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Misconceptions about HIV/AIDS
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===HIV is not the cause of AIDS=== {{Main|AIDS denialism}} There is broad [[scientific consensus]] that HIV is the cause of AIDS, but some individuals reject this consensus, including biologist [[Peter Duesberg]], biochemist [[David Rasnick]], journalist/activist [[Celia Farber]], conservative writer [[Tom Bethell]], and [[intelligent design]] advocate [[Phillip E. Johnson]]. (Some one-time skeptics have since rejected AIDS denialism, including physiologist [[Robert Root-Bernstein]], and physician and AIDS researcher [[Joseph Sonnabend]].){{cn|date=January 2021}} A great deal is known about the [[pathogenesis]] of HIV disease, even though important details remain to be elucidated. However, a complete understanding of the pathogenesis of a disease is not a prerequisite to knowing its cause. Most infectious agents have been associated with the disease they cause long before their pathogenic mechanisms have been discovered. Because research in pathogenesis is difficult when precise animal models are unavailable, the disease-causing mechanisms in many diseases, including [[tuberculosis]] and [[hepatitis B]], are poorly understood, but the pathogens responsible are very well established.<ref name="NIAID, 1994-2003">{{cite web |url=https://www.niaid.nih.gov/topics/HIVAIDS/Understanding/howHIVCausesAIDS/Pages/HIVcausesAIDS.aspx |title=The Evidence that HIV Causes AIDS |date=4 September 2009|publisher=[[National Institute of Allergy and Infectious Disease]] |access-date=29 May 2015}}</ref> ====AZT and other antiretroviral drugs, not HIV, cause AIDS==== {{Main|Duesberg hypothesis}} The vast majority of people with AIDS never received antiretroviral drugs, including those in developed countries prior to the licensure of [[Zidovudine|AZT]] in 1987. Even today, very few individuals in developing countries have access to these medications.<ref name="UNAIDS, 2003">[http://www.unaids.org/html/pub/publications/fact-sheets04/fs_treatment_en_pdf.pdf UNAIDS, 2003] {{webarchive|url=https://web.archive.org/web/20070614103019/http://www.unaids.org/html/pub/publications/fact-sheets04/fs_treatment_en_pdf.pdf |date=2007-06-14 }}</ref> In the 1980s, [[clinical trial]]s enrolling patients with AIDS found that AZT given as single-drug therapy conferred a survival advantage compared to [[placebo]], albeit modest and short-lived. Among HIV-infected patients who had not yet developed AIDS, placebo-controlled trials found that AZT given as a single-drug therapy delayed, for a year or two, the onset of AIDS-related illnesses. The lack of excess AIDS cases and death in the AZT arms of these placebo-controlled trials effectively counters the argument that AZT causes AIDS.<ref name="NIAID, 1995"/> Subsequent clinical trials found that patients receiving two-drug combinations had up to 50% increases in time to progression to AIDS and in survival when compared to people receiving single-drug therapy. In more recent years, three-drug combination therapies have produced another 50–80% improvements in progression to AIDS and in survival when compared to two-drug regimens in clinical trials.<ref name="HHS, 2005">{{Cite web |url=http://www.hivatis.org/guidelines/adult/AA_040705.pdf |title=HHS, 2005 |access-date=2005-08-23 |archive-url=https://web.archive.org/web/20171004135919/http://www.hivatis.org/guidelines/adult/AA_040705.pdf |archive-date=2017-10-04 |url-status=dead }}</ref> Use of potent anti-HIV combination therapies has contributed to dramatic reductions in the incidence of AIDS and AIDS-related deaths in populations where these drugs are widely available, an effect which would be unlikely if antiretroviral drugs ''caused'' AIDS.