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Side effects differ from person to person. The most common are dizziness and headache. Serious side effects may include swelling of the mouth and tongue and liver damage. Drug interactions and drug resistance are also possible.

Screening of blood and organs: Transmission by blood transfusion is still remotely possible in the US because antibody results may be false-negative during early infection. Currently, screening blood for antibody and p24 antigen is mandated in the US and probably further reduces risk of transmission. Risk is reduced further by asking people with risk factors for HIV infection, even those with recent negative HIV antibody test results, not to donate blood or organs for transplantation. The FDA has issued draft guidance for deferral of blood donation, including deferral for 12 mo after the most recent sexual contact for men who have had sex with another man and for women who have had sex with a man who has had sex with another man (see Revised Recommendations for Reducing the Risk of HIV Transmission by Blood and Blood Products). However, use of sensitive HIV screening tests and deferral of donors of organs, blood, and blood products have not been implemented consistently in developing countries.

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.

Each virus can be contracted individually, or they can be contracted together in what is referred to as co-infection. HIV-2 seems to have lower mortality rates, less severe symptoms and slower progression to AIDS than HIV-1 alone or the co-infection. In co-infection, however, this is largely dependent on which virus was contracted first. HIV-1 tends to out compete HIV-2 for disease progression. Co-infection seems to be a growing problem globally as time progresses, with most cases being identified in West African countries, as well as some cases in the US.[24]

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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 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.

Jump up ^ Woods, S.; Moore, D.; Weber, E.; Grant, I. (2009). “Cognitive neuropsychology of HIV-associated neurocognitive disorders”. Neuropsychology review. 19 (2): 152–168. doi:10.1007/s11065-009-9102-5. PMC 2690857 . PMID 19462243.

Once infection has progressed to AIDS, the survival period is usually less than 2 years in untreated patients. Persons in whom the infection does not progress long-term may not develop AIDS for 15 years or longer, although many still exhibit laboratory evidence of CD4 T-cell decline or dysfunction. [79, 80, 81, 82]

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.

Finkel TH, Tudor-Williams G, Banda NK, et al. Apoptosis occurs predominantly in bystander cells and not in productively infected cells of HIV- and SIV-infected lymph nodes. Nat Med. 1995 Feb. 1(2):129-34. [Medline].

Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Darunavir for HIV (Prezista) article more useful, or one of our other health articles.

Jump up ^ “Quick Reference Guide—Laboratory Testing for the Diagnosis of HIV Infection: Updated Recommendations” (PDF). cdc.gov. New York State Department of Health. June 27, 2014. pp. 1–2. Retrieved April 13, 2017.

According to data published by the World Health Organization (WHO), about 36.9 million people were living with HIV, approximately 2 million people were newly infected with HIV, and about 1.2 million people died of HIV-related causes in 2014. Since 1981 more than 34 million people have died from HIV infection. A 2014 United Nations report on AIDS indicated that between 2001 and 2013, however, the annual number of new infections in some 27 countries dropped by at least half, and since about 2005 the annual number of deaths from AIDS globally has also declined. The latter trend has been largely due to improved access to treatment for the afflicted. Thus, there has been an increase in the overall number of people living with AIDS.

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Some viruses do not produce rapid lysis of host cells, but rather remain latent for long periods in the host before the appearance of clinical symptoms. This carrier state can take any of several different forms. The term latency is used to denote the interval from infection to clinical manifestations. In the lentiviruses, it was formerly mistakenly believed that virus was inactive during this period. The true situation is that lentiviruses are rapidly replicating and spawning dozens of quasi-species until a particularly effective one overruns the ability of the host’s immune system to defeat it. Other viruses, however, such as the herpesviruses, actually enter a time known as “viral latency,” when little or no replication is taking place until further replication is initiated by a specific trigger. For many years all forms of latency were thought to be identical, but now it has been discovered that there are different types with basic and important distinctions.

Jump up ^ Zhu T, Korber BT, Nahmias AJ, Hooper E, Sharp PM, Ho DD (1998). “An African HIV-1 Sequence from 1959 and Implications for the Origin of the epidemic”. Nature. 391 (6667): 594–7. Bibcode:1998Natur.391..594Z. doi:10.1038/35400. PMID 9468138.

There are six additional known HIV-2 groups, each having been found in just one person. They all seem to derive from independent transmissions from sooty mangabeys to humans. Groups C and D have been found in two people from Liberia, groups E and F have been discovered in two people from Sierra Leone, and groups G and H have been detected in two people from the Ivory Coast. Each of these HIV-2 strains, for which humans are probably dead-end hosts, is most closely related to SIVsmm strains from sooty mangabeys living in the same country where the human infection was found.[20][21]

HIV infection does not immediately cause AIDS, and the issues of how it does, and whether all HIV-infected patients will progress to overt disease, remain controversial. Nevertheless, accumulating evidence clearly implicates the growth of the virus in CD4 T cells, and the immune response to it, as the central keys to the puzzle of AIDS. HIV is a worldwide pandemic and, although great strides are being made in understanding the pathogenesis and epidemiology of the disease, the number of infected people around the world continues to grow at an alarming rate, presaging the death of many people from AIDS for many years to come. Estimates from the World Health Organization are that 16.3 million people have died from AIDS since the beginning of the epidemic and that there are currently around 34.3 million people alive with HIV infection (Fig. 11.19), of whom the majority are living in sub-Saharan Africa, where approximately 7% of young adults are infected. In some countries within this region, such as Zimbabwe and Botswana, over 25% of adults are infected. (AIDS in Mother and Child, in Case Studies in Immunology, see Preface for details)

HIV (human immunodeficiency virus) is a virus that attacks the immune system, the body’s natural defense system. Without a strong immune system, the body has trouble fighting off disease. Both the virus and the infection it causes are called HIV.

