User:Dak/aids

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NOTE! THIS ISN'T THE MAIN AIDS ARTICLE, THIS IS A COPY FOR ME TO WORK ON. TO SEE WIKIPEDIA'S ACTUAL ARTICLE ON AIDS, CLICK HERE --> AIDS

Dak/aids
List of abbreviations used in this article

AIDS: Acquired immune deficiency syndrome
HIV: Human immunodeficiency virus
CD4+: CD4+ T helper cells
CCR5: Chemokine (C-C motif) receptor 5
CDC: Centers for Disease Control and Prevention
WHO: World Health Organization
PCP: Pneumocystis pneumonia
TB: Tuberculosis
MTCT: Mother-to-child transmission
HAART: Highly active antiretroviral therapy
STI/STD: Sexually transmitted infection/disease

Acquired immune deficiency syndrome or acquired immunodeficiency syndrome (AIDS) is a set of symptoms and infections resulting from the damage to the human immune system caused by the human immunodeficiency virus (HIV).[1]

This condition progressively reduces the effectiveness of the immune system and leaves individuals susceptible to opportunistic infections and tumors. HIV is transmitted through direct contact of a mucous membrane or the bloodstream with a bodily fluid containing HIV, such as blood, semen, vaginal fluid, preseminal fluid, and breast milk.[2][3]

This transmission can involve anal, vaginal or oral sex, blood transfusion, contaminated hypodermic needles, exchange between mother and baby during pregnancy, childbirth, or breastfeeding, or other exposure to one of the above bodily fluids.

AIDS is now a pandemic.[4] In 2007, an estimated 33.2 million people lived with the disease worldwide, and it killed an estimated 2.1 million people, including 330,000 children.[5] Over three-quarters of these deaths occurred in sub-Saharan Africa,[5] retarding economic growth and destroying human capital.[6]

Most researchers believe that HIV originated in sub-Saharan Africa during the twentieth century.[7] AIDS was first recognized by the U.S. Centers for Disease Control and Prevention in 1981 and its cause, HIV, identified by American and French scientists in the early 1980s.[8]

Although treatments for AIDS and HIV can slow the course of the disease, there is currently no vaccine or cure. Antiretroviral treatment reduces both the mortality and the morbidity of HIV infection, but these drugs are expensive and routine access to antiretroviral medication is not available in all countries.[9] Due to the difficulty in treating HIV infection, preventing infection is a key aim in controlling the AIDS epidemic, with health organizations promoting safe sex and needle-exchange programmes in attempts to slow the spread of the virus.



Diagnosis[edit]

The diagnosis of AIDS in a person infected with HIV is based on the presence of certain signs or symptoms. Since June 5, 1981, many definitions have been developed for epidemiological surveillance such as the Bangui definition and the 1994 expanded World Health Organization AIDS case definition. However, clinical staging of patients was not an intended use for these systems as they are neither sensitive, nor specific. In developing countries, the World Health Organization staging system for HIV infection and disease, using clinical and laboratory data, is used and in developed countries, the Centers for Disease Control (CDC) Classification System is used.

WHO disease staging system[edit]

In 1990, the World Health Organization (WHO) grouped these infections and conditions together by introducing a staging system for patients infected with HIV-1.[10] An update took place in September 2005. Most of these conditions are opportunistic infections that are easily treatable in healthy people.

CDC classification system[edit]

There are two main definitions for AIDS, both produced by the Centers for Disease Control and Prevention (CDC). The older definition is to referring to AIDS using the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus.[11][12] In 1993, the CDC expanded their definition of AIDS to include all HIV positive people with a CD4+ T cell count below 200 per µL of blood or 14% of all lymphocytes.[13] The majority of new AIDS cases in developed countries use either this definition or the pre-1993 CDC definition. The AIDS diagnosis still stands even if, after treatment, the CD4+ T cell count rises to above 200 per µL of blood or other AIDS-defining illnesses are cured.

HIV test[edit]

Many people are unaware that they are infected with HIV.[14] Less than 1% of the sexually active urban population in Africa has been tested, and this proportion is even lower in rural populations. Furthermore, only 0.5% of pregnant women attending urban health facilities are counseled, tested or receive their test results. Again, this proportion is even lower in rural health facilities.[14] Therefore, donor blood and blood products used in medicine and medical research are screened for HIV.