<ref name="Palella, 1998">{{cite journal | doi = 10.1056/NEJM199803263381301 | last1 = Palella | first1 = F.J. Jr | last2 = Delaney | first2 = K.M. | last3 = Moorman | first3 = A.C. | last4 = Loveless | first4 = M.O. | last5 = Fuhrer | first5 = J. | last6 = Satten | first6 = G.A. | last7 = Aschman | first7 = D.J. | last8 = Holmberg | first8 = S.D. | year = 1998 | title = Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. HIV Outpatient Study Investigators | journal = N. Engl. J. Med. | volume = 338 | issue = 13| pages = 853–60 | pmid = 9516219 | doi-access = free }}</ref><ref name="Mocroft, 1998">{{cite journal | doi = 10.1016/S0140-6736(98)03201-2 | last1 = Mocroft | first1 = A. | last2 = Vella | first2 = S. | last3 = Benfield | first3 = T.L. | last4 = Chiesi | first4 = A. | last5 = Miller | first5 = V. | last6 = Gargalianos | first6 = P. | last7 = Arminio Monforte | first7 = A. | last8 = Yust | first8 = I. | last9 = Bruun | first9 = J.N. | last10 = Phillips | first10 = AN | last11 = Lundgren | first11 = JD | year = 1998 | title = Changing patterns of mortality across Europe in patients infected with HIV-1. EuroSIDA Study Group | journal = Lancet | volume = 352 | issue = 9142| pages = 1725–30 | pmid = 9848347 | s2cid = 32223916 | display-authors = 9 }}</ref><ref name="Mocroft, 2000">{{cite journal | doi = 10.1016/S0140-6736(00)02504-6 | last1 = Mocroft | first1 = A. | last2 = Katlama | first2 = C. | last3 = Johnson | first3 = A.M. | last4 = Pradier | first4 = C. | last5 = Antunes | first5 = F. | last6 = Mulcahy | first6 = F. | last7 = Chiesi | first7 = A. | last8 = Phillips | first8 = A.N. | last9 = Kirk | first9 = O. | last10 = Lundgren | first10 = JD | year = 2000 | title = AIDS across Europe, 1994–98: the EuroSIDA study | journal = Lancet | volume = 356 | issue = 9226| pages = 291–96 | pmid = 11071184 | s2cid = 8167162 | display-authors = 9 }}</ref><ref name="Vittinghoff, 1999">{{cite journal | doi = 10.1086/314623 | last1 = Vittinghoff | first1 = E. | last2 = Scheer | first2 = S. | last3 = O'Malley | first3 = P. | last4 = Colfax | first4 = G. | last5 = Holmberg | first5 = S.D. | last6 = Buchbinder | first6 = S.P. | year = 1999 | title = Combination antiretroviral therapy and recent declines in AIDS incidence and mortality | journal = J. Infect. Dis. | volume = 179 | issue = 3| pages = 717–20 | pmid = 9952385 | doi-access = free }}</ref><ref name="Detels, 1998">{{cite journal | doi = 10.1001/jama.280.17.1497 | last1 = Detels | first1 = R. | last2 = Munoz | first2 = A. | last3 = McFarlane | first3 = G. | last4 = Kingsley | first4 = L.A. | last5 = Margolick | first5 = J.B. | last6 = Giorgi | first6 = J. | last7 = Schrager | first7 = L.K. | last8 = Phair | first8 = J.P. | year = 1998 | title = Effectiveness of potent antiretroviral therapy on time to AIDS and death in men with known HIV infection duration. Multicenter AIDS Cohort Study Investigators | journal = JAMA | volume = 280 | issue = 17| pages = 1497–503 | pmid = 9809730 | doi-access = free }}</ref><ref name="de Martino, 2000">{{cite journal | last1 = De Martino | first1 = M | last2 = Tovo | first2 = PA | last3 = Balducci | first3 = M | last4 = Galli | first4 = L | last5 = Gabiano | first5 = C | last6 = Rezza | first6 = G | last7 = Pezzotti | first7 = P | title = Reduction in mortality with availability of antiretroviral therapy for children with perinatal HIV-1 infection. Italian Register for HIV Infection in Children and the Italian National AIDS Registry | journal = JAMA | volume = 284 | issue = 2 | pages = 190–97 | year = 2000 | pmid = 10889592 | doi=10.1001/jama.284.2.190| doi-access = free }}</ref><ref name="Hogg, 1999">{{cite journal | last1 = Hogg | first1 = R.S. | last2 = Yip | first2 = B. | last3 = Kully | first3 = C. | last4 = Craib | first4 = K.J. | last5 = O'Shaughnessy | first5 = M.V. | last6 = Schechter | first6 = M.T. | last7 = Montaner | first7 = J.S. | year = 1999 | title = Improved survival among HIV-infected patients after initiation of triple-drug antiretroviral regimens | journal = CMAJ | volume = 160 | issue = 5| pages = 659–65 | pmid = 10102000 | pmc = 1230111 }}</ref><ref