“Sexually Transmitted Diseases Chlamydia _Gonorrhea”

Circumcision in Sub-Saharan Africa “reduces the acquisition of HIV by heterosexual men by between 38% and 66% over 24 months”.[115] Due to these studies, both the World Health Organization and UNAIDS recommended male circumcision as a method of preventing female-to-male HIV transmission in 2007 in areas with a high rates of HIV.[116] However, whether it protects against male-to-female transmission is disputed,[117][118] and whether it is of benefit in developed countries and among men who have sex with men is undetermined.[119][120][121] The International Antiviral Society, however, does recommend for all sexually active heterosexual males and that it be discussed as an option with men who have sex with men.[122] Some experts fear that a lower perception of vulnerability among circumcised men may cause more sexual risk-taking behavior, thus negating its preventive effects.[123]

Bonhoeffer et al.[76] suggested that template switching by reverse transcriptase acts as a repair process to deal with breaks in the single-stranded RNA genome. In addition, Hu and Temin[72] suggested that recombination is an adaptation for repair of damage in the RNA genomes. Strand switching (copy-choice recombination) by reverse transcriptase could generate an undamaged copy of genomic DNA from two damaged single-stranded RNA genome copies. This view of the adaptive benefit of recombination in HIV could explain why each HIV particle contains two complete genomes, rather than one. Furthermore, the view that recombination is a repair process implies that the benefit of repair can occur at each replication cycle, and that this benefit can be realized whether or not the two genomes differ genetically. On the view that recombination in HIV is a repair process, the generation of recombinational variation would be a consequence, but not the cause of, the evolution of template switching.[76]

Details of the origin of HIV unclear. However, a lentivirus that is genetically similar to HIV has been found in chimpanzees and gorillas in western equatorial Africa. That virus is known as simian immunodeficiency virus (SIV), and it was once widely thought to be harmless in chimpanzees. However, in 2009 a team of researchers investigating chimpanzee populations in Africa found that SIV in fact causes AIDS-like illness in the animals. SIV-infected chimpanzees have a death rate that is 10 to 16 times higher than their uninfected counterparts. The practice of hunting, butchering, and eating the meat of chimpanzees may have allowed transmission of the virus to humans, probably in the late 19th or early 20th century. The strain of SIV found in gorillas is known as SIVgor, and it is distinct from the strain found in chimpanzees. Because primates are suspected of being the source of HIV, AIDS is considered a zoonosis, an infection that is shared by humans and other vertebrate animals.

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.

It is widely believed that HIV originated in Kinshasa, in the Democratic Republic of Congo around 1920 when HIV crossed species from chimpanzees to humans. Up until the 1980s, we do not know how many people were infected with HIV or developed AIDS. HIV was unknown and transmission was not accompanied by noticeable signs or symptoms.

In people with AIDS, HIV itself may cause symptoms. Some people experience relentless fatigue and weight loss, known as “wasting syndrome.” Others may develop confusion or sleepiness due to infection of the brain with HIV, known as HIV encephalopathy. Both wasting syndrome and HIV encephalopathy are AIDS-defining illnesses.

Moreover never loose hope for life as is the only chance which we got, who knows about the second life, if got infected accediently do not loose hope and do the best u can do for yourself and the society.

by mother to baby before or during birth or by means of the milk. Drug users and homosexuals are high-risk groups, but in central Africa it is now widespread amongst heterosexuals where a second virus, HIV 2 is also present. This is endemic throughout West Africa but does not appear to have resulted in an epidemic of the disease.

Rarely, HIV has been transmitted via transplantation of organs from HIV-seropositive donors. Infection has developed in recipients of kidney, liver, heart, pancreas, bone, and skin—all of which contain blood—but screening for HIV greatly reduces risk of transmission. HIV transmission is even more unlikely from transplantation of cornea, ethanol-treated and lyophilized bone, fresh-frozen bone without marrow, lyophilized tendon or fascia, or lyophilized and irradiated dura mater.

