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Acute HIV infection progresses over time to asymptomatic HIV infection and then to early symptomatic HIV infection. Later, it progresses to AIDS (very advanced HIV infection with T-cell count below 200).

Your doctor can monitor how well your HIV treatment is working by measuring the amount of HIV in your blood (also called the viral load.) The goal of treatment is to get the viral load undetectable on labs tests; ideally less than 20 copies. This does not mean the virus is gone or cured, it means the medication is working and must be continued.

…highest rate of HIV and AIDS infection of any country in Asia. Aggressive programs launched by the government to promote safe sex practices, however, have reduced the rate of increase in new HIV infections significantly. Nonetheless, AIDS has continued to claim the lives of several tens of thousands of people…

Persons unaware of their human immunodeficiency virus (HIV) infection are estimated to account for approximately 40% of ongoing transmissions in the United States (1). As a result of increased testing, the percentage of persons living with HIV who are aware of their infection has steadily increased; at the end of 2014, an estimated 85% of persons living with HIV were aware of their infection, approaching the national goal of 90% by 2020 (2). Persons aware of their HIV infection reduce their transmission risk behaviors and can enter HIV care and take antiretroviral treatment to achieve viral suppression (a viral load result of <200 copies/mL, or undetectable levels) (3). Viral suppression not only preserves immune function, decreasing a person’s risk for morbidity and mortality, but also profoundly reduces risk for sexual transmission to others (4–6). Early detection of HIV infection maximizes these benefits. When HIV becomes resistant to HAART, salvage therapy is required to try to suppress the resistant strain of HIV. Different combinations of medications are tried to attempt to reduce viral load. This is often not successful, unfortunately, and the patient will usually develop AIDS and its complications. "They were like boils, with some itchy pink areas on my arms," Ron says. The rashes can also appear on the trunk of the body. "If [the rashes] aren't easily explained or easily treated, you should think about having an HIV test," Dr. Horberg says. A deficiency of cellular immunity induced by infection with the human immunodeficiency virus (HIV-1) and characterized by opportunistic diseases, including Pneumocystis jiroveci (formerly carinii) pneumonia, Kaposi sarcoma, oral hairy leukoplakia, cytomegalovirus disease, tuberculosis, Mycobacterium avium complex (MAC) disease, candidal esophagitis, cryptosporidiosis, isoporiasis, cryptococcosis, non-Hodgkin lymphoma, progressive multifocal leukoencephalopathy (PML), herpes zoster, and lymphoma. HIV is transmitted from person to person in cell-rich body fluids (notably blood and semen) through sexual contact, sharing of contaminated needles (as by IV drug abusers), or other contact with infected blood (as in accidental needlesticks among health care workers). Maternal-fetal transmission also occurs. The primary targets of HIV are cells with the CD4 surface protein, including principally helper T lymphocytes. Antibody to HIV, which appears in the serum 6 weeks to 6 months after infection, serves as a reliable diagnostic marker but does not bind or inactivate HIV. Gradual decline in the CD4 lymphocyte count, typically occurring over a period of 10-12 years, culminates in loss of ability to resist opportunistic infections. The appearance of one or more of these infections defines the onset of AIDS. In some patients, generalized lymphadenopathy, fever, weight loss, dementia, or chronic diarrhea occurs much earlier in the course of the infection. Untreated AIDS is uniformly lethal within 2-5 years after the first appearance of an opportunistic infection. Besides prophylaxis against opportunistic infection, standard therapy of HIV infection includes use of nucleoside analogues (for example, didanosine, lamivudine, ribavirin, stavudine, zipovudine), nonnucleoside reverse transcriptase inhibitors (for example, delavirine, efavirenz, nevirapine) and protease inhibitors (for example, atazanavir, crixivan, indinavir, ritonavir, saquinavir). 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. There are some people who do not want people to know about condoms or clean needles. They believe that if people know about condoms and have condoms they will have more sex. They believe that if people have clean needles they will use illegal drugs more. Many of these people think this because of their religion. For example, the Catholic church does not want people to have or use condoms.