Steeds meer wetenschappers krijgen in de gaten dat HIV- en AIDS-onderzoek de sleutel zijn tot grotere onderzoeksbudgetten en dikkere auto’s. Aan HIV is daarom –zonder enig succes overigens- al zoveel onderzocht en aan het virus zijn inmiddels al zoveel bizarre eigenschappen toegekend, dat het lastig is nog iets nieuws te bedenken. Wetenschappers moeten tegenwoordig echt creatief zijn. Heel creatief. En dat waren ze bij de Universiteit van San Diego. Zij bedachten weer iets nieuws. HIV is nog gevaarlijker dan we al moeten denken.
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"Aan HIV is daarom –zonder enig succes overigens- al zoveel onderzocht en aan het virus zijn inmiddels al zoveel bizarre eigenschappen toegekend" En weer wordt dezelfde dommigheid herhaald. NA 25 jaar is bereikt dat AIDS geen dodelijke ziekte is, maar een hanteerbare, weliswaar chronisch, maar toch. In landen waar AIDS-remmers voorhanden zijn sterven er slechts weinigen nog aan AIDS. In landen waar die ontbreken sterven ze wel. De HIV->AIDS->dood is al lang verbroken, maar de AIDS-ontkennertjes kiezen ervoor om oogkleppen op te zetten en doen net alsof dat nog steeds het geval is. Namens de HIV-geïnfecteerden (die toch al moeten vechten tegen allerlei vooroordelen); BEDANKT HE! (maar niet heus).
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Wel goed lezen floeper. Ik ontken geen AIDS. Ik ontken alleen dat het van een virus komt en dat het besmettelijk is. En met mij een heeeeeeeeeeleboel echte wetenschappers. Je mag nu naar Zapruder waar op dit moment een ex-AIDS patient en een virus-expert in de comments meedoen. Je kan namelijk gewoon weer beter worden van AIDS. Stoppen met de medicijnen. Dus wees een vent en ga ik discussie met hen... Op Zapruder hebben we denk ik zo 7, 8 ex-AIDS patienten aanwezig. Mensen die nu weer kerngezond zijn, Stoppen met de AIDS-remmers (dat is chemokuur) is de oplossing. Dus, ga jij hen even vertellen hoe het zit. Jouw commentaar is complete nonsense trouwens.
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http://www.quackwatch.org/04ConsumerEducation/h... Op deze pagina vind je een goed overzicht met bewijzen dat het HIV virus AIDS veroorzaakt, compleet met bronvermeldingen. Het gaat onder andere in op de volgende zaken: -HIV voldoet aan Koch's postulaten als de oorzaak van AIDS -AIDS en HIV zijn zonder uitzondering gecorrelleerd in tijd, plaats en bevolkingsgroep -Veel studies bevestigen dat er maar één factor is, HIV, die voorspelt of iemand AIDS zal ontwikkelen. -In groepsstudies komen ernstige immunosuppressie en AIDS-gedefinieerde ziekten vrijwel alleen voor in individuen die HIV-geinfecteerd zijn. -Voor de verschijning van HIV kwamen AIDS-gerelateerde ziekten zoals PCP, KS en MAC zeer zelden voor in westerse landen; vandaag de dag zijn ze veel voorkomend bij HIV-geinfecteerden. -In ontwikkelingslanden, de verspreiding van zeldzame en endemische ziekten is dramatisch veranderd sinds de verspreiding van HIV, met name onder de jonge en middle aged bevolking, inclusief leden van de hoog opgeleide middenklasse. -Uit studies blijkt dat zowel in ontwikkelde als in ontwikkelingslanden het sterftepercentage van HIV-seropositiven duidelijk hoger ligt dan HIV-seronegatieven. -HIV kan gedetecteerd worden in vrijwel iedereen die AIDS heeft. -Talrijke studies tonen an dat wanneer iemand een hoge concentratie HIV, antigenen en HIV nucleaire zuren (DNA en RNA) in z'n lichaam heeft dat er een zeer verhoogd risico aanwezig is dat het immuunsysteem verslechterd en AIDS-gerelateerde ziekten ontwikkelen. Andersom, wanneer de concentraties laag zijn, is dat risico ook veel lager. -De beschikbaarheid