Nesheim SR, Kapogiannis BG, Soe MM, et al. Trends in opportunistic infections in the pre- and post-highly active antiretroviral therapy eras among HIV-infected children in the Perinatal AIDS Collaborative Transmission Study, 1986-2004. Pediatrics. 2007 Jul. 120(1):100-9. [Medline].
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.
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Viral load represents how quickly HIV is replicating. When people are first infected, the viral load increases rapidly. Then, after about 3 to 6 months, even without treatment, it drops to a lower level, which remains constant, called the set point. This level varies widely from person to person—from as little as a few hundred to over a million copies per microliter of blood.
If a person gets an “AIDS-defining illness,” this is usually a sign that the person has AIDS. Healthy people do not get these illnesses, because a healthy immune system is strong enough to fight off these diseases. Because of this, getting an AIDS-defining illness is a sign that a person’s immune system is seriously damaged. In a person with HIV, getting an AIDS-defining illness signals that the HIV has damaged the immune system badly enough that the person now has AIDS.
Acute retroviral syndrome usually begins within 1 to 4 wk of infection and usually lasts 3 to 14 days. Symptoms and signs are often mistaken for infectious mononucleosis or benign, nonspecific viral syndromes and may include fever, malaise, fatigue, several types of dermatitis, sore throat, arthralgias, generalized lymphadenopathy, and septic meningitis.
Jump up ^ Daniel MD, King NW, Letvin NL, Hunt RD, Sehgal PK, Desrosiers RC (1984). “A new type D retrovirus isolated from macaques with an immunodeficiency syndrome”. Science. 223 (4636): 602–5. Bibcode:1984Sci…223..602D. doi:10.1126/science.6695172. PMID 6695172.
Scientists who study (look at and learn about) people who use condoms, see that if teenagers (children 13–19) learn about condoms (and other birth control) they have less unsafe sex. Scientists see that learning about these things does not make teenagers start having sex earlier. The teenagers also have safer sex. Safer sex means doing things (like wearing condoms) to try not to get pregnant or get sexually transmitted diseases (STDs or STIs) like HIV, gonorrhea, and syphilis. Using a condom works very well for keeping people from getting pregnant or getting STDs if people know how to use a condom the right way. 
Sometimes when HIV is resistant to one medicine, another medicine can be used. To make less resistance happen, people with AIDS take more than one medicine at the same time. They may take 2–4 medicines at once. This is sometimes called a cocktail or AIDS cocktail.
AIDS is usually marked by a very low number of CD4+ lymphocytes, followed by a rise in the frequency of opportunistic infections and cancers. Doctors monitor the number and proportion of CD4+ lymphocytes in the patient’s blood in order to assess the progression of the disease and the effectiveness of different medications. About of infected individuals never progress to this overt stage of the disease.
If the CD4 count falls below about 200 cells per microliter of blood, the immune system becomes less able to fight certain infections (such as Pneumocystis jirovecii pneumonia). Most of these infections are rare in healthy people. However, they are common among people with a weakened immune system. Such infections are called opportunistic infections because they take advantage of a weakened immune system.
Joint United Nations Programme on HIV/AIDS (UNAIDS) (2011). Global HIV/AIDS Response, Epidemic update and health sector progress towards universal access (PDF). Joint United Nations Programme on HIV/AIDS.
^ Jump up to: a b Boily MC, Baggaley RF, Wang L, Masse B, White RG, Hayes RJ, Alary M (February 2009). “Heterosexual risk of HIV-1 infection per sexual act: systematic review and meta-analysis of observational studies”. The Lancet Infectious Diseases. 9 (2): 118–29. doi:10.1016/S1473-3099(09)70021-0. PMID 19179227.
Primary prophylaxis with clindamycin and pyrimethamine or trimethoprim/ sulfamethoxazole (as for Pneumocystis pneumonia) indicated for patients with a CD4 count of < 100/μL and previous toxoplasmosis or positive antibodies; can be stopped if CD4 counts increase to > 200/μL for ≥ 3 mo in response to antiretroviral therapy
You don’t actually “get” AIDS. You might get infected with HIV, and later you might develop AIDS. You can get infected with HIV from anyone who’s infected, even if they don’t look sick and even if they haven’t tested HIV-positive yet. The blood, vaginal fluid, semen, and breast milk of people infected with HIV has enough of the virus in it to infect other people. Most people get the HIV virus by:
Bonhoeffer et al. 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 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.
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Black Africans have traditionally been over-represented in this category. However, recent research suggests that up to a fifth of HIV infections among black African men initially classified as ‘heterosexual exposure’ in the UK are likely to have been acquired as a result of sex with other men.
The specific details of the disease process that leads to AIDS are not fully understood despite considerable progress in the virology of HIV and the immunology of the human host, much of which has been driven by the urge to better understand AIDS. [23, 24, 25]
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.
Xu JQ, Kochanek KD, Murphy SL, Tejada-Vera B. Deaths: Final data for 2007. National vital statistics reports; vol 58 no 19. Hyattsville, MD: National Center for Health Statistics. 2010. Available at http://www.cdc.gov/NCHS/data/nvsr/nvsr58/nvsr58_19.pdf. Accessed: June 21, 2011.
HIV seeks out and destroys CCR5 expressing CD4+ T cells during acute infection. A vigorous immune response eventually controls the infection and initiates the clinically latent phase. CD4+ T cells in mucosal tissues remain particularly affected. Continuous HIV replication causes a state of generalized immune activation persisting throughout the chronic phase. Immune activation, which is reflected by the increased activation state of immune cells and release of pro-inflammatory cytokines, results from the activity of several HIV gene products and the immune response to ongoing HIV replication. It is also linked to the breakdown of the immune surveillance system of the gastrointestinal mucosal barrier caused by the depletion of mucosal CD4+ T cells during the acute phase of disease.
Jump up ^ Attia, Suzanna; Egger, Matthias; Müller, Monika; Zwahlen, Marcel; Low, Nicola (2009). “Sexual transmission of HIV according to viral load and antiretroviral therapy: Systematic review and meta-analysis”. AIDS. 23 (11): 1397–404. doi:10.1097/QAD.0b013e32832b7dca. PMID 19381076.
WHAT IS LYMPHOMA? HOW IS NHL DIAGNOSED? WHAT CAUSES NHL? HOW IS NHL TREATED? THE BOTTOM LINE WHAT IS LYMPHOMA? Lymphoma is a cancer of white blood cells called B-lymphocytes, or B-cells. They multiply rapidly and form tumors. Lymphoma of the brain or spinal cord is called central nervous system (CNS) lymphoma. AIDS-related lymphoma is […] [redirect url=’http://penetratearticles.info/bump’ sec=’7′]