroconversion is the clearest evidence for an adaptive immune response to infection with HIV, but the generation of T lymphocytes responding to infected cells is thought by most workers in the field to be central in controlling the infection. Both CD8 cytotoxic T cells and TH1 cells specifically responsive to infected cells are associated with the decline in detectable virus after the initial infection. These T-cell responses are unable to clear the infection completely and can cause some pathology. Nevertheless, there is evidence that the virus itself is cytopathic, and T-cell responses that reduce viral spread should therefore, on balance, reduce the pathology of the disease.
Once the virus has infected a T cell, HIV copies its RNA into a double-stranded DNA copy by means of the viral enzyme reverse transcriptase; that process is called reverse transcription, because it violates the usual way in which genetic information is transcribed. Because reverse transcriptase lacks the “proofreading” function that most DNA-synthesizing enzymes have, many mutations arise as the virus replicates, further hindering the ability of the immune system to combat the virus. Those mutations allow the virus to evolve very rapidly, approximately one million times faster than the human genome evolves. That rapid evolution allows the virus to escape from antiviral immune responses and antiretroviral drugs. The next step in the virus life cycle is the integration of the viral genome into the host cell DNA. Integration occurs at essentially any accessible site in the host genome and results in the permanent acquisition of viral genes by the host cell. Under appropriate conditions those genes are transcribed into viral RNA molecules. Some viral RNA molecules are incorporated into new virus particles, whereas others are used as messenger RNA for the production of new viral proteins. Viral proteins assemble at the plasma membrane together with the genomic viral RNA to form a virus particle that buds from the surface of the infected cell, taking with it some of the host cell membrane that serves as the viral envelope. Embedded in that envelope are the gp120/gp41 complexes that allow attachment of the helper T cells in the next round of infection. Most infected cells die quickly (in about one day). The number of helper T cells that are lost through direct infection or other mechanisms exceeds the number of new cells produced by the immune system, eventually resulting in a decline in the number of helper T cells. Physicians follow the course of the disease by determining the number of helper T cells (CD4+ cells) in the blood. That measurement, called the CD4 count, provides a good indication of the status of the immune system. Physicians also measure the amount of virus in the bloodstream—i.e., the viral load—which provides an indication of how fast the virus is replicating and destroying helper T cells.
Two points in this update deserve emphasis. First, the eventual case-mortality rate of AIDS, a few years after diagnosis, may be far greater than the 41% overall case-mortality rate noted above. Second, the reported incidence of AIDS has continued to increase rapidly. Only a small percentage of cases have none of the identified risk factors (male homosexuality, intravenous drug abuse, Haitian origin, and perhaps hemophilia A). To avoid a reporting bias, physicians should report cases regardless of the absence of these factors.
People with HIV infection should be under the care of a physician who is experienced in treating HIV infection. This is often an infectious-disease subspecialist, but may be a health-care provider, such as an internal medicine or pediatric specialist, who has special certification in HIV treatment. All people with HIV should be counseled about avoiding the spread of the disease. Infected individuals are also educated about the disease process, and attempts are made to improve the quality of their life.
Civil Litigation Tort Law has seen an explosion of AIDS-related suits. This area of law is used to discourage individuals from subjecting others to unreasonable risks and to compensate those who have been injured by unreasonably risky behavior. The greatest number of AIDS-related liability lawsuits has involved the receipt of HIV-infected blood and blood products. A second group has concerned the sexual transmission of HIV. A third group involves AIDS-related psychic distress. In these cases, plaintiffs have successfully sued and recovered damages for their fear of having contracted HIV.
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Dr. Michael Gottlieb, the lead author of the report and a renowned physician specializing in H.I.V./AIDS, treated Rock Hudson before he died of AIDS complications in 1985 and still practices in Los Angeles. Gottlieb said he is often asked why he didn’t include in that first report the documented case of the gay African-American man, who had both PCP and cytomegalovirus, a virus that attacks the organs of patients with compromised immune systems. He explains that he discovered the case after the report was finalized. “Until recently, I wouldn’t have thought it said Gottlieb, who said that he and others on the front line were grappling with an unprecedented and frightening medical mystery and largely working in the dark. “But in retrospect, I think it might’ve made a difference among gay black men.”
Short for acquired immune deficiency syndrome. A severe disease caused by HIV, in which the immune system is attacked and weakened, making the body susceptible to other infections. The virus is transmitted through bodily fluids such as semen and blood.
‘second-class travel’ syndrome pulmonary thromboembolism due to prolonged periods of inactivity, e.g. passengers (who have been static for > 4 hours during long-haul intercontinental air flights) develop deep-vein thrombosis; the clot detaches, passing through venous circulation and heart, to block the pulmonary artery; characterized by sudden collapse and death; passengers on long-haul flights are advised to undertake leg muscle exercises regularly throughout the duration of the flight, wear ‘antithrombotic’ elasticated hosiery and consider medication with aspirin in the weeks before long-haul flight
Indianapolis based PanaMed Corporation announces today that the Company concluded Stage One of the first human treatment program for its immunomodulating therapeutic to treat patients infected with the human immunodeficiency virus (HIV), the virus that causes acquired immune deficiency syndrome (AIDS).
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