van medicijncocktails die specifiek de HIV-replicatie blokkeren heeft de prognose van HIV-geinfecteerden dramatisch verbeterd. Dit effect zou je niet zien als HIV geen centrale rol speelde in het veroorzaken van AIDS. -Bij HIV-geinfecteerden die anti-HIV medicatie ontvangen is het duidelijk dat bij de patienten waar de behandelmethode aanslaat de virus-concentratie daalt, en dat de kans op AIDS verkleint. Bij degenen bij wie de medicijnen niet aanslaan zie je die daling niet. Dit effect zou je niet zien als HIV geen centrale rol speelde in het veroorzaken van AIDS. -Bijna iedereen met AIDS heeft HIV antilichamen -Talrijke bloedonderzoeken tonen aan dat AIDS veel voorkomt op die plekken waar veel individuen HIV-antilichamen hebben. Andersom, in populaties waar HIV-antilichamen bijna niet voorkomen is AIDS extreem zeldzaam. -Het specifieke immunologische kenmerk van AIDS - een langdurig lage CD4+ T-cell count - is buitengewoon zeldzaam bij afwezigheid van HIV-infectie of een andere bekende oorzaak van onderdrukking van het immuunsysteem. -Pasgeboren kinderen hebben geen 'risicogedrag' getoond, toch hebben veel kinderen wiens moeder HIV-geinfecteerd waren AIDS gekregen en zijn overleden. -HIV-geinfecteerde kinderen ontwikkelden AIDS terwijl de niet-geinfecteerde tweelingbroer/zus geen AIDS ontwikkelde. -Talrijke studies naar mensen die AIDS ontwikkelde na een bloedtransfusie hebben herhaaldelijk geleid tot de ontdekking van HIV zowel in het bloed van de patient als in het bloed van de donor. -HIV veroorzaakt de dood en beschadiging van CD4+ T lymphocyten zowel in vitro als in vivo. (voor uitgebreidere uitleg en bronnen, zie de link)
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"Je kan namelijk gewoon weer beter worden van AIDS." Dit is trouwens een onhandige uitspraak van mij, want AIDS in de Westerse wereld is wat anders dan AIDS in Afrika waar het wel echte AIDS is maar wordt veroorzaakt door langdurige ondervoeding, blootstelling aan chemicalieen en medicijnen en infectieziekheid.
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AIDS voldoet niet aan Kochs postulaten, daarover hebben we al veel geschreven., De rest is ook makkelijk te debunken: http://zapruder.nl/AIDS Je verhaal is echt te dom voor woorden. Ik pik er één uit: "-Talrijke studies naar mensen die AIDS ontwikkelde na een bloedtransfusie hebben herhaaldelijk geleid tot de ontdekking van HIV zowel in het bloed van de patient als in het bloed van de donor. " Daar is nooit HIV ontdekt, daar is seropositiviteit vastgesteld. Dat is wat anders. Er bestaan geen HIV-tests. HIV kan op geen enkele manier gedetecteerd worden hoewel de orthodoxie volhoudt dat het wel kan. Maar doe deze discussie gewoon bij ons. Daar zijn echte experts aanwezig.
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"Jouw commentaar is complete nonsense trouwens." yeah right. Nog een keer: doen alsof AIDS een dodelijke ziekte is in Westerse landen, dat is onzin. Die "heeeeeeleboel" wetenschappers zijn een paar handenvol schreeuwlelijks. Of wil je weer gaan schermen met je Nobelprijswinnaars? Wil je er Duesberg weer bijhalen? Wie was het ook alweer die de claims van de Perth-groep over het niet bestaan van HIV in 1997 categorisch naar de prullenbak verwees? O ja, diezelfde Duesberg! Een Godschalk is een narcistische idioot die al meer dan 30 jaar niet wetenschappelijk actief is op z'n vakgebied; in de tijd dat HIV ontdekt werd lag ie er allang uit. Het is dan ook niet zo raar dat dit soort "experts" aan de kant van de aids-ontkenners staan. En ja, AIDS ONTKENNERS, want je ontkent glashard de aids-epidemie in Afrika, dus doe nou maar niet alsof dat niet zo is.