People with HIV/AIDS often develop prolonged diarrhoea which are sometimes not caused by infections. This is more so in the sub‐Saharan Africa where drugs for controlling HIV itself i.e. antiretroviral drugs (ARV) may not be widely available or affordable. prolonged diarrhoea often results in prolonged illness and death due to loss of fluids, if not treated effectively and on time. Antimotility drugs and adsorbents are readily available and are used to try to control this condition while efforts are made to receive ARVs. We did not find enough evidence to support or refute their use in controlling this condition.

After the first month or so, HIV enters the clinical latency stage. This stage can last from a few years to a few decades. Progression can be slowed with antiretroviral therapy. Some people have symptoms. Many people do not, but it’s still contagious.

It appears that macrophage-tropic isolates of HIV are preferentially transmitted by sexual contact as they are the dominant viral phenotype found in newly infected individuals. Virus is disseminated from an initial reservoir of infected dendritic cells and macrophages and there is evidence for an important role for mucosal lymphoid tissue in this process. Mucosal epithelia, which are constantly exposed to foreign antigens, provide a milieu of immune system activity in which HIV replication occurs readily. Infection of CD4 T cells via CCR5 occurs early in the course of infection and continues to occur, with activated CD4 T cells accounting for the major production of HIV throughout infection. Late in infection, in approximately 50% of cases, the viral phenotype switches to a T-lymphocyte-tropic type that utilizes CXCR4 co-receptors, and this is followed by a rapid decline in CD4 T-cell count and progression to AIDS.

Groups outside the Collaboratories who are testing ways to cure AIDS share their results with the N.I.H. teams. In parallel with the Seattle group, Carl June, the director of translational research at the Abramson Cancer Center, at the University of Pennsylvania, and his colleagues have used genetic engineering to close off the CCR5 passageway. In the New England Journal of Medicine this past March, they reported on their recent clinical trial, which showed that the modified T cells could survive in people with H.I.V. for years. Similar work on knocking down CCR5 is being done by Calimmune, a California-based company devoted to curing AIDS. (One of its founders is David Baltimore, who received the Nobel Prize for the discovery of reverse transcriptase, a crucial enzyme in retroviral reproduction.) Groups in Denmark and Spain have made progress, too, and in 2012 researchers in France analyzed the Visconti study, which had put the early intervention received by the Mississippi baby to a formal test. A subset of fourteen H.I.V. patients had been treated within weeks of their infection, and then HAART was interrupted. They remained free of the virus for several years.

Preexposure prophylaxis with antiretrovirals (PrEP): In PrEP, people who are not infected with HIV but are at high risk (eg, by having an HIV-infected sexual partner) take an antiretroviral drug daily to reduce their risk of infection. The combination of tenofovir disoproxil fumarate plus emtricitabine (TDF/FTC) can be used. Use of PrEP does not eliminate the need to use other methods of reducing risk of HIV infection, including using condoms and avoiding high-risk behaviors (eg, needle sharing). Data concerning infants of HIV-negative mothers taking TDF/FTC PrEP during pregnancy are incomplete, but currently, no adverse effects have been reported in children born to HIV-infected women treated with TDF/FTC. Use of PrEP to reduce the risk of HIV infection in injection drug users is being studied. For the current CDC recommendations, see Pre-Exposure Prophylaxis (PrEP).

Compared with HIV-negative patients, HIV-infected patients with Mycobacterium tuberculosis infection are markedly (21–34 times) more likely to develop active tuberculosis disease.48 The epidemic of HIV has fuelled an increase in tuberculosis disease in countries with a high HIV prevalence. Many southern and eastern African countries experienced a dramatic increase in the rates of tuberculosis disease and mortality from 1980 to 2004.48 In 2010, WHO estimated that approximately 12.5% of the 8.8 million incident cases of tuberculosis worldwide were among HIV-infected persons but that 25% of the 1.4 million people who died of tuberculosis had HIV infection.48 Since 2004, reductions in both the incidence of and mortality from tuberculosis among HIV-infected patients have been attributed to improved tuberculosis diagnosis and treatment, increased HIV testing of patients with tuberculosis, and increased access to ART and cotrimoxazole prophylaxis in HIV/tuberculosis co-infected patients. The epidemiology of these syndemics illustrates the importance of considering and testing for tuberculosis in patients with HIV as well as the importance of HIV testing in all patients with active tuberculosis disease.