HIV tests are usually performed on venous blood. Many laboratories use fourth generation screening tests which detect anti-HIV antibody (IgG and IgM) and the HIV p24 antigen. The detection of HIV antibody or antigen in a patient previously known to be negative is evidence of HIV infection. Individuals whose first specimen indicates evidence of HIV infection will have a repeat test on a second blood sample to confirm the results.

The window period (the time between initial infection and the development of detectable antibodies against the infection) can vary since it can take 3–6 months to seroconvert and to test positive. Detection of the virus using polymerase chain reaction (PCR) during the window period is possible, and evidence suggests that an infection may often be detected earlier than when using a fourth generation EIA screening test.

Positive results obtained by PCR are confirmed by antibody tests.[15] Routinely used HIV tests for infection in neonates, born to HIV-positive mothers, have no value because of the presence of maternal antibody to HIV in the child's blood. HIV infection can only be diagnosed by PCR, testing for HIV pro-viral DNA in the children's lymphocytes.[16]

Prevention[edit]

Estimated per act risk for acquisition
of HIV by exposure route[17]
Exposure Route Estimated infections
per 10,000 exposures
to an infected source
Blood Transfusion 9,000[18]
Childbirth 2,500[19]
Needle-sharing injection drug use 67[20]
Percutaneous needle stick 30[21]
Receptive anal intercourse* 50[22][23]
Insertive anal intercourse* 6.5[22][23]
Receptive penile-vaginal intercourse* 10[22][23][24]
Insertive penile-vaginal intercourse* 5[22][23]
Receptive oral intercourse 1[23]
Insertive oral intercourse 0.5[23]
* assuming no condom use
§ source refers to oral intercourse
performed on a man

The three main transmission routes of HIV are sexual contact, exposure to infected body fluids or tissues, and from mother to fetus or child during perinatal period. It is possible to find HIV in the saliva, tears, and urine of infected individuals, but there are no recorded cases of infection by these secretions, and the risk of infection is negligible.[25]

Sexual contact[edit]

The majority of HIV infections are acquired through unprotected sexual relations between partners, one of whom has HIV. The primary mode of HIV infection worldwide is through sexual contact between members of the opposite sex.[26][27][28]

During a sexual act, only male or female condoms can reduce the chances of infection with HIV and other STDs and the chances of becoming pregnant. The best evidence to date indicates that typical condom use reduces the risk of heterosexual HIV transmission by approximately 80% over the long-term, though the benefit is likely to be higher if condoms are used correctly on every occasion.[29]

The male latex condom, if used correctly without oil-based lubricants, is the single most effective available technology to reduce the sexual transmission of HIV and other sexually transmitted infections. Manufacturers recommend that oil-based lubricants such as petroleum jelly, butter, and lard not be used with latex condoms, because they dissolve the latex, making the condoms porous. If necessary, manufacturers recommend using water-based lubricants.

Oil-based lubricants can however be used with polyurethane condoms.[30]

The female condom is an alternative to the male condom and is made from polyurethane, which allows it to be used in the presence of oil-based lubricants. They are larger than male condoms and have a stiffened ring-shaped opening, and are designed to be inserted into the vagina.

The female condom contains an inner ring, which keeps the condom in place inside the vagina – inserting the female condom requires squeezing this ring. However, at present availability of female condoms is very low and the price remains prohibitive for many women.

Preliminary studies suggest that, where female condoms are available, overall protected sexual acts increase relative to unprotected sexual acts, making them an important HIV prevention strategy.[31]

Studies on couples where one partner is infected show that with consistent condom use, HIV infection rates for the uninfected partner are below 1% per year.[32] Prevention strategies are well-known in developed countries, but epidemiological and behavioral studies in Europe and North America suggest that a substantial minority of young people continue to engage in high-risk practices despite HIV/AIDS knowledge, underestimating their own risk of becoming infected with HIV.[33][34]

Randomized controlled trials have shown that male circumcision lowers the risk of HIV infection among heterosexual men by up to 60%.[35] It is expected that this procedure will be actively promoted in many of the countries affected by HIV, although doing so will involve confronting a number of practical, cultural and attitudinal issues.