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"En ja, AIDS ONTKENNERS, want je ontkent glashard de aids-epidemie in Afrika, dus doe nou maar niet alsof dat niet zo is." Het is eigenlijk andersom. Jullie zijn de mensen die op basis van een pharmafabel half Afrika willen uitmoorden met dodelijke medicijnen. AIDS-remmers kunnen nooit iemand beter maken. Hun principiele werking is dat ze mensen dood maken. Transcriptases-toppers en weet ik wat al niet meer. Het is dodeliljke chemokuur en op basis van de goedgelovigeheid van mensen zoals jij moet nu heel Afrika daarmee worden volgepropt. Terwijl die mensen gewoon ziek van ondervoeding en slechte hygiene zijn. Wat in Afrika een AIDS_indicator is gemaakt. Het woord genocide komt in me op.
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Ga dat verhaal houden in Groningen.... bij de rechtbank. Tegen de mensen die het slachtoffer zijn geworden van die idioten. Kijk dan eens hoeveel bijval je krijgt.
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"AIDS voldoet niet aan Kochs postulaten, daarover hebben we al veel geschreven., De rest is ook makkelijk te debunken: http://zapruder.nl/AIDS" Als je echte informatie wil over AIDS ga je naar: http://www.quackwatch.org/04ConsumerEducation/h... DAAR zitten de experts. DAAR zijn de links naar de ECHTE informatie. Op Zapruder is het eenzijdigheid troef. Patman weet niet eens dat AIDS in NL geen dodelijke ziekte meer is (zoiets komt 'm niet uit dus wordt het maar ontkend!), Patman weet niet wat de stand van zaken is in de medische wereld. Patman laat z'n oor hangen naar morosofen als Godschalk en laat zich door hem vertellen wat de stand van zaken is in de wetenschappelijke onderzoeken, maar verzuimt het ten enen male om dat dan ook te tjekken. Patman WEET helemaal niet wat er nu wel en niet bekend is over HIV en AIDS; hij weet alleen wat de AIDS-ontkenners 'm vertellen over wat zij denken dat er bekend is over HIV en AIDS. En dan krijg je dus dingen dat je dom de Perth Group gaat napraten over "de klassieke methode" om virussen te identificeren. En wie heeft die "klassieke methode" verzonnen? Jawel: de Perth Group zelf! Maar hola nee, Patman tjekt zoiets niet, die kopieert het gospel van de AIDS-ontkenners en probeert dat te verkopen als "informatie". Het is te walgelijk voor woorden.
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"Het is eigenlijk andersom. Jullie zijn de mensen die op basis van een pharmafabel half Afrika willen uitmoorden met dodelijke medicijnen. " Tjongejonge.. jij bent echt op de hoogte he? Die medicijnen ontbreken er juist. In landen waar medicijnen voorhanden zijn sterven ze niet (of nauwelijks). rara! Denk toch eens na, idioot! "AIDS-remmers kunnen nooit iemand beter maken. Hun principiele werking is dat ze mensen dood maken." Dat eerste klopt; daarom is AIDS nu (voorlopig) een chronische ziekte; niet te genezen maar wel in de hand te houden. Dat tweede is natuurlijk weer van de pot gerukte onzin. Voor je eigen gewin zit je nu al maanden te proberen om HIV-patienten ten dode op te schrijven; lekker een bevolkingsgroep stigmatiseren die toch al zo moet vechten tegen vooroordelen!. AIDS in Nederland is EEN CHRONISCHE ZIEKTE; je kan er oud mee worden, dankzij de ontwikkelingen op medisch gebied. Krijg dat toch eens in die botte kop van je.
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"Tjongejonge.. jij bent echt op de hoogte he? Die medicijnen ontbreken er juist. In landen waar medicijnen voorhanden zijn sterven ze niet (of nauwelijks). rara! Denk toch eens na, idioot! " Dat zijn de statistieken van de AIDS-pushers zoals jij. Mensen die er geweest zijn, zeggen wat anders... AIDS is in Nederland niets anders dan één van die 29 ziektes en het kan gewoon genezen worden. We hebben een forum vol zulke mensen bij ons., Ik geloof liever hun dan zo iemand als jij die alles voor zoete koek slikt...
