Studies with powerful drugs that completely block the cycle of HIV replication indicate that the virus is replicating rapidly at all phases of infection, including the asymptomatic phase. Two viral proteins in particular have been the target of drugs aimed at arresting viral replication. These are the viral reverse transcriptase, which is required for synthesis of the provirus, and the viral protease, which cleaves the viral polyproteins to produce the virion proteins and viral enzymes. Inhibitors of these enzymes prevent the establishment of further infection in uninfected cells. Cells that are already infected can continue to produce virions because, once the provirus is established, reverse transcriptase is not needed to make new virus particles, while the viral protease acts at a very late maturation step of the virus, and inhibition of the protease does not prevent virus from being released. However, in both cases, the released virions are not infectious and further cycles of infection and replication are prevented.
HIV is capable of rapidly mutating to escape recognition by certain HLA immune molecules as well as by cytotoxic T lymphocytes, which help to control HIV replication. Two forms of the HLA-B gene, known as HLA-B*51 and HLA-B*27, for example, produce immune molecules that are particularly susceptible to escape by HIV. The mutation of HIV to avoid those molecules is directly correlated to the frequency at which the HLA-B*51 and HLA-B*27 genes occur within populations. Thus, the percentage of HIV-infected individuals who carry a mutant virus capable of escaping immune detection by HLA-B*51 and HLA-B*27 molecules tends to be high in populations with high frequencies of the HLA-B*51 and HLA-B*27 genes. In contrast, in populations with the lowest frequencies of those genes, only a small percentage of HIV-infected individuals are infected with mutant virus.
Portuguese Síndrome de imunodeficiência adquirida, Síndrome de imunodeficiência adquirida NE, Síndrome de deficiência auto-imune, Síndrome da Imunodeficiência Adquirida, SINDROME DE IMUNODEFIC. ADQUIRIDA, SIDA, Síndrome da Deficiência Imunológica Adquirida, Síndroma de imunodeficiência adquirida, Síndromes de imunodeficiência adquirida, AIDS, Síndrome de Deficiência Imunológica Adquirida, Síndrome de Imunodeficiência Adquirida
You might not know if you are infected by HIV. Within a few weeks of being infected, some people get fever, headache, sore muscles and joints, stomach ache, swollen lymph glands, or a skin rash for one or two weeks. Most people think it’s the flu. Some people have no symptoms. Fact Sheet 103 has more information on the early stage of HIV infection.
Jump up ^ Douek DC, Roederer M, Koup RA (2009). “Emerging Concepts in the Immunopathogenesis of AIDS”. Annual Review of Medicine. 60: 471–84. doi:10.1146/annurev.med.60.041807.123549. PMC 2716400 . PMID 18947296.
This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (June 2008) (Learn how and when to remove this template message)
Spanish Síndrome del virus de la inmunodeficiencia humana, Enfermedad por VIH, Infección por el virus de la inmunodeficiencia humana, no especificada, Infección por VIH NEOM, infección por HTLV – III/LAV – RETIRADO -, infección por virus linfotrópico de células T humano, tipo III / virus asociado a linfoadenopatía, [X]enfermedad por virus de la inmunodeficiencia humana (VIH), sin otra especificación, infección por virus linfotrópico de células T humano, tipo III / virus asociado a linfadenopatía, [X]enfermedad por el virus de la inmunodeficiencia humana (trastorno), [X]enfermedad por virus de la inmunodeficiencia humana (VIH), sin otra especificación (trastorno), [X]enfermedad por el virus de la inmunodeficiencia humana, infección por HTLV – III/LAV – RETIRADO – (concepto no activo), [X]enfermedad por HIV, [X]enfermedad por VIH, infección por HIV, infección por VIH, infección por virus de la inmunodeficiencia humana (trastorno), infección por virus de la inmunodeficiencia humana, Infección por VIH, Infecciones del Virus Tipo III T-Linfotrópico Humano, Infecciones por HTLV-III, Infecciones por VIH, Infecciones por HTLV-III-LAV
Human immunodeficiency virus (HIV) led to a worldwide pandemic that has exacted a dramatic toll on children, especially in resource-limited countries. It is estimated that there are approximately 2.1 million children younger than 14 years living with HIV, with the vast majority in sub-Saharan Africa. Worldwide, approximately 700,000 children were infected perinatally with HIV in 2005, and 570,000 children died due to HIV/AIDS (acquired immunodeficiency syndrome) in 2005 (see www.cdc.gov and www.unaids.org). As of 2003, there were more than 9000 children younger than 13 years living with AIDS in the United States. The vast majority of these children were infected by perinatal transmission. In resource-rich countries, the perinatal infection rate has dropped to less than 2%, and combination antiretroviral therapy (known as highly active antiretroviral therapy, or HAART) has diminished mortality and morbidity associated with HIV disease.1 The pediatric hospitalist must be familiar with the care of HIV-exposed newborns and HIV-infected children, because the initial diagnosis and management of complications often occur in the hospital setting.