name="Schwarcz, 2000">{{cite journal | doi = 10.1093/aje/152.2.178 | last1 = Schwarcz | first1 = S.K. | last2 = Hsu | first2 = L.C. | last3 = Vittinghoff | first3 = E. | last4 = Katz | first4 = M.H. | year = 2000 | title = Impact of protease inhibitors and other antiretroviral treatments on acquired immunodeficiency syndrome survival in San Francisco, California, 1987–1996 | journal = Am. J. Epidemiol. | volume = 152 | issue = 2| pages = 178–85 | pmid = 10909955 | doi-access = free }}</ref><ref name="Kaplan, 2000">{{cite journal | last1 = Kaplan | first1 = JE | last2 = Hanson | first2 = D | last3 = Dworkin | first3 = MS | last4 = Frederick | first4 = T | last5 = Bertolli | first5 = J | last6 = Lindegren | first6 = ML | last7 = Holmberg | first7 = S | last8 = Jones | first8 = JL | title = Epidemiology of human immunodeficiency virus-associated opportunistic infections in the United States in the era of highly active antiretroviral therapy | journal = Clinical Infectious Diseases | volume = 30 | pages = S5–S14 | year = 2000 | issue = Suppl 1 | pmid = 10770911 | doi = 10.1086/313843 | doi-access = free }}</ref><ref name="McNaghten, 1999">{{cite journal | doi = 10.1097/00002030-199909100-00012 | last1 = McNaghten | first1 = A.D. | last2 = Hanson | first2 = D.L. | last3 = Jones | first3 = J.L. | last4 = Dworkin | first4 = M.S. | last5 = Ward | first5 = J.W. | last6 = The Adultadolescent Spectrum Of Disease Group +/ | year = 1999 | title = Effects of antiretroviral therapy and opportunistic illness primary chemoprophylaxis on survival after AIDS diagnosis. Adult/Adolescent Spectrum of Disease Group | journal = AIDS | volume = 13 | issue = 13| pages = 1687–95 | pmid = 10509570 | doi-access = free }}</ref>{{citation overkill|date=January 2021}} ====Behavioral factors such as recreational drug use and multiple sexual partners—not HIV—account for AIDS==== The proposed behavioral causes of AIDS, such as multiple sexual partners and long-term [[recreational drug use]], have existed for many years. The epidemic of AIDS, characterized by the occurrence of formerly rare opportunistic infections such as ''[[Pneumocystis carinii]]'' pneumonia (PCP), did not occur in the United States until a previously unknown human [[retrovirus]]—HIV—spread through certain communities.<ref>{{Cite web |url=https://www.niaid.nih.gov/publications/hivaids/21.htm |title=NIAID }}</ref> Compelling evidence against the hypothesis that behavioral factors cause AIDS comes from recent studies that have followed cohorts of [[homosexual]] men for long periods of time and found that only HIV-seropositive men develop AIDS. For example, in a prospectively studied cohort in [[Vancouver, British Columbia]], 715 homosexual men were followed for a median of 8.6 years. Among 365 HIV-positive individuals, 136 developed AIDS. No AIDS-defining illnesses occurred among 350 seronegative men, despite the fact that these men reported appreciable use of [[nitrite inhalants]] ("poppers") and other recreational drugs, and frequent receptive [[anal intercourse]] (Schechter et al., 1993).<ref name="Schechter, 1993">{{cite journal | doi = 10.1016/0140-6736(93)90421-C | last1 = Schechter | first1 = M.T. | last2 = Craib | first2 = K.J. | last3 = Gelmon | first3 = K.A. | last4 = Montaner | first4 = J.S. | last5 = Le | first5 = T.N. | last6 = O'Shaughnessy | first6 = M.V. | year = 1993 | title = HIV-1 and the aetiology of AIDS | journal = Lancet | volume = 341 | issue = 8846| pages = 658–59 | pmid = 8095571 | last7 = Schechter | first7 = M.T. | last8 = Gelmon | first8 = K.A. | last9 = Montaner | first9 = J.S.G. | s2cid = 23141531 }}</ref> Other studies show that among homosexual men and injection-drug users, the specific immune deficit that leads to AIDS—a progressive and sustained loss of [[CD4]]+ [[T-cell]]s—is extremely rare in the absence of other immunosuppressive conditions. For example, in the [[Multicenter AIDS Cohort Study]], more than 22,000 T-cell determinations in 2,713 HIV-seronegative homosexual men revealed only one individual with a CD4+ T-cell count persistently lower than 300 cells/μL of blood, and this individual was receiving [[immunosuppressive therapy]].