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"Dat zijn de statistieken van de AIDS-pushers zoals jij. Mensen die er geweest zijn, zeggen wat anders... " Mensen zoals ik zeggen iets anders??? Oooo je bedoelt het minderheidsgroepje waar jij je oor naar laat hangen zonder naar de realiteit te kijken! "We hebben een forum vol zulke mensen bij ons.," Nee, je hebt, zoals je zelf al zei 7-8 personen bij je, van de ong. 13.000 seropositieven in NL. Dat is 0.05% En ja, net zoals je mensen met kanker hebt die dat liever ontkennen (of met wat voor ernstige ziekte dan ook) heb je een groepje dat het comfortabeler vindt hun ziekte te ontkennen, of om die te genezen met iets buiten de reguliere medische wereld om (zoals een knoflook en citroenendieetje). Tegenover dat cultachtige clubje van je staan duizenden nederlandse HIV-patienten die wel enig realisme tonen. En wie slikt hier nu alles voor zoete koek? Wie slikt die (door Duesberg in 1997 bewezen) flagrante onzin van de Perth Group? Wie slikt het woord van morosoof Godschalk? Je zou ook eens naar de echte onderzoeksresultaten kunnen kijken ipv blind te vertrouwen op je "experts" en wat zij erover zeggen. Maar dat doe je niet; het verhaal van de ontkenners spreekt je aan, dus staar je je er volkomen blind op.
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10 Scientific Reasons Why HIV Cannot Cause AIDS For anyone convinced that HIV has been isolated. 1. HIV is neutralized by antibody immunity. When a person tests "positive" to HIV, it means they carry antibodies to the virus. Which means that they have immunity. This is clear from the fact that there is so little virus to be found in HIV antibody positive people.* The antibodies have done their job and the virus is well under control. There are no known viruses that cause illness in every case only long after antibodies appear, which is how AIDS is defined. One has to question why 12 years and billions of dollars have been spent developing a vaccine against HIV when the best vaccine possible already exists when a person tests positive. 2. HIV does not kill the T cells it infects. HIV can only kill T cells under rare laboratory conditions. In fact, HIV researchers use T cells to grow the virus because T cells live quite compatibly with HIV. 3. HIV does not infect enough T cells to cause AIDS. HIV never infects more than 1 out of 1000 T cells; commonly just 1 out of 10,000 T cells.* People replace 5% of their T cells per day. Simple math shows that HIV cannot infect enough T cells to cause them to die off and bring down the whole immune system. Even supporters of the HIV/AIDS theory admit that this low level of T cell infection is a challenge to explain. * The recent invention of "viral load" testing is an attempt to explain away the fact that almost no sign of HIV can be found by standard measurements. Viral load tests do not measure viable virus and have not been approved by the FDA to diagnose HIV infection. 4. HIV has no AIDS causing gene. HIV has no specific gene or unique reason to cause AIDS. All retroviruses have only 3 major genes, GAG, ENV and POL and only 6 minor genes. Because the genes and genetic sequences are so limited in these simple organisms, they need all their genes to replicate. HIV is almost identical to all other retroviruses genetically. There are 50 to 100 different retroviruses that can be found in every healthy human body. All have been brought under control by antibody response. HIV behaves no differently than any of these others. If none of these other retroviruses cause AIDS, why should HIV? And vice versa, if HIV causes AIDS, why don't all the rest? So there is no genetic reason why HIV would cause AIDS. 5. There is no such thing as a "slow virus". HIV is claimed to take 10 to 20 years (the "latency period") after infection to cause AIDS. The only way to explain this is to give HIV magical abilities to reactivate, mutate, migrate and hibernate. These slow virus hypotheses were devised by scientists who used them to buy time when their viruses failed to perform. The slow virus proponents point to examples like the herpes viruses that smolder and hide and then reemerge in persons when they have suppressed immunity and cannot generate a sufficient defense. These differ greatly from HIV because large amounts of active virus can be found causing specific symptoms. By contrast, a slow virus is an invention credited with the ability to cause disease only years after infection - termed the latency period - in previously healthy persons, regardless of their state of immunity. Such a concept allows scientists to blame a long-neutralized virus for any disease that appears decades after infection. HIV is inactive, then is said to cause 30 different diseases 10 years later. None of which are specific to HIV itself. 6. HIV is not a new virus, so it could not cause a new epidemic. AIDS cases went from almost none in 1980 to a reported half a million in North America alone by 1995. Therefore, scientists claim HIV must be a new virus or we would have had an epidemic years or centuries ago. However, this claim does not stand up to the principals of Farr's Law. Farr's Law asserts that new infections spread exponentially through the population. HIV has been reported at more or less 1 million infected in the USA each year since they had a test for it in 1984. So it cannot be a new virus. 7. HIV fails Koch's postulates. The universal test used by scientists to determine if a disease is truly being caused by an infection was designed over one hundred years ago by Robert Koch. Koch's postulates state: The organism: 1. must be found in all cases of the disease. 