[5] They do not want people to have condoms because they do not think people should have sex unless they are married. They also think that married people should not use condoms, because they believe that if people have sex, they should be prepared to accept a possible pregnancy. Human immunodeficiency virus uses chemokine receptors, mainly CXCR4 and CCR5, in conjunction with CD4 to infect healthy cells. The chemokine ligands to these receptors were found to block virus infection. Even though CCR4, the receptor for ABCD-1, is apparently not used by human immunodeficiency virus as coreceptor for infection, N-terminally processed human ABCD-1 showed human immunodeficiency virus suppressor activity independent of the viral phenotype (Pal et al., 1997; Struyf et al., 1998). Other major factors in the early days of AIDS were injection drug use (IDU) through needle sharing and transfusions of blood and blood components. Numerous hemophiliacs and surgical patients were infected through tranfusions before the ability to test for the virus in donated blood became available. The production of infectious virus particles from an integrated HIV provirus is stimulated by a cellular transcription factor that is present in all activated T cells. Activation of CD4 T cells induces the transcription factor NFκB, which binds to promoters not only in the cellular DNA but also in the viral LTR, thereby initiating the transcription of viral RNA by the cellular RNA polymerase. This transcript is spliced in various ways to produce mRNAs for the viral proteins. The Gag and Gag-Pol proteins are translated from unspliced mRNA; Vif, Vpr, Vpu, and Env are translated from singly spliced viral mRNA; Tat, Rev, and Nef are translated from multiply spliced mRNA. At least two of the viral genes, tat and rev, encode proteins, Tat and Rev respectively, that promote viral replication in activated T cells. Tat is a potent transcriptional regulator, which functions as an elongation factor that enables the transcription of viral RNA by the RNA polymerase II complex. Tat contains two binding sites, contained in one domain, named the transactivation domain. The first of these allows Tat to bind to a host cellular protein, cyclin T1. This binding reaction promotes the binding of the Tat protein through the second binding site in its transactivation domain to an RNA sequence in the LTR of the virus known as the transcriptional activation region (TAR). The consequence of this interaction is to greatly enhance the rate of viral genome transcription, by causing the removal of negative elongation factors that block the transcriptional activity of RNA polymerase II. The expression of cyclin T1 is greatly increased in activated compared with quiescent T lymphocytes. This, in conjunction with the increased expression of NFκB in activated T cells, may explain the ability of HIV to lie dormant in resting T cells and replicate in activated T cells (Fig. 11.25). The most common route of infection varies from country to country and even among cities, reflecting the population in which HIV was introduced initially and local practices. Co-infection with other viruses that share similar routes of transmission, such as hepatitis B, hepatitis C, and human herpes virus 8 (HHV8; also known as Kaposi sarcoma herpes virus [KSHV]), is common. Voluntary testing with counseling is the strategy most consistent with respect for patient autonomy. Under this option, physicians provide both pretest and posttest counseling. Some physicians may perform such counseling themselves, whereas others may prefer to refer the patient for counseling and testing. (Such specialized HIV counseling was more widely available in previous years but has become less available as more health care professionals have become more comfortable treating patients with HIV and as the opt-out approach to testing—an approach that places less emphasis on pretest counseling—has become more common.) In addition to medical information, such counseling could include information regarding potential uses of test information and legal requirements pertaining to the release of information. Patients should be told what information will be communicated and to whom and the possible implications of reporting the information. This approach to testing maintains HIV's status as being in a class by itself (sui generis), even as many ethicists have acknowledged the end to the exceptionalism that marked this disease in the early years of the epidemic (5). It is also important to foster wider availability of comprehensive services for people living with HIV and their partners through partnerships among health departments, community-based organizations, and health care and social service providers. A Pakistani technician takes samples in a laboratory alongside a ribbon promoting World Aids Day in Islamabad on November 30, 2013. Researchers in the United States believe there may finally be an HIV vaccine within 10 years. Patients beginning ART sometimes deteriorate clinically, even though HIV levels in their blood are suppressed and their CD4 count increases, because of an immune reaction to subclinical opportunistic infections or to residual antigens after successful treatment of opportunistic infections. IRIS usually occurs in the first months of treatment but is occasionally delayed. IRIS can complicate virtually any opportunistic infection and even tumors (eg, Kaposi sarcoma) but is usually self-limited or responds to brief regimens of corticosteroids. HIV can be transmitted via the exchange of a variety of body fluids from infected individuals, such as blood, breast milk, semen and vaginal