<ref name="Vermund, 1993">{{cite journal | last1 = Vermund | first1 = S.H. | last2 = Hoover | first2 = D.R. | last3 = Chen | first3 = K. | year = 1993 | title = CD4+ counts in seronegative homosexual men. The Multicenter AIDS Cohort Study | journal = N. Engl. J. Med. | volume = 328 | issue = 6| page = 442 | pmid = 8093639 | doi = 10.1056/NEJM199302113280615 | doi-access = free }}</ref> In a survey of 229 HIV-seronegative injection-drug users in [[New York City]], mean CD4+ T-cell counts of the group were consistently more than 1000 cells/μL of blood. Only two individuals had two CD4+ T-cell measurements of less than 300/μL of blood, one of whom died with cardiac disease and [[non-Hodgkin's lymphoma]] listed as the cause of death.<ref name="Des Jarlais, 1993">{{cite journal | last1 = Des Jarlais | first1 = D.C. | last2 = Friedman | first2 = S.R. | last3 = Marmor | first3 = M. | last4 = Mildvan | first4 = D. | last5 = Yancovitz | first5 = S. | last6 = Sotheran | first6 = J.L. | last7 = Wenston | first7 = J. | last8 = Beatrice | first8 = S. | year = 1993 | title = CD4 lymphocytopenia among injecting drug users in New York City | journal = J. Acquir. Immune Defic. Syndr. | volume = 6 | issue = 7| pages = 820–22 | pmid = 8099613 }}</ref> ====AIDS among transfusion recipients is due to underlying diseases that necessitated the transfusion, rather than to HIV==== This notion is contradicted by a report by the Transfusion Safety Study Group (TSSG), which compared HIV-negative and HIV-positive blood recipients who had been given [[blood transfusions]] for similar diseases. Approximately 3 years following blood transfusion, the mean CD4+ T-cell count in 64 HIV-negative recipients was 850/μL of blood, while 111 HIV-seropositive individuals had average CD4+ T-cell counts of 375/μL of blood. By 1993, there were 37 cases of AIDS in the HIV-infected group, but not a single AIDS-defining illness in the HIV-seronegative transfusion recipients.<ref name="Donegan, 1990">{{cite journal | last1 = Donegan | first1 = E. | last2 = Stuart | first2 = M. | last3 = Niland | first3 = J.C. | last4 = Sacks | first4 = H.S. | last5 = Azen | first5 = S.P. | last6 = Dietrich | first6 = S.L. | last7 = Faucett | first7 = C. | last8 = Fletcher | first8 = M.A. | last9 = Kleinman | first9 = S.H. |display-authors=etal | year = 1990 | title = Infection with human immunodeficiency virus type 1 (HIV-1) among recipients of antibody-positive blood donations | journal = Annals of Internal Medicine | volume = 113 | issue = 10| pages = 733–39 | pmid = 2240875 | doi=10.7326/0003-4819-113-10-733}}</ref><ref name="Cohen, 1994">{{cite journal | doi = 10.1126/science.7992044 | last1 = Cohen | first1 = J. | year = 1994 | title = Duesberg and critics agree: hemophilia is the best test | journal = Science | volume = 266 | issue = 5191| pages = 1645–46 | pmid = 7992044 | bibcode=1994Sci...266.1645C}}</ref> ====High usage of clotting factor concentrate, not HIV, leads to CD4+ T-cell depletion and AIDS in hemophiliacs==== This view is contradicted by many studies. For example, among HIV-seronegative patients with [[hemophilia A]] enrolled in the Transfusion Safety Study, no significant differences in CD4+ T-cell counts were noted between 79 patients with no or minimal factor treatment and 52 with the largest amount of lifetime treatments. Patients in both groups had CD4+ T-cell-counts within the normal range.