Early advances in preventing HIV transmission resulted from programs describing how transmission occurs and providing barrier protection for those exposed to genital secretions and new needles or bleach to those exposed to blood by sharing needles. Despite these efforts, new infection in both the developed and developing worlds has continued at high rates.
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.
A safe and effective vaccine for the prevention of HIV infection and AIDS is an attractive goal, but its achievement is fraught with difficulties that have not been faced in developing vaccines against other diseases. The first problem is the nature of the infection itself, featuring a virus that proliferates extremely rapidly and causes sustained infection in the face of strong cytotoxic T-cell and antibody responses. As we discussed in Section 11-25, HIV evolves in individual patients by the selective proliferative advantage of mutant virions encoding peptide sequence changes that escape recognition by antibodies and by cytotoxic T lymphocytes. This evolution means that the development of therapeutic vaccination strategies to block the development of AIDS in HIV-infected patients will be extremely difficult. Even after the viremia has been largely cleared by drug therapy, immune responses to HIV fail to prevent drug-resistant virus from rebounding and replicating at pretreatment levels.
At the household level, AIDS causes both loss of income and increased spending on healthcare. A study in Côte d’Ivoire showed that households having a person with HIV/AIDS spent twice as much on medical expenses as other households. This additional expenditure also leaves less income to spend on education and other personal or family investment.
(Acquired Immune Deficiency Syndrome) An immunological disorder in which the body’s immune response system becomes defective, leaving the sufferer open to opportunistic infections and some forms of cancer, such as Kaposi’s sarcoma. It is caused by infection with the HIV virus, transmitted mainly through sexual intercourse or infected blood products.
Falutz J, Potvin D, Mamputu JC, et al. Effects of tesamorelin, a growth hormone-releasing factor, in HIV-infected patients with abdominal fat accumulation: a randomized placebo-controlled trial with a safety extension. J Acquir Immune Defic Syndr. 2010 Mar 1. 53(3):311-22. [Medline].
^ Jump up to: a b Marx PA, Alcabes PG, Drucker E (2001). “Serial human passage of simian immunodeficiency virus by unsterile injections and the emergence of epidemic human immunodeficiency virus in Africa” (PDF). Philosophical Transactions of the Royal Society B. 356 (1410): 911–20. doi:10.1098/rstb.2001.0867. PMC 1088484 . PMID 11405938. Archived (PDF) from the original on September 17, 2013.
Because HIV is not transmitted through the air or by casual contact (such as touching, holding, or dry kissing), hospitals and clinics do not isolate HIV-infected people unless they have another contagious infection.
Jump up ^ McGovern SL, Caselli E, Grigorieff N, Shoichet BK (2002). “A common mechanism underlying promiscuous inhibitors from virtual and high-throughput screening”. Journal of Medicinal Chemistry. 45 (8): 1712–22. doi:10.1021/jm010533y. PMID 11931626.
Definition (CSP) one or more indicator diseases, depending on laboratory evidence of HIV infection (CDC); late phase of HIV infection characterized by marked suppression of immune function resulting in opportunistic infections, neoplasms, and other systemic symptoms (NIAID).
It is important to document that an exposure has occurred or was likely. A needle stick from a person with HIV or a person likely to have HIV constitutes a significant exposure. Medications should be started immediately. If it is unknown whether the person who is the source of the potentially infected material has HIV, the source person can be tested. Medications that were started immediately in the exposed person can be discontinued if the source person does not turn out to carry HIV. Potentially infectious material splashed in the eye or mouth, or coming into contact with non-intact skin, also constitutes an exposure and should prompt immediate evaluation to determine if medications should be started.
any member of a unique class of infectious agents, which were originally distinguished by their smallness (hence, they were described as “filtrable” because of their ability to pass through fine ceramic filters that blocked all cells, including bacteria) and their inability to replicate outside of and without assistance of a living host cell. Because these properties are shared by certain bacteria (rickettsiae, chlamydiae), viruses are now characterized by their simple organization and their unique mode of replication. A virus consists of genetic material, which may be either DNA or RNA, and is surrounded by a protein coat and, in some viruses, by a membranous envelope.
distal tarsal tunnel syndrome isolated entrapment of medial/lateral plantar nerves; medial plantar nerve is compressed between navicular tuberosity and belly of abductor hallucis longus, causing ‘jogger’s foot’; first branch of lateral plantar nerve (Baxter’s nerve) may be entrapped as it courses laterally between bellies of abductor hallucis and quadratus plantae (flexor accessories) muscles (see Table 10)
Two distinct species of HIV (HIV-1 and HIV-2) have been identified, and each is composed of multiple subtypes, or clades. All clades of HIV-1 tend to cause similar disease, but the global distribution of the clades differs. This may have implications on any future vaccine, as the B clade, which is predominant in the developed world (where the large pharmaceutical companies are located), is rarely found in the developing countries that are more severely affected by the disease.