Some experts fear that a lower perception of vulnerability among circumcised men may result in more sexual risk-taking behavior, thus negating its preventive effects.[36] However, one randomized controlled trial indicated that adult male circumcision was not associated with increased HIV risk behavior.[37]

Exposure to infected body fluids[edit]

Health care workers can reduce exposure to HIV by employing precautions to reduce the risk of exposure to contaminated blood. These precautions include barriers such as gloves, masks, protective eyeware or shields, and gowns or aprons which prevent exposure of the skin or mucous membranes to blood borne pathogens. Frequent and thorough washing of the skin immediately after being contaminated with blood or other bodily fluids can reduce the chance of infection. Finally, sharp objects like needles, scalpels and glass, are carefully disposed of to prevent needlestick injuries with contaminated items.[38] Since intravenous drug use is an important factor in HIV transmission in developed countries, harm reduction strategies such as needle-exchange programmes are used in attempts to reduce the infections caused by drug abuse.[39][40]

Mother-to-child transmission (MTCT)[edit]

Current recommendations state that when replacement feeding is acceptable, feasible, affordable, sustainable and safe, HIV-infected mothers should avoid breast-feeding their infant. However, if this is not the case, exclusive breast-feeding is recommended during the first months of life and discontinued as soon as possible.[41]

Treatment[edit]

See also HIV Treatment and Antiretroviral drug.
Abacavir – a nucleoside analog reverse transcriptase inhibitor (NARTI or NRTI)

There is currently no vaccine or cure for HIV or AIDS. The only known methods of prevention are based on avoiding exposure to the virus or, failing that, an antiretroviral treatment directly after a highly significant exposure, called post-exposure prophylaxis (PEP).[42] PEP has a very demanding four week schedule of dosage. It also has very unpleasant side effects including diarrhea, malaise, nausea and fatigue.[43]

Antiviral therapy[edit]

Current treatment for HIV infection consists of highly active antiretroviral therapy, or HAART.[44] This has been highly beneficial to many HIV-infected individuals since its introduction in 1996 when the protease inhibitor-based HAART initially became available.[9] Current optimal HAART options consist of combinations (or "cocktails") consisting of at least three drugs belonging to at least two types, or "classes," of antiretroviral agents. Typical regimens consist of two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). Because HIV disease progression in children is more rapid than in adults, and laboratory parameters are less predictive of risk for disease progression, particularly for young infants, treatment recommendations are more aggressive for children than for adults.[45] In developed countries where HAART is available, doctors assess the viral load, rapidity in CD4 decline, and patient readiness while deciding when to recommend initiating treatment.[46]

Standard goals of HAART include improvement in the patient’s quality of life, reduction in complications, and reduction of HIV viremia below the limit of detection, but it does not cure the patient of HIV nor does it prevent the return, once treatment is stopped, of high blood levels of HIV, often HAART resistant.[47][48] Moreover, it would take more than the lifetime of an individual to be cleared of HIV infection using HAART.[49] Despite this, many HIV-infected individuals have experienced remarkable improvements in their general health and quality of life, which has led to the plummeting of HIV-associated morbidity and mortality.[50][51][52] In the absence of HAART, progression from HIV infection to AIDS occurs at a median of between nine to ten years and the median survival time after developing AIDS is only 9.2 months.[53] HAART is thought to increase survival time by between 4 and 12 years.[54][55]

For some patients, which can be more than fifty percent of patients, HAART achieves far less than optimal results, due to medication intolerance/side effects, prior ineffective antiretroviral therapy and infection with a drug-resistant strain of HIV. Non-adherence and non-persistence with therapy are the major reasons why some people do not benefit from HAART.[56] The reasons for non-adherence and non-persistence are varied. Major psychosocial issues include poor access to medical care, inadequate social supports, psychiatric disease and drug abuse. HAART regimens can also be complex and thus hard to follow, with large numbers of pills taken frequently.[57][58][59] Side effects can also deter people from persisting with HAART, these include lipodystrophy, dyslipidaemia, diarrhoea, insulin resistance, an increase in cardiovascular risks and birth defects.[60] Anti-retroviral drugs are expensive, and the majority of the world's infected individuals do not have access to medications and treatments for HIV and AIDS.