Viral load in peripheral blood is used as a surrogate marker of viral replication rate; however, quantitative viral-load assays should not be used as a diagnostic tool. Clinical relevance is as follows:

The second problem is our uncertainty over what form protective immunity to HIV might take. It is not known whether antibodies, cytotoxic T lymphocyte responses, or both are necessary to achieve protective immunity, and which epitopes might provide the targets of protective immunity. Third, if strong cytotoxic responses are necessary to provide protection against HIV, these might be difficult to develop and sustain through vaccination. Other effective viral vaccines rely on the use of live, attenuated viruses and there are concerns over the safety of pursuing this approach for HIV. Another possible approach is the use of DNA vaccination, a technique that we discuss in Section 14-25. Both of these approaches are being tested in animal models.

Once HIV is in the immune system, it multiplies inside the CD4 cells, disabling and killing them in the course of the infection, and thus interfering with their normal function. The immune system gradually deteriorates until it reaches a point where it can no longer fight off any infection.

Although most HIV-1 infected individuals have a detectable viral load and in the absence of treatment will eventually progress to AIDS, a small proportion (about 5%) retain high levels of CD4+ T cells (T helper cells) without antiretroviral therapy for more than 5 years.[28][33] These individuals are classified as HIV controllers or long-term nonprogressors (LTNP).[33] Another group consists of those who maintain a low or undetectable viral load without anti-retroviral treatment, known as “elite controllers” or “elite suppressors”. They represent approximately 1 in 300 infected persons.[34]

Safer sex practices, such as using latex condoms, are effective in preventing the spread of HIV. But there is still a risk of getting the infection, even with the use of condoms (for example, condoms can tear). Abstinence is the only sure way to prevent sexual transmission of HIV.

In 1997, amid euphoria about HAART, people first started thinking seriously about a cure. Sooner or later, all infected cells die on their own. Could the right drugs in the right combination rout the virus for good? That year, David Ho published a paper in Nature in which he mathematically predicted that an H.I.V. patient on the HAART regimen should be able to conquer the detectable virus in twenty-eight to thirty-seven months. That issue also contained a very different report from Robert Siliciano, currently a Howard Hughes investigator at the Johns Hopkins School of Medicine. Using an uncommonly sensitive measurement technique that he’d invented, Siliciano located H.I.V. in a type of helper T cell that provides memory to our immune system and normally survives for decades. Memory T cells are uniquely important: they recognize the antigens in infections and orchestrate speedy responses. But the virus proved to be even cleverer. It lay dormant in strands of host DNA, untouched by the drug cocktail, later springing back to life and degrading the immune system.

Jump up ^ Beard, J; Feeley, F; Rosen, S (November 2009). “Economic and quality of life outcomes of antiretroviral therapy for HIV/AIDS in developing countries: a systematic literature review”. AIDS Care. 21 (11): 1343–56. doi:10.1080/09540120902889926. PMID 20024710.

A previous estimate¶ of diagnosis delays among persons who received a diagnosis of HIV infection in 2011 indicated that half had been infected for 3.6 years. The median diagnosis delay of 3.0 years among HIV diagnoses in 2015 reflects an absolute reduction of 0.6 years (7 months) and a relative reduction of 17%, representing a considerable decrease over a 4-year period (8). Earlier detection of HIV combined with prompt linkage to care and initiation of antiretroviral treatment enhances preservation of immune function and, if viral suppression is achieved and maintained, reduces risk for sexual transmission of HIV (4). In addition, persons who know they have HIV infection substantially reduce their HIV-related risk behaviors: the prevalence of unprotected anal or vaginal intercourse was found to be 53% lower among persons aware of their HIV status than among those who were unaware of their status (17).

The ability of HIV to mutate and rapidly evolve to escape immune detection by the most-prevalent HLA molecules is similar to the rapid adaptation and mutation of other infectious viruses, such as influenza. There is some evidence, however, that within populations the adaptation of HIV to protective HLA variants may reduce its replicative capacity. In Botswana, for instance, where HIV has adapted to overcome the protective effects of the HLA-B*57 variant, seroprevalence (the frequency of HIV infection) is increased but viral replication capacity is reduced. Researchers have speculated that declines in HIV replication capacity and virulence may be attributed to not only rapid adaptation to protective variants but also increasing use of antiretroviral treatments.

Treating infected women with HIV drugs can dramatically reduce the risk of transmission. Infected pregnant women should be treated during the 2nd and 3rd trimesters of pregnancy, during delivery, and during breastfeeding. Doing a cesarean delivery and treating the baby for several weeks after birth also reduce the risk.

The patient with HIV may present with signs and symptoms of any of the stages of HIV infection. No physical findings are specific to HIV infection; the physical findings are those of the presenting infection or illness. Manifestations include the following:

RNA testing (viral load test) detects HIV RNA in the blood. It is not commonly used for screening but can be helpful in detecting early HIV infection when a person is in the window period or if the screening tests are unclear.

Macrophages. Tissue macrophages are one of the target cells for HIV. These macrophages harbour the virus and are known to be the source of viral proteins. However, the infected macrophages are shown to lose their ability to ingest and kill foreign microbes and present antigen to T cells. This could have a major contribution in overall immune dysfunction caused by HIV infection.

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 10% of infected individuals never progress to this overt stage of the disease. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]

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