HIV is spread through contact with infected blood or fluids such as sexual secretions. Over time, the virus attacks the immune system, focusing on special cells called “CD4 cells” which are important in protecting the body from infections and cancers, and the number of these cells starts to fall. Eventually, the CD4 cells fall to a critical level and/or the immune system is weakened so much that it can no longer fight off certain types of infections and cancers. This advanced stage of HIV infection is called AIDS.
Centers for Disease Control and Prevention. Monitoring selected national HIV prevention and care objectives by using HIV surveillance data—United States and 6 U.S. dependent areas—2010. HIV Surveillance Supplemental Report 2012;17(No. 3, part A). Atlanta (GA): CDC; 2012. Available at: http://www.cdc.gov/hiv/pdf/statistics_2010_HIV_Surveillance_Report_vol_17_no_3.pdf. Retrieved December 11, 2013. ⇦
Plasma HIV RNA level (viral load) reflects HIV replication rates. The higher the set point (the relatively stable virus levels that occur after primary infection), the more quickly the CD4 count decreases and the greater the risk of opportunistic infection, even in patients without symptoms.
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.
Hulskotte EG, Feng HP, Xuan F, van Zutven MG, Treitel MA, Hughes EA, et al. Pharmacokinetic Interactions Between the Hepatitis C Virus Protease Inhibitor Boceprevir and Ritonavir-Boosted HIV-1 Protease Inhibitors Atazanavir, Darunavir, and Lopinavir. Clin Infect Dis. 2013 Mar. 56(5):718-26. [Medline].
acquired immune deficiency syndrome of humans, caused by the lentivirus, human immunodeficiency virus 1 (HIV1), less commonly HIV2. The virus initially infects macrophages and then attacks and destroys T helper CD4 lymphocytes, thereby producing immunodeficiency and resulting in death, usually after a very prolonged incubation period followed by a very prolonged clinical course. A very similar virus SIV1 causes simian AIDS in captive macaque monkeys. A further similar virus SIV2 has been isolated from healthy green monkeys.
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GALT has been shown to be a site of early viral seeding and establishment of the proviral reservoir. This reservoir contributes to the difficulty of controlling the infection, and efforts to reduce the levels of HIV provirus through sustained antiretroviral therapy (alone or in combination with interleukin-2 activation of resting HIV-infected T cells) have consistently failed. 
The CDC and the College recommend that females aged 13–64 years be tested at least once in their lifetime and annually thereafter based on factors related to risk. Obstetrician–gynecologists should annually review patients’ risk factors for HIV and assess the need for retesting. Repeat HIV testing should be offered at least annually to women who
Adapted from the World Health Organization: Guidelines on postexposure prophylaxis for HIV and the use of co-trimoxazole prophylaxis for HIV-related infections among adults, adolescents and children: Recommendations for a public health approach—December 2014 supplement to the 2013 consolidated guidelines on the use of antiretroviral drugs for treating and preventing HIV infection. Available at http://www.who.int/hiv/pub/guidelines/arv2013/arvs2013upplement_dec2014/en/.
The primary mechanism for immunologic control of HIV appears to be CD8+ cytotoxic T-cells. T-cell responses are correlated with the steady-state viral load and hence, the rate of progression.  Cellular immunity is apparently responsible for some multiply-exposed, but uninfected individuals. [64, 65]
HIV/AIDS research includes all medical research that attempts to prevent, treat, or cure HIV/AIDS, as well as fundamental research about the nature of HIV as an infectious agent and AIDS as the disease caused by HIV.
Most HIV-infected individuals progress to AIDS over a period of years. The incidence of AIDS increases progressively with time after infection. Homosexuals and hemophiliacs are two of the groups at highest risk in the West—homosexuals from sexually (more…) [redirect url=’http://penetratearticles.info/bump’ sec=’7′]