Experimental and proposed treatments[edit]

It has been postulated that only a vaccine can halt the pandemic because a vaccine would possibly cost less, thus being affordable for developing countries, and would not require daily treatments. However, even after almost 30 years of research, HIV-1 remains a difficult target for a vaccine.[61]

Research to improve current treatments includes decreasing side effects of current drugs, further simplifying drug regimens to improve adherence, and determining the best sequence of regimens to manage drug resistance. A number of studies have shown that measures to prevent opportunistic infections can be beneficial when treating patients with HIV infection or AIDS. Vaccination against hepatitis A and B is advised for patients who are not infected with these viruses and are at risk of becoming infected.[62] Patients with substantial immunosuppression are also advised to receive prophylactic therapy for Pneumocystis jiroveci pneumonia (PCP), and many patients may benefit from prophylactic therapy for toxoplasmosis and Cryptococcus meningitis as well.[43]

Researchers have discovered an abzyme that can destroy the protein gp120 CD4 binding site. This protein is common to all HIV variants as it is the attachment point for B lymphocytes and subsequent compromising of the immune system.[63]

In Berlin, Germany, a 42-year-old leukemia patient infected with HIV for more than a decade was given an experimental transplant of bone marrow with cells that contained an unusual natural variant of the CCR5 cell-surface receptor. This CCR5-Δ32 variant has been shown to make some cells from people who are born with it resistant to infection with some strains of HIV. Almost two years after the transplant, and even after the patient reportedly stopped taking antiretroviral medications, HIV has not been detected in the patient's blood. [64]

Alternative medicine[edit]

Various forms of alternative medicine have been used to treat symptoms or alter the course of the disease.[65] Acupuncture has been used to alleviate some symptoms, such peripheral neuropathy, but cannot cure the HIV infection.[66] Several randomized clinical trials testing the effect of herbal medicines have shown that there is no evidence that these herbs have any effect on the progression of the disease, but may instead produce serious side-effects.[67]

Some data suggest that multivitamin and mineral supplements might reduce HIV disease progression in adults, although there is no conclusive evidence on if they reduce mortality among people with good nutritional status.[68] Vitamin A supplementation in children probably has some benefit.[68] Daily doses of selenium can suppress HIV viral burden with an associated improvement of the CD4 count. Selenium can be used as an adjunct therapy to standard antiviral treatments, but cannot itself reduce mortality and morbidity.[69]

Current studies indicate that that alternative medicine therapies have little effect on the mortality or morbidity of the disease, but may improve the quality of life of individuals afflicted with AIDS. The psychological benefits of these therapies are the most important use.[65]




Notes and references[edit]