2. must be isolated from the host and grown in pure culture. 3. must cause the same disease when injected into a new, healthy host. 4. must be found growing again in the newly diseased host. Here is how HIV does on this test: 1. The germ must be found in all cases of the diseases. FAILS. * 10 to 20% of AIDS patients have no HIV at all. * Only tiny amounts of HIV, usually dormant, can be found in any AIDS patient. 2. The germ must be isolated from the host and grown in pure culture. PASSES - but only on a technicality. * Huge amounts of cell tissue are needed to find HIV. * HIV needs a chemically induced process to reactivate. * By contrast, large amounts of active virus can be found with other viruses. 3. The germ must cause the same disease when injected into a new, healthy host. FAILS - hands down. * HIV does not cause AIDS in test animals like chimpanzees. * human health care workers accidentally infected with HIV rarely get AIDS unless they use recreational drugs ... or AZT. 4. The germ must be found growing again in the newly diseased host. FAILS - for not passing postulate 3. HIV fails this test. HIV scientists claim that Koch's postulates are old and out of date with modern science. But they have stood the test of time. Disease hypotheses that ignored Koch's postulates have been a failure. The infectious theories of scurvy, pellagra, beriberi, SMON and virus/cancer research have all ignored Koch's postulates and all have been a dismal failure. And now HIV/AIDS? 8. AIDS has remained in the original risk groups for over 15 years. If a disease does not spread it must be caused by something non-infectious. The US CDC reports (1997) confirm that AIDS is not spreading into the general population. AIDS cases by risk group (US): Admitted gay males 54% Admitted IV drug users 32% Hemophiliacs 1% Transfusion recipients 1% Claimed heterosexual contact 9% Pediatric 1% Total: 97% If AIDS is truly caused by a virus AIDS patients not in a risk group should be growing above an estimated 10% as the disease spreads. Note that the US army has found that when testing recruits HIV positive results were divided equally between men (50%) and women (50%). Yet 85% of AIDS cases in the US are male. Note too that in the US men use over 80% of all hard drugs. Among women with AIDS 60% (admit they) use hard drugs. 9. International comparisons of AIDS differ greatly. A germ related disease would effect the population in the same way around the world. An outbreak of cholera in India and Honduras would be much the same. But AIDS is totally different in the USA or western industrialized countries and Africa. USA AFRICA Aids by sexual percentage 85% male 50% male 15% female 50% female AIDS among risk groups At least 90% No risk group risk groups (at random) AIDS diseases caused by microbes 62% 90% Estimated HIV Infections 1 million 14 million Official documented cases of AIDS (1995/96) 513,486 442,735 AIDS in Africa should be 14 times higher than in the US. Instead, people with HIV in the US develop AIDS 10 to 20 times faster than in Africa. This means that whereas the latency period in the US is predicted at 10 -15 years, in Africa it is at least 100 to 150 years! 10. AIDS occurs without HIV Infection and most people with HIV never develop AIDS. The evidence for the HIV/AIDS hypothesis is based solely on correlation. Because the virus is found in most AIDS patients, it is thought to cause AIDS. But the logic of that assumption is flawed because CORRELATION DOES NOT PROVE CAUSATION. The common presence of HIV in AIDS patients is no more proof that HIV causes AIDS than the presence of birds on power lines is proof that birds cause power failures. So, if HIV and AIDS are only correlated, we should find AIDS without HIV and healthy people who have HIV and never get AIDS. That is exactly what is happening. In Africa studies have shown over 65% of AIDS patients are not HIV positive. In Africa a positive HIV antibody test result is not necessary for reporting AIDS cases; prolonged symptoms are enough. 4621 cases of AIDS without HIV were found in the US Center for Disease Control (CDC) reports up to 1993. And the number could be much larger but the official definition of AIDS is designed to eliminate AIDS cases without HIV. AIDS is distinguished from virtually every other disease in history by the fact that it has no constant specific symptoms. AIDS is an umbrella term for 29 old diseases and one non-disease (a T4 cell count of less than 200/ul of blood) when a person has an HIV-positive antibody test result. The official CDC definition of AIDS excludes HIV-negative AIDS by definition. How the CDC's AIDS definition works: * Kaposi's Sarcoma + HIV = AIDS * Kaposi's Sarcoma - HIV = Kaposi's Sarcoma * Pneumonia + HIV = AIDS * Pneumonia - HIV = Pneumonia * Dementia + HIV = AIDS * Dementia - HIV = Dementia and so on... * <200 T4 cell count + HIV = AIDS * <200 T4 cell count - HIV = no disease There is no disease that is only caused by HIV. HIV is said to cause 29 old diseases when it is present. When it is not, the original causes of these diseases are responsible for them. The official definition of AIDS creates a 100% correlation between the virus and AIDS. This "correlation" is not objective or scientific, but is artificial and deceptively self-fulfilling. Estimated total HIV infected worldwide: 28,000,000 ? Total of reported AIDS cases worldwide: 1,400,000 95% percent of people with HIV do not have AIDS.