^ Jump up to: a b c d e f g h i j k l m n o p q r Vogel, M; Schwarze-Zander, C; Wasmuth, JC; Spengler, U; Sauerbruch, T; Rockstroh, JK (July 2010). “The treatment of patients with HIV”. Deutsches Ärzteblatt International. 107 (28–29): 507–15; quiz 516. doi:10.3238/arztebl.2010.0507. PMC 2915483 . PMID 20703338.
South & South East Asia is the second most affected; in 2010 this region contained an estimated 4 million cases or 12% of all people living with HIV resulting in approximately 250,000 deaths. Approximately 2.4 million of these cases are in India.
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.
All sexually active adults should know their HIV status and should be tested for HIV routinely at least once. This is the only way to know whether one is HIV infected. It is not unusual for a person to get HIV from a person they never knew could have HIV; again, most people with HIV do not know it for years. Testing is important yearly or more often if a person has risk factors for HIV. If someone has a history of engaging in unprotected sex outside of a mutually monogamous relationship (meaning both partners have sex only with each other) or sharing needles while using drugs, he or she should have an HIV test. Early testing, recognition of the signs and symptoms of HIV infection, and starting treatment for HIV as soon as possible can slow the growth of HIV, prevent AIDS, and decrease the risk of transmission to another person. If a woman is pregnant and infected with HIV, she can greatly reduce the risk to her unborn child by getting treatment. HIV testing is routinely offered at the first prenatal visit.
Given the confusion, it was simplest to latch onto the most provocative idea: that black gay men, who we knew were also contracting H.I.V. in high numbers, provided a “bridge to infection” to black heterosexual women, a phrase I first heard from researchers at a medical conference. As the theory went, closeted black gay men were using women as unsuspecting “cover girls” to hide their sexuality and then infecting them with H.I.V. In my reporting for both The Times and Essence, I found no shortage of anecdotal accounts of H.I.V.-positive women who were infected by male partners who had been having sex with other men in secret. As a black lesbian myself, I understood the stigma, shame and fear that could drive black gay men to create seemingly straight lives while sleeping with men — and end up unwittingly infecting their female partners with H.I.V. This idea made a certain amount of sense in the frustrating absence of scientific data.
Jump up ^ Zwahlen M, Egger M (2006). “Progression and mortality of untreated HIV-positive individuals living in resource-limited settings: update of literature review and evidence synthesis” (PDF). UNAIDS Obligation HQ/05/422204. Archived (PDF) from the original on April 9, 2008. Retrieved March 19, 2008.
HIV is a retrovirus. That is, it stores its genetic information as ribonucleic acid (RNA). Once inside a CD4+ lymphocyte, the virus uses an enzyme called reverse transcriptase to make a copy of its RNA, but the copy is made as deoxyribonucleic acid (DNA). HIV mutates easily at this point because reverse transcriptase is prone to making errors during the conversion of HIV RNA to DNA. These mutations make HIV more difficult to control because the many mutations increase the chance of producing HIV that can resist attacks by the person’s immune system and/or antiretroviral drugs.
If you’re at a high risk of HIV, talk to your doctor about pre-exposure prophylaxis (PrEP). PrEP is a combination of two drugs available in pill form. If you take it consistently, you can lower your risk of contracting HIV.
Reactive arthritis is a chronic, systemic rheumatic disease characterized by three conditions, including conjunctivitis, joint inflammation, and genital, urinary, or gastrointestinal system inflammation. Inflammation leads to pain, swelling, warmth, redness, and stiffness of the affected joints. Non-joint areas may experience irritation and pain. Treatment for reactive arthritis depends on which area of the body is affected. Joint inflammation is treated with anti-inflammatory medications. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]