  1. ^ Weiss RA (May 1993). "How does HIV cause AIDS?". Science (Journal). 260 (5112): 1273–9. doi:10.1126/science.8493571. PMID 8493571.{{cite journal}}: CS1 maint: date and year (link)
  2. ^ Divisions of HIV/AIDS Prevention (2003). "HIV and Its Transmission". Centers for Disease Control & Prevention. Retrieved 2006-05-23.
  3. ^ San Francisco AIDS Foundation (2006-04-14). "How HIV is spread". Retrieved 2006-05-23. {{cite web}}: Check date values in: |date= (help)
  4. ^ Cite error: The named reference Kallings was invoked but never defined (see the help page).
  5. ^ a b Cite error: The named reference UNAIDS2007 was invoked but never defined (see the help page).
  6. ^ Cite error: The named reference Bell-et-al-2003 was invoked but never defined (see the help page).
  7. ^ Gao F, Bailes E, Robertson DL; et al. (1999). "Origin of HIV-1 in the Chimpanzee Pan troglodytes troglodytes". Nature. 397 (6718): 436–441. doi:10.1038/17130. PMID 9989410. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  8. ^ Gallo RC (2006). "A reflection on HIV/AIDS research after 25 years". Retrovirology. 3: 72. doi:10.1186/1742-4690-3-72. PMC 1629027. PMID 17054781.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  9. ^ a b Palella FJ Jr, Delaney KM, Moorman AC; et al. (1998). "Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. HIV Outpatient Study Investigators". N. Engl. J. Med. 338 (13): 853–860. doi:10.1056/NEJM199803263381301. PMID 9516219. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  10. ^ World Health Organization (1990). "Interim proposal for a WHO staging system for HIV infection and disease". WHO Wkly Epidem. Rec. 65 (29): 221–228. PMID 1974812.
  11. ^ Centers for Disease Control (CDC) (1982). "Persistent, generalized lymphadenopathy among homosexual males". MMWR Morb Mortal Wkly Rep. 31 (19): 249–251. PMID 6808340.
  12. ^ Barré-Sinoussi F, Chermann JC, Rey F; et al. (1983). "Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS)". Science. 220 (4599): 868–871. doi:10.1126/science.6189183. PMID 6189183. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  13. ^ "1993 Revised Classification System for HIV Infection and Expanded Surveillance Case Definition for AIDS Among Adolescents and Adults". CDC. 1992. Retrieved 2006-02-09.
  14. ^ a b Kumaranayake L, Watts C (2001). "Resource allocation and priority setting of HIV/AIDS interventions: addressing the generalized epidemic in sub-Saharan Africa". J. Int. Dev. 13 (4): 451–466. doi:10.1002/jid.798.
  15. ^ Weber B (2006). "Screening of HIV infection: role of molecular and immunological assays". Expert Rev. Mol. Diagn. 6 (3): 399–411. doi:10.1586/14737159.6.3.399. PMID 16706742.
  16. ^ Tóth FD, Bácsi A, Beck Z, Szabó J (2001). "Vertical transmission of human immunodeficiency virus". Acta Microbiol Immunol Hung. 48 (3–4): 413–27. doi:10.1556/AMicr.48.2001.3-4.10. PMID 11791341.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  17. ^ Smith DK, Grohskopf LA, Black RJ; et al. (2005). "Antiretroviral Postexposure Prophylaxis After Sexual, Injection-Drug Use, or Other Nonoccupational Exposure to HIV in the United States". MMWR. 54 (RR02): 1–20. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  18. ^ Donegan E, Stuart M, Niland JC; et al. (1990). "Infection with human immunodeficiency virus type 1 (HIV-1) among recipients of antibody-positive blood donations". Ann. Intern. Med. 113 (10): 733–739. doi:10.7326/0003-4819-113-10-733. PMID 2240875. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  19. ^ Coovadia H (2004). "Antiretroviral agents—how best to protect infants from HIV and save their mothers from AIDS". N. Engl. J. Med. 351 (3): 289–292. doi:10.1056/NEJMe048128. PMID 15247337.
  20. ^ Kaplan EH, Heimer R (1995). "HIV incidence among New Haven needle exchange participants: updated estimates from syringe tracking and testing data". J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. 10 (2): 175–176. doi:10.1097/00042560-199510020-00010. PMID 7552482.
  21. ^ Bell DM (1997). "Occupational risk of human immunodeficiency virus infection in healthcare workers: an overview". Am. J. Med. 102 (5B): 9–15. doi:10.1016/s0002-9343(97)89441-7. PMID 9845490.
  22. ^ a b c d European Study Group on Heterosexual Transmission of HIV (1992). "Comparison of female to male and male to female transmission of HIV in 563 stable couples". BMJ. 304 (6830): 809–813. doi:10.1136/bmj.304.6830.809. PMC 1881672. PMID 1392708.