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The Evidence That HIV Causes AIDS BACKGROUND The acquired immunodeficiency syndrome (AIDS) was first recognized in 1981 and has since become a major worldwide pandemic. AIDS is caused by the human immunodeficiency virus (HIV). By leading to the destruction and/or functional impairment of cells of the immune system, notably CD4+ T cells, HIV progressively destroys the body's ability to fight infections and certain cancers. An HIV-infected person is diagnosed with AIDS when his or her immune system is seriously compromised and manifestations of HIV infection are severe. The U.S. Centers for Disease Control and Prevention (CDC) currently defines AIDS in an adult or adolescent age 13 years or older as the presence of one of 26 conditions indicative of severe immunosuppression associated with HIV infection, such as Pneumocystis carinii pneumonia (PCP), a condition extraordinarily rare in people without HIV infection. Most other AIDS-defining conditions are also "opportunistic infections" which rarely cause harm in healthy individuals. A diagnosis of AIDS also is given to HIV-infected individuals when their CD4+ T-cell count falls below 200 cells/cubic millimeter (mm3) of blood. Healthy adults usually have CD4+ T-cell counts of 600-1,500/mm3 of blood. In HIV-infected children younger than 13 years, the CDC definition of AIDS is similar to that in adolescents and adults, except for the addition of certain infections commonly seen in pediatric patients with HIV. (CDC. MMWR 1992;41(RR-17):1; CDC. MMWR 1994;43(RR-12):1). In many developing countries, where diagnostic facilities may be minimal, healthcare workers use a World Health Organization (WHO) AIDS case definiton based on the presence of clinical signs associated with immune deficiency and the exclusion of other known causes of immunosuppression, such as cancer or malnutrition. An expanded WHO AIDS case definition, with a broader spectrum of clinical manifestations of HIV infection, is employed in settings where HIV antibody tests are available (WHO. Wkly Epidemiol Rec. 1994;69:273). As of the end of 2000, an estimated 36.1 million people worldwide - 34.7 million adults and 1.4 million children younger than 15 years - were living with HIV/AIDS. Through 2000, cumulative HIV/AIDS-associated deaths worldwide numbered approximately 21.8 million - 17.5 million adults and 4.3 million children younger than 15 years. In the United States, an estimated 800,000 to 900,000 people are living with HIV infection. As of December 31, 1999, 733,374 cases of AIDS and 430,441 AIDS-related deaths had been reported to the CDC. AIDS is the fifth leading cause of death among all adults aged 25 to 44 in the United States. Among African-Americans in the 25 to 44 age group, AIDS is the leading cause of death for men and the second leading cause of death for women (UNAIDS. AIDS epidemic update: December 2000; CDC. HIV/AIDS Surveillance Report 1999;11[2]:1; CDC. MMWR 1999;48[RR13]:1). This document summarizes the abundant evidence that HIV causes AIDS. Questions and answers at the end of this document address the specific claims of those who assert that HIV is not the cause of AIDS. EVIDENCE THAT HIV CAUSES AIDS HIV fulfills Koch's postulates as the cause of AIDS. Among many criteria used over the years to prove the link between putative pathogenic (disease-causing) agents and disease, perhaps the most-cited are Koch's postulates, developed in the late 19th century. Koch's postulates have been variously interpreted by many scientists, and modifications have been suggested to accommodate new technologies, particularly with regard to viruses (Harden. Pubbl Stn Zool Napoli [II] 1992;14:249; O'Brien, Goedert. Curr Opin Immunol 1996;8:613). However, the basic tenets remain the same, and for more than a century Koch's postulates, as listed below, have served as the litmus test for determining the cause of any epidemic disease: 1. Epidemiological association: the suspected cause must be strongly associated with the disease. 