Branson BM, Handsfield HH, Lampe MA, Janssen RS, Taylor AW, Lyss SB, et al. Revised recommendations for HIV testing of adults, adolescents, and pregnant women in health-care settings. MMWR Recomm Rep 2006;55 (RR–14):1–17; quiz CE1–4.

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.

He told me, “I’m no longer that concerned about the virus itself. I’m more concerned about my internal organs and premature aging.” In 1999, at fifty, he learned that fatty deposits had substantially constricted the blood flow in a major artery that supplies the heart’s left ventricle. He began to experience crippling pain when he walked, because the blood supply to his bone tissue had diminished—a condition called avascular necrosis. In 2002, he had his first hip replacement, and the second in 2010. His muscles have shrunk, and sitting can be uncomfortable, so he sometimes wears special foam-padded underwear. Every other year, he has his face injected with poly-L-lactic acid, which replaces lost connective tissue.

In summary, patients with a CD4 cell count of less than 200 cells/mm3 should receive preventative treatment against Pneumocystis jiroveci with trimethoprim/sulfamethoxazole (Bactrim, Septra), given once daily or three times weekly. If they are intolerant to that drug, patients can be treated with an alternative drug such as dapsone or atovaquone (Mepron). Those patients with a CD4 cell count of less than 100 cells/mm3 who also have evidence of past infection with Toxoplasma gondii, which is usually determined by the presence of Toxoplasma antibodies in the blood, should receive trimethoprim/sulfamethoxazole. Toxoplasmosis is an opportunistic parasitic disease that affects the brain and liver. If a person is using dapsone to prevent Pneumocystis jiroveci, pyrimethamine and leucovorin can be added once a week to dapsone to prevent toxoplasmosis. Finally, patients with a CD4 cell count of less than 50 cells/mm3 should receive preventive treatment for Mycobacterium avium complex (MAC) infection with weekly azithromycin (Zithromax), or as an alternative, twice daily clarithromycin (Biaxin) or rifabutin (Mycobutin). MAC is an opportunistic bacterium that causes infection throughout the body. Many of these drugs can be stopped if initial antiviral therapy results in good viral suppression and sustained increases in CD4 cells.

The only drug in this class is T-20, which is administered as a twice-daily subcutaneous injection. The most common side effects are redness and pain at the site of injection. Rarely, infection can occur at the injection site. There also are reports of generalized allergic reactions.

HIV-2’s closest relative is SIVsm, a strain of SIV found in sooty mangabees. Since HIV-1 is derived from SIVcpz, and HIV-2 from SIVsm, the genetic sequence of HIV-2 is only partially homologous to HIV-1 and more closely resembles that of SIVsm.[citation needed][102]

Jump up ^ editors, Alexander Krämer, Mirjam Kretzschmar, Klaus Krickeberg, (2010). Modern infectious disease epidemiology concepts, methods, mathematical models, and public health (Online-Ausg. ed.). New York: Springer. p. 88. ISBN 9780387938356. Archived from the original on September 24, 2015.

* Past year testing was assessed during the interview by asking participants, “When did you have your most recent HIV test? Please tell me the month and year.” A missed opportunity was defined as a visit to a health care provider in the past 12 months for a person who did not report past year HIV testing or as not being offered an HIV test at any health care visits for a person who did not report past year HIV testing and had visited a health care provider in the past year.

The human immunodeficiency virus (HIV) causes HIV infection and the acquired immunodeficiency syndrome (AIDS). Symptoms and signs of HIV infection include fatigue, enlarged lymph glands, and recurrent vaginal yeast infections. Highly active antiretroviral therapy (ART) is the standard treatment for HIV infection.

Jump up ^ “Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents” (pdf). Department of Health and Human Services. February 12, 2013. p. i. Archived (PDF) from the original on November 1, 2016. Retrieved January 3, 2014. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]

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