  23. ^ a b c d e f Varghese B, Maher JE, Peterman TA, Branson BM,Steketee RW (2002). "Reducing the risk of sexual HIV transmission: quantifying the per-act risk for HIV on the basis of choice of partner, sex act, and condom use". Sex. Transm. Dis. 29 (1): 38–43. doi:10.1097/00007435-200201000-00007. PMID 11773877.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  24. ^ Leynaert B, Downs AM, de Vincenzi I (1998). "Heterosexual transmission of human immunodeficiency virus: variability of infectivity throughout the course of infection. European Study Group on Heterosexual Transmission of HIV". Am. J. Epidemiol. 148 (1): 88–96. doi:10.1093/oxfordjournals.aje.a009564. PMID 9663408.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. ^ "Facts about AIDS & HIV". avert.org. Retrieved 2007-11-30.
  26. ^ Johnson AM, Laga M (1988). "Heterosexual transmission of HIV". AIDS. 2 (suppl. 1): S49–S56. doi:10.1136/bmj.296.6628.1017. PMC 2545554. PMID 3130121.
  27. ^ N'Galy B, Ryder RW (1988). "Epidemiology of HIV infection in Africa". Journal of Acquired Immune Deficiency Syndromes. 1 (6): 551–558. PMID 3225742.
  28. ^ Deschamps MM, Pape JW, Hafner A, Johnson WD Jr. (1996). "Heterosexual transmission of HIV in Haiti". Annals of Internal Medicine. 125 (4): 324–330. doi:10.7326/0003-4819-125-4-199608150-00011. PMID 8678397.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  29. ^ Cayley WE Jr. (2004). "Effectiveness of condoms in reducing heterosexual transmission of HIV". Am. Fam. Physician. 70 (7): 1268–1269. PMID 15508535.
  30. ^ "Module 5/Guidelines for Educators" (Microsoft Word). Durex. Retrieved 2006-04-17.
  31. ^ PATH (2006). "The female condom: significant potential for STI and pregnancy prevention". Outlook. 22 (2).
  32. ^ "Condom Facts and Figures". WHO. August 2003. Retrieved 2006-01-17.{{cite web}}: CS1 maint: date and year (link)
  33. ^ Patel VL, Yoskowitz NA, Kaufman DR, Shortliffe EH (2008). "Discerning patterns of human immunodeficiency virus risk in healthy young adults". Am J Med. 121 (4): 758–764. doi:10.1016/j.amjmed.2008.04.022. PMC 2597652. PMID 18724961.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  34. ^ Dias SF, Matos MG, Goncalves, A. C. (2005). "Preventing HIV transmission in adolescents: an analysis of the Portuguese data from the Health Behaviour School-aged Children study and focus groups". Eur. J. Public Health. 15 (3): 300–304. doi:10.1093/eurpub/cki085. PMID 15941747.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  35. ^ Weiss HA (February 2007). "Male circumcision as a preventive measure against HIV and other sexually transmitted diseases". Curr. Opin. Infect. Dis. 20 (1): 66–72. doi:10.1097/QCO.0b013e328011ab73. PMID 17197884.{{cite journal}}: CS1 maint: date and year (link)
  36. ^ Eaton LA, Kalichman S (December 2007). "Risk compensation in HIV prevention: implications for vaccines, microbicides, and other biomedical HIV prevention technologies". Curr HIV/AIDS Rep. 4 (4): 165–72. doi:10.1007/s11904-007-0024-7. PMC 2937204. PMID 18366947.{{cite journal}}: CS1 maint: date and year (link)
  37. ^ Mattson, C. L.; Campbell, R. T.; Bailey, R. C.; Agot, K.; Ndinya-Achola, J. O.; Moses, S. (2008). "Risk compensation is not associated with male circumcision in Kisumu, Kenya: a multi-faceted assessment of men enrolled in a randomized controlled trial". PLOS ONE. 3 (6): e2443. doi:10.1371/journal.pone.0002443. PMC 2409966. PMID 18560581. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: date and year (link)
  38. ^ "Recommendations for Prevention of HIV Transmission in Health-Care Settings". Retrieved 2008-04-28.
  39. ^ Kerr T, Kimber J, Debeck K, Wood E (December 2007). "The role of safer injection facilities in the response to HIV/AIDS among injection drug users". Curr HIV/AIDS Rep. 4 (4): 158–64. doi:10.1007/s11904-007-0023-8. PMID 18366946.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  40. ^ Wodak A, Cooney A (2006). "Do needle syringe programs reduce HIV infection among injecting drug users: a comprehensive review of the international evidence". Subst Use Misuse. 41 (6–7): 777–813. doi:10.1080/10826080600669579. PMID 16809167.