<ref name="Hasset, 1993">{{cite journal | last1 = Hassett | first1 = J. | last2 = Gjerset | first2 = G.F. | last3 = Mosley | first3 = J.W. | last4 = Fletcher | first4 = M.A. | last5 = Donegan | first5 = E. | last6 = Parker | first6 = J.W. | last7 = Counts | first7 = R.B. | last8 = Aledort | first8 = L.M. | last9 = Lee | first9 = H. |display-authors=etal | year = 1993 | title = Effect on lymphocyte subsets of clotting factor therapy in human immunodeficiency virus-1-negative congenital clotting disorders. The Transfusion Safety Study Group | journal = Blood | volume = 82 | issue = 4| pages = 1351–57 | pmid = 8353293 | doi = 10.1182/blood.V82.4.1351.1351 | doi-access = free }}</ref> In another report from the Transfusion Safety Study, no instances of AIDS-defining illnesses were seen among 402 HIV-seronegative hemophiliacs who had received factortherapy.<ref name="Aledort, 1993">{{cite journal | last1 = Aledort | first1 = L.M. | last2 = Operskalski | first2 = E.A. | last3 = Dietrich | first3 = S.L. | last4 = Koerper | first4 = M.A. | last5 = Gjerset | first5 = G.F. | last6 = Lusher | first6 = J.M. | last7 = Lian | first7 = E.C. | last8 = Mosley | first8 = J.W. | year = 1993 | title = Low CD4+ counts in a study of transfusion safety. The Transfusion Safety Study Group | journal = N. Engl. J. Med. | volume = 328 | issue = 6| pages = 441–42 | pmid = 8093638 | doi = 10.1056/NEJM199302113280614 | doi-access = free }}</ref> In a cohort in the [[United Kingdom]], researchers matched 17 HIV-seropositive [[hemophiliac]]s with 17 HIV-seronegative hemophiliacs with regard to clotting factor concentrate usage over a ten-year period. During this time, 16 AIDS-defining clinical events occurred in 9 patients, all of whom were HIV-seropositive. No AIDS-defining illnesses occurred among the HIV-negative patients. In each pair, the mean CD4+ T-cell count during follow-up was, on average, 500 cells/μL lower in the HIV-seropositive patient.<ref name="Sabin, 1996">{{cite journal | last1 = Sabin | first1 = C.A. | last2 = Pasi | first2 = K.J. | last3 = Phillips | first3 = A.N. | last4 = Lilley | first4 = P. | last5 = Bofill | first5 = M. | last6 = Lee | first6 = C.A. | year = 1996 | title = Comparison of immunodeficiency and AIDS defining conditions in HIV negative and HIV positive men with haemophilia A | journal = BMJ | volume = 312 | issue = 7025| pages = 207–10 | pmid = 8563582 | pmc = 2349998 | doi=10.1136/bmj.312.7025.207}}</ref> Among HIV-infected hemophiliacs, Transfusion Safety Study investigators found that neither the purity nor the amount of factor VIII therapy had a deleterious effect on CD4+ T-cell counts.<ref name="Gjerset, 1994">{{cite journal | last1 = Gjerset | first1 = G.F. | last2 = Pike | first2 = M.C. | last3 = Mosley | first3 = J.W. | last4 = Hassett | first4 = J. | last5 = Fletcher | first5 = M.A. | last6 = Donegan | first6 = E. | last7 = Parker | first7 = J.W. | last8 = Counts | first8 = R.B. | last9 = Zhou | first9 = Y. |display-authors=etal | year = 1994 | title = Effect of low- and intermediate-purity clotting factor therapy on progression of human immunodeficiency virus infection in congenital clotting disorders. Transfusion Safety Study Group | journal = Blood | volume = 84 | issue = 5| pages = 1666–71 | pmid = 7915149 | doi = 10.1182/blood.V84.5.1666.1666 | doi-access = free }}</ref> Similarly, the Multicenter Hemophilia Cohort Study found no association between the cumulative dose of plasma concentrate and incidence of AIDS among HIV-infected hemophiliacs.<ref name="Goedert, 1989">{{cite journal | last1 = Goedert | first1 = JJ | last2 = Kessler | first2 = CM | last3 = Aledort | first3 = LM | last4 = Biggar | first4 = RJ | last5 = Andes | first5 = WA | last6 = White Gc | first6 = 2nd | last7 = Drummond | first7 = JE | last8 = Vaidya | first8 = K | last9 = Mann | first9 = DL | last10 = Eyster | first10 = M. Elaine | last11 = Ragni | first11 = Margaret V. | last12 = Lederman | first12 = Michael M. | last13 = Cohen | first13 = Alan R. | last14 = Bray | first14 = Gordon L. | last15 = Rosenberg | first15 = Philip S. | last16 = Friedman | first16 = Robert M. | last17 = Hilgartner | first17 = Margaret W. | last18 = Blattner | first18 = William A. | last19 = Kroner | first19 = Barbara | last20 = Gail | first20 = Mitchell H. | title = A