2. Isolation: the suspected pathogen can be isolated - and propagated - outside the host. 3. Transmission pathogenesis: transfer of the suspected pathogen to an uninfected host, man or animal, produces the disease in that host. With regard to postulate #1, numerous studies from around the world show that virtually all AIDS patients are HIV-seropositive; that is they carry antibodies that indicate HIV infection. With regard to postulate #2, modern culture techniques have allowed the isolation of HIV in virtually all AIDS patients, as well as in almost all HIV-seropositive individuals with both early- and late-stage disease. In addition, the polymerase chain (PCR) and other sophisticated molecular techniques have enabled researchers to document the presence of HIV genes in virtually all patients with AIDS, as well as in individuals in earlier stages of HIV disease. Postulate #3 has been fulfilled in tragic incidents involving three laboratory workers with no other risk factors who have developed AIDS or severe immunosuppression after accidental exposure to concentrated, cloned HIV in the laboratory. In all three cases, HIV was isolated from the infected individual, sequenced and shown to be the infecting strain of virus. In another tragic incident, transmission of HIV from a Florida dentist to six patients has been documented by genetic analyses of virus isolated from both the dentist and the patients. The dentist and three of the patients developed AIDS and died, and at least one of the other patients has developed AIDS. Five of the patients had no HIV risk factors other than multiple visits to the dentist for invasive procedures (O'Brien, Goedert. Curr Opin Immunol 1996;8:613; O'Brien, 1997; Ciesielski et al. Ann Intern Med 1994;121:886). In addition, through December 1999, the CDC had received reports of 56 health care workers in the United States with documented, occupationally acquired HIV infection, of whom 25 have developed AIDS in the absence of other risk factors. The development of AIDS following known HIV seroconversion also has been repeatedly observed in pediatric and adult blood transfusion cases, in mother-to-child transmission, and in studies of hemophilia, injection-drug use and sexual transmission in which seroconversion can be documented using serial blood samples (CDC. HIV AIDS Surveillance Report 1999;11[2]:1; AIDS Knowledge Base, 1999). For example, in a 10-year study in the Netherlands, researchers followed 11 children who had become infected with HIV as neonates by small aliquots of plasma from a single HIV-infected donor. During the 10-year period, eight of the children died of AIDS. Of the remaining three children, all showed a progressive decline in cellular immunity, and two of the three had symptoms probably related to HIV infection (van den Berg et al. Acta Paediatr 1994;83:17). Koch's postulates also have been fulfilled in animal models of human AIDS. Chimpanzees experimentally infected with HIV have developed severe immunosuppression and AIDS. In severe combined immunodeficiency (SCID) mice given a human immune system, HIV produces similar patterns of cell killing and pathogenesis as seen in people. HIV-2, a less virulent variant of HIV which causes AIDS in people, also causes an AIDS-like syndrome in baboons. More than a dozen strains of simian immunodeficiency virus (SIV), a close cousin of HIV, cause AIDS in Asian macaques. In addition, chimeric viruses known as SHIVs, which contain an SIV backbone with various HIV genes in place of the corresponding SIV genes, cause AIDS in macaques. Further strengthening the association of these viruses with AIDS, researchers have shown that SIV/SHIVs isolated from animals with AIDS cause AIDS when transmitted to uninfected animals (O'Neil et al. J Infect Dis 2000;182:1051; Aldrovandi et al. Nature 1993;363:732; Liska et al. AIDS Res Hum Retroviruses 1999;15:445; Locher et al. Arch Pathol Lab Med 1998;22:523; Hirsch et al. Virus Res 1994;32:183; Joag et al. J Virol 1996;70:3189). AIDS and HIV infection are invariably linked in time, place and population group. Historically, the occurence of AIDS in human populations around the world has closely followed the appearance of HIV. In the United States, the first cases of AIDS were reported in 1981 among homosexual men in New York and California, and retrospective examination of frozen blood samples from a U.S. cohort of gay men showed the presence of HIV antibodies as early as 1978, but not before then. Subsequently, in every region, country and city where AIDS has appeared, evidence of HIV infection has preceded AIDS by just a few years (CDC. MMWR 1981;30:250; CDC. MMWR 1981;30:305; Jaffe et al. Ann Intern Med 1985;103:210; U.S. Census Bureau; UNAIDS). Many studies agree that only a single factor, HIV, predicts whether a person will develop AIDS. Other