  41. ^ WHO HIV and Infant Feeding Technical Consultation (2006). "Consensus statement" (PDF). Retrieved 2008-03-12.
  42. ^ Hamlyn E, Easterbrook P (August 2007). "Occupational exposure to HIV and the use of post-exposure prophylaxis". Occup Med (Lond). 57 (5): 329–36. doi:10.1093/occmed/kqm046. PMID 17656498.{{cite journal}}: CS1 maint: date and year (link)
  43. ^ a b "A Pocket Guide to Adult HIV/AIDS Treatment February 2006 edition". Department of Health and Human Services. February 2006. Retrieved 2006-09-01.{{cite web}}: CS1 maint: date and year (link) Cite error: The named reference "PEPpocketguide" was defined multiple times with different content (see the help page).
  44. ^ "A Pocket Guide to Adult HIV/AIDS Treatment February 2006 edition". Department of Health and Human Services. February 2006. Retrieved 2006-09-01.{{cite web}}: CS1 maint: date and year (link)
  45. ^ "Guidelines for the Use of Antiretroviral Agents in Pediatric HIV Infection" (PDF). Department of Health and Human Services Working Group on Antiretroviral Therapy and Medical Management of HIV-Infected Children. 2005-11-03. Retrieved 2006-01-17.
  46. ^ "Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents" (PDF). Department of Health and Human Services Panel on Clinical Practices for Treatment of HIV Infection. 2005-10-06. Retrieved 2006-01-17.
  47. ^ Martinez-Picado J, DePasquale MP, Kartsonis N; et al. (2000). "Antiretroviral resistance during successful therapy of human immunodeficiency virus type 1 infection". Proc. Natl. Acad. Sci. U. S. A. 97 (20): 10948–10953. doi:10.1073/pnas.97.20.10948. PMC 27129. PMID 11005867. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  48. ^ Dybul M, Fauci AS, Bartlett JG, Kaplan JE, Pau AK; Panel on Clinical Practices for Treatment of HIV. (2002). "Guidelines for using antiretroviral agents among HIV-infected adults and adolescents". Ann. Intern. Med. 137 (5 Pt 2): 381–433. doi:10.7326/0003-4819-137-5_part_2-200209031-00001. PMID 12617573.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  49. ^ Blankson JN, Persaud D, Siliciano RF (2002). "The challenge of viral reservoirs in HIV-1 infection". Annu. Rev. Med. 53: 557–593. doi:10.1146/annurev.med.53.082901.104024. PMID 11818490.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  50. ^ Palella FJ, Delaney KM, Moorman AC, Loveless MO, Fuhrer J, Satten GA, Aschman DJ, Holmberg SD (1998). "Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection". N. Engl. J. Med. 338 (13): 853–860. doi:10.1056/NEJM199803263381301. PMID 9516219.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  51. ^ Wood E, Hogg RS, Yip B, Harrigan PR, O'Shaughnessy MV, Montaner JS (2003). "Is there a baseline CD4 cell count that precludes a survival response to modern antiretroviral therapy?". AIDS. 17 (5): 711–720. doi:10.1097/00002030-200303280-00009. PMID 12646794.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  52. ^ Chene G, Sterne JA, May M, Costagliola D, Ledergerber B, Phillips AN, Dabis F, Lundgren J, D'Arminio Monforte A, de Wolf F, Hogg R, Reiss P, Justice A, Leport C, Staszewski S, Gill J, Fatkenheuer G, Egger ME and the Antiretroviral Therapy Cohort Collaboration (2003). "Prognostic importance of initial response in HIV-1 infected patients starting potent antiretroviral therapy: analysis of prospective studies". Lancet. 362 (9385): 679–686. doi:10.1016/S0140-6736(03)14229-8. PMID 12957089.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  53. ^ Cite error: The named reference Morgan2 was invoked but never defined (see the help page).
  54. ^ King JT, Justice AC, Roberts MS, Chang CH, Fusco JS and the CHORUS Program Team (2003). "Long-Term HIV/AIDS Survival Estimation in the Highly Active Antiretroviral Therapy Era". Medical Decision Making. 23 (1): 9–20. doi:10.1177/0272989X02239652. PMID 12583451.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  55. ^ Tassie JM, Grabar S, Lancar R, Deloumeaux J, Bentata M, Costagliola D and the Clinical Epidemiology Group from the French Hospital Database on HIV (2002). "Time to AIDS from 1992 to 1999 in HIV-1-infected subjects with known date of infection". Journal of Acquired Immune Deficiency Syndromes. 30 (1): 81–7. doi:10.1097/00042560-200205010-00011. PMID 12048367.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  56. ^ Becker SL, Dezii CM, Burtcel B, Kawabata H, Hodder S. (2002). "Young HIV-infected adults are at greater risk for medication nonadherence". MedGenMed. 