prospective study of human immunodeficiency virus type 1 infection and the development of AIDS in subjects with hemophilia | journal = The New England Journal of Medicine | volume = 321 | issue = 17 | pages = 1141–48 | year = 1989 | pmid = 2477702 | doi = 10.1056/NEJM198910263211701 | display-authors = 8 }}</ref> ====The distribution of AIDS cases casts doubt on HIV as the cause. Viruses are not gender-specific, yet only a small proportion of AIDS cases are among women==== The distribution of AIDS cases, whether in the United States or elsewhere in the world, invariably mirrors the prevalence of HIV in a population. In the United States, HIV first appeared in populations of [[injection-drug]] users (a majority of whom are male) and [[gay]] men. HIV is spread primarily through unprotected sex, the exchange of HIV-contaminated needles, or cross-contamination of the drug solution and infected blood during intravenous drug use. Because these behaviors show a gender skew—Western men are more likely to take illegal drugs intravenously than Western women, and men are more likely to report higher levels of the riskiest sexual behaviors, such as unprotected [[anal intercourse]]—it is not surprising that a majority of U.S. AIDS cases have occurred in men.<ref>{{Cite web |url=https://www.census.gov/population/international/ |title=U.S. Census Bureau }}</ref> Women in the United States, however, are increasingly becoming HIV-infected, usually through the exchange of HIV-contaminated needles or sex with an HIV-infected male. The [[Centers for Disease Control and Prevention|CDC]] estimates that 30 percent of new HIV infections in the United States in 1998 were in women. As the number of HIV-infected women has risen, so too has the number of female AIDS patients in the United States. Approximately 23% of U.S. adult/adolescent AIDS cases reported to the CDC in 1998 were among women. In 1998, AIDS was the fifth leading cause of death among women aged 25 to 44 in the United States, and the third leading cause of death among African-American women in that age group.<ref>{{Cite web |url=https://www.niaid.nih.gov/factsheets/aidsstat.htm |title=AIDS/HIV Statics }}</ref> In Africa, HIV was first recognized in sexually active [[heterosexual]]s, and AIDS cases in Africa have occurred at least as frequently in women as in men. Overall, the worldwide distribution of HIV infection and AIDS between men and women is approximately 1 to 1.<ref>{{Cite web |url=https://www.census.gov/population/international/ |title=U.S. Bureau Census }}</ref> In [[sub-Saharan Africa]], 57% of adults with HIV are women, and young women aged 15 to 24 are more than three times as likely to be infected as young men.<ref name="UNAIDS, 2005">{{Cite web |url=http://www.unfpa.org/upload/lib_pub_file/308_filename_women_aids1.pdf |title=UNAIDS, 2005 |access-date=2005-08-24 |archive-date=2013-12-02 |archive-url=https://web.archive.org/web/20131202144406/http://www.unfpa.org/upload/lib_pub_file/308_filename_women_aids1.pdf |url-status=dead }}</ref> ====HIV is not the cause of AIDS because many individuals with HIV have not developed AIDS==== HIV infections have a prolonged and variable course. The median period of time between infection with HIV and the onset of clinically apparent disease is approximately 10 years in [[industrialized countries]], according to prospective studies of homosexual men in which dates of [[seroconversion]] are known. Similar estimates of asymptomatic periods have been made for HIV-infected blood-transfusion recipients, injection-drug users and adult hemophiliacs.