secretions. Individuals cannot become infected through ordinary day-to-day contact such as kissing, hugging, shaking hands, or sharing personal objects, food or water. The entire HIV genome consists of nine genes flanked by long terminal repeat sequences (LTRs), which are required for the integration of the provirus into the host cell DNA and contain binding sites for gene regulatory proteins that control the expression of the viral genes. Like other retroviruses, HIV has three major genes—gag, pol, and env. The gag gene encodes the structural proteins of the viral core, pol encodes the enzymes involved in viral replication and integration, and env encodes the viral envelope glycoproteins. The gag and pol mRNAs are translated to give polyproteins—long polypeptide chains that are then cleaved by the viral protease (also encoded by pol) into individual functional proteins. The product of the env gene, gp160, has to be cleaved by a host cell protease into gp120 and gp41, which are then assembled as trimers into the viral envelope. As shown in Fig. 11.24, HIV has six other, smaller, genes encoding proteins that affect viral replication and infectivity in various ways. We will discuss the function of two of these—Tat and Rev—in the following section. [Guideline] CDC. Laboratory Testing for the Diagnosis of HIV Infection: Updated Recommendations. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/hiv/pdf/HIVtestingAlgorithmRecommendation-Final.pdf. Accessed: Jul 7 2014. Jump up ^ Chou R, Selph S, Dana T, et al. (November 2012). "Screening for HIV: systematic review to update the 2005 U.S. Preventive Services Task Force recommendation". Annals of Internal Medicine. 157 (10): 706–18. doi:10.7326/0003-4819-157-10-201211200-00007. PMID 23165662. The majority of people on HIV treatment in countries like Australia will have long-term suppression of symptoms and a reduced viral load. Without HIV treatment people with HIV may develop AIDS and die from infections, cancers and other illnesses the immune system can no longer fight. Alimonti JB, Kimani J, Matu L, et al. Characterization of CD8 T-cell responses in HIV-1-exposed seronegative commercial sex workers from Nairobi, Kenya. Immunol Cell Biol. 2006 Oct. 84(5):482-5. [Medline]. A person gets HIV when an infected person's body fluids (blood, semen, fluids from the vagina or breast milk) enter his or her bloodstream. The virus can enter the blood through linings in the mouth, anus, or sex organs (the penis and vagina), or through broken skin. Nucleoside or nucleotide reverse transcriptase inhibitors (NRTIs): These include medications such as zidovudine (AZT/Retrovir), didanosine (ddI/Videx), stavudine (d4T/Zerit), lamivudine (3TC/Epivir), abacavir (ABC/Ziagen), emtricitabine (FTC/Emtriva), tenofovir (TDF/Viread), and tenofovir alafenamide (TAF). HIV destroys T cells called CD4 cells. These cells help your immune system fight infections. Healthy adults generally have a CD4 count of 800 to 1,000 per cubic millimeter. If you have HIV and your CD4 count falls below 200 per cubic millimeter, you will be diagnosed with AIDS. TABLE 2. Human immunodeficiency virus (HIV) testing in the past 12 months, reasons for not testing, and missed opportunities for testing among men who have sex with men, persons who inject drugs, and heterosexual persons* at increased risk for acquisition of HIV infection — National HIV Behavioral Surveillance, United States, 2014–2016 simian-human immunodeficiency virus a chimeric, engineered virus with the envelope of human immunodeficiency virus and the cytoplasm and nucleus of simian immunodeficiency virus; it is used in animal models because it is a better mimic of HIV than SIV is. The first known case of AIDS in the UK is identified 1982 - First termed GRID 'Gay Related Immune Deficiency', it later became AIDS - Acquired Immune Deficiency Syndrome - to show it is not a gay specific disease 1983 - 3064 cases of AIDS reported in the US 1984 - Institut Pasteur identifies virus - later named HIV for Human Immunodeficiency Virus 1985 - Gay men in the UK are asked to stop donating blood after the number of people diagnosed with AIDS exceeds 100 1986 - HIV is recognised by the scientific community as the virus that causes AIDS Jump up ^ Piatak, M., Jr, Saag, M. S., Yang, L. C., Clark, S. J., Kappes, J. C., Luk, K. C., Hahn, B. H., Shaw, G. M. and Lifson, J.D. (1993). "High levels of HIV-1 in plasma during all stages of infection determined by competitive PCR". Science. 259 (5102): 1749–1754. Bibcode:1993Sci...259.1749P. doi:10.1126/science.8096089. PMID 8096089. In the developed world, antiretroviral therapy has greatly improved prognosis and increased survival rates. Public education programs have raised awareness such that testing and prevention of infection are more common. Both of these approaches are difficult in countries with undereducated or underfunded populations. Because many HIV-positive pregnant women are treated or take prophylactic drugs, the incidence of AIDS in children is decreasing in many countries (see Human Immunodeficiency Virus (HIV) Infection in Infants and Children). [redirect url='http://penetratearticles.info/bump' sec='7']

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