viral infections, bacterial infections, sexual behavior patterns and drug abuse patterns do not predict who develops AIDS. Individuals from diverse backgrounds, including heterosexual men and women, homosexual men and women, hemophiliacs, sexual partners of hemophiliacs and transfusion recipients, injection-drug users and infants have all developed AIDS, with the only common denominator being their infection with HIV (NIAID, 1995). In cohort studies, severe immunosuppression and AIDS-defining illnesses occur almost exclusively in individuals who are HIV-infected. For example, analysis of data from more than 8,000 participants in the Multicenter AIDS Cohort Study (MACS) and the Women's Interagency HIV Study (WIHS) demonstrated that participants who were HIV-seropositive were 1,100 times more likely to develop an AIDS-associated illness than those who were HIV-seronegative. These overwhelming odds provide a clarity of association that is unusual in medical research (MACS and WIHS Principal Investigators, 2000). In a Canadian cohort, investigators followed 715 homosexual men for a median of 8.6 years. Every case of AIDS in this cohort occurred in individuals who were HIV-seropositive. No AIDS-defining illnesses occurred in men who remained negative for HIV antibodies, despite the fact that these individuals had appreciable patterns of illicit drug use and receptive anal intercourse (Schechter et al. Lancet 1993;341:658). Before the appearance of HIV, AIDS-related diseases such as PCP, KS and MAC were rare in developed countries; today, they are common in HIV-infected individuals. Prior to the appearance of HIV, AIDS-related conditions such as Pneumocystis carinii pneumonia (PCP), Kaposi's sarcoma (KS) and disseminated infection with the Mycobacterium avium complex (MAC) were extraordinarily rare in the United States. In a 1967 survey, only 107 cases of PCP in the United States had been described in the medical literature, virtually all among individuals with underlying immunosuppressive conditions. Before the AIDS epidemic, the annual incidence of Kaposi's sarcoma in the United States was only 0.2 to 0.6 cases per million population, and only 32 individuals with disseminated MAC disease had been described in the medical literature (Safai. Ann NY Acad Sci 1984;437:373; Le Clair. Am Rev Respir Dis 1969;99:542; Masur. JAMA 1982;248:3013). By the end of 1999, CDC had received reports of 166,368 HIV-infected patients in the United States with definitive diagnoses of PCP, 46,684 with definitive diagnoses of KS, and 41,873 with definitive diagnoses of disseminated MAC (personal communication). In developing countries, patterns of both rare and endemic diseases have changed dramatically as HIV has spread, with a far greater toll now being exacted among the young and middle-aged, including well-educated members of the middle class. In developing countries, the emergence of the HIV epidemic has dramatically changed patterns of disease in affected communities. As in developed countries, previously rare, "opportunistic" diseases such as PCP and certain forms of meningitis have become more commonplace. In addition, as HIV seroprevalence rates have risen, there have been significant increases in the burden of endemic conditions such as tuberculosis (TB), particularly among young people. For example, as HIV seroprevalence increased sharply in Blantyre, Malawi from 1986 to 1995, tuberculosis admissions at the city's main hospital rose more than 400 percent, with the largest increase in cases among children and young adults. In the rural Hlabisa District of South Africa, admissions to tuberculosis wards increased 360 percent from 1992 to 1998, concomitant with a steep rise in HIV seroprevalence. High rates of mortality due to endemic conditions such as TB, diarrheal diseases and wasting syndromes, formerly confined to the elderly and malnourished, are now common among HIV-infected young and middle-aged people in many developing countries (UNAIDS, 2000; Harries et al. Int J Tuberc Lung Dis 1997;1:346; Floyd et al. JAMA 1999;282:1087). In studies conducted in both developing and developed countries, death rates are markedly higher among HIV-seropositive individuals than among HIV-seronegative individuals. For example, Nunn and colleagues (BMJ 1997;315:767) assessed the impact of HIV infection over five years in a rural population in the Masaka District of Uganda. Among 8,833 individuals of all ages