<ref name="Alcabes, 1993">{{cite journal | last1 = Alcabes | first1 = P. | last2 = Munoz | first2 = A. | last3 = Vlahov | first3 = D. | last4 = Friedland | first4 = G.H. | year = 1993 | title = Incubation period of human immunodeficiency virus | journal = Epidemiol. Rev. | volume = 15 | issue = 2| pages = 303–18 | pmid = 8174659 | doi = 10.1093/oxfordjournals.epirev.a036122 }}</ref> As with many diseases, a number of factors can influence the course of HIV disease. Factors such as age or genetic differences between individuals, the level of virulence of the individual strain of virus, as well as exogenous influences such as co-infection with other microbes may determine the rate and severity of HIV disease expression. Similarly, some people infected with [[hepatitis B]], for example, show no symptoms or only [[jaundice]] and clear their infection, while others suffer disease ranging from chronic [[liver]] inflammation to [[cirrhosis]] and hepatocellular carcinoma. Co-factors probably also determine why some smokers develop [[lung cancer]] while others do not.<ref name="Levy, 1993"/><ref name="Evans, 1982">{{cite journal | last1 = Evans | first1 = A.S. | year = 1982 | title = The clinical illness promotion factor: a third ingredient | journal = Yale J. Biol. Med. | volume = 55 | issue = 3–4| pages = 193–99 | pmid = 6295003 | pmc = 2596440 }}</ref><ref name="Fauci, 1996">{{cite journal | doi = 10.1038/384529a0 | last1 = Fauci | first1 = A.S. | year = 1996 | title = Host factors and the pathogenesis of HIV-induced disease | url = https://zenodo.org/record/1233194| journal = Nature | volume = 384 | issue = 6609| pages = 529–34 | pmid = 8955267 |bibcode = 1996Natur.384..529F | s2cid = 4370482 }}</ref> ====HIV is not the cause of AIDS because some people have symptoms associated with AIDS but are not infected with HIV==== Most AIDS symptoms result from the development of [[opportunistic infection]]s and [[cancer]]s associated with severe [[immunosuppression]] secondary to HIV.{{cn|date=January 2021}} However, immunosuppression has many other potential causes. Individuals who take [[glucocorticoid]]s or immunosuppressive drugs to prevent [[organ transplant|transplant]] rejection or to treat [[autoimmune disease]]s can have increased susceptibility to unusual infections, as do individuals with certain [[genetics|genetic]] conditions, severe [[malnutrition]] and certain kinds of cancers. There is no evidence suggesting that the numbers of such cases have risen, while abundant [[epidemiologic]] evidence shows a very large rise in cases of immunosuppression among individuals who share one characteristic: HIV infection.<ref name="NIAID, 1995"/><ref name="UNAIDS, 2000"/> ====The spectrum of AIDS-related infections seen in different populations proves that AIDS is actually many diseases not caused by HIV==== [[File:Pneumocystis jiroveci infection (3833203709).jpg|thumb|[[Pneumocystis jiroveci pneumonia|''Pneumocystis jiroveci'' pneumonia]] ]] [[File:Bacteria on Warthin–Starry stain.jpg|thumb|[[Mycobacterium avium complex|''Mycobacterium avium'' complex]] ]] The diseases associated with AIDS, such as [[Pneumocystis jiroveci pneumonia|''Pneumocystis jiroveci'' pneumonia]] (PCP) and [[Mycobacterium avium complex|''Mycobacterium avium'' complex]] (MAC), are not caused by HIV, but rather result from the immunosuppression caused by HIV disease. As the immune system of an HIV-infected individual weakens, he or she becomes susceptible to the particular [[virus|viral]], [[fungus|fungal]], and [[bacteria]]l infections common in the community. For example, HIV-infected people in the [[Midwestern United States]] are much more likely than people in [[New York City]] to develop [[histoplasmosis]], which is caused by a fungus. A person in Africa is exposed to pathogens different from individuals in an American city. Children may be exposed to different infectious agents compared to adults.<ref>{{Cite web |url=http://hivatis.org/guidelines/op_infections/OI_112801.html |title=USPHS/IDSA }}</ref> HIV is the underlying cause of the condition named AIDS, but the additional conditions that may affect an AIDS patient are dependent upon the [[endemic (epidemiology)|endemic]] [[pathogens]] to which the patient may be exposed.{{cn|date=January 2021}}
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