4 (3): 21. PMID 12466764.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  57. ^ Nieuwkerk P, Sprangers M, Burger D, Hoetelmans RM, Hugen PW, Danner SA, van Der Ende ME, Schneider MM, Schrey G, Meenhorst PL, Sprenger HG, Kauffmann RH, Jambroes M, Chesney MA, de Wolf F, Lange JM and the ATHENA Project (2001). "Limited Patient Adherence to Highly Active Antiretroviral Therapy for HIV-1 Infection in an Observational Cohort Study". Arch. Intern. Med. 161 (16): 1962–1968. doi:10.1001/archinte.161.16.1962. PMID 11525698.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  58. ^ Kleeberger C, Phair J, Strathdee S, Detels R, Kingsley L, Jacobson LP (2001). "Determinants of Heterogeneous Adherence to HIV-Antiretroviral Therapies in the Multicenter AIDS Cohort Study". J. Acquir. Immune Defic. Syndr. 26 (1): 82–92. doi:10.1097/00126334-200101010-00012. PMID 11176272.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  59. ^ Heath KV, Singer J, O'Shaughnessy MV, Montaner JS, Hogg RS (2002). "Intentional Nonadherence Due to Adverse Symptoms Associated With Antiretroviral Therapy". J. Acquir. Immune Defic. Syndr. 31 (2): 211–217. doi:10.1097/00126334-200210010-00012. PMID 12394800.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  60. ^ Burgoyne RW, Tan DH (March 2008). "Prolongation and quality of life for HIV-infected adults treated with highly active antiretroviral therapy (HAART): a balancing act". J. Antimicrob. Chemother. 61 (3): 469–73. doi:10.1093/jac/dkm499. PMID 18174196.{{cite journal}}: CS1 maint: date and year (link)
  61. ^ Karlsson Hedestam GB, Fouchier RA, Phogat S, Burton DR, Sodroski J, Wyatt RT (February 2008). "The challenges of eliciting neutralizing antibodies to HIV-1 and to influenza virus". Nat. Rev. Microbiol. 6 (2): 143–55. doi:10.1038/nrmicro1819. PMID 18197170.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  62. ^ Laurence J (2006). "Hepatitis A and B virus immunization in HIV-infected persons". AIDS Reader. 16 (1): 15–17. PMID 16433468.
  63. ^ Planque S, Nishiyama Y, Taguchi H, Salas M, Hanson C, Paul S (June 2008). "Catalytic antibodies to HIV: Physiological role and potential clinical utility". Autoimmun Rev. 7 (6): 473–9. doi:10.1016/j.autrev.2008.04.002. PMC 2527403. PMID 18558365.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  64. ^ "A Doctor, a Mutation and a Potential Cure for AIDS: A Bone Marrow Transplant to Treat a Leukemia Patient Also Gives Him Virus-Resistant Cells; Many Thanks, Sample 61". Wall Street Journal. November 2008. Retrieved 2008-11-12.{{cite news}}: CS1 maint: date and year (link)
  65. ^ a b Power R, Gore-Felton C, Vosvick M, Israelski DM, Spiegel D (June 2002). "HIV: effectiveness of complementary and alternative medicine". Prim. Care. 29 (2): 361–78. doi:10.1016/s0095-4543(01)00013-6. PMID 12391716.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  66. ^ Nicholas PK, Kemppainen JK, Canaval GE; et al. (February 2007). "Symptom management and self-care for peripheral neuropathy in HIV/AIDS". AIDS Care. 19 (2): 179–89. doi:10.1080/09540120600971083. PMID 17364396. Retrieved 2008-04-28. {{cite journal}}: Explicit use of et al. in: |author= (help); Text "1B69BA326FFE69C3F0A8F227DF8201D0" ignored (help)CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  67. ^ Liu JP, Manheimer E, Yang M (2005). "Herbal medicines for treating HIV infection and AIDS". Cochrane Database Syst Rev. 2010 (3): CD003937. doi:10.1002/14651858.CD003937.pub2. PMC 8759069. PMID 16034917.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  68. ^ a b Irlam JH, Visser ME, Rollins N, Siegfried N (2005). Irlam, James JH (ed.). "Micronutrient supplementation in children and adults with HIV infection". Cochrane Database Syst Rev (4): CD003650. doi:10.1002/14651858.CD003650.pub2. PMID 16235333.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  69. ^ Hurwitz BE, Klaus JR, Llabre MM; et al. (January 2007). "Suppression of human immunodeficiency virus type 1 viral load with selenium supplementation: a randomized controlled trial". Arch. Intern. Med. 167 (2): 148–54. doi:10.1001/archinte.167.2.148. PMID 17242315. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)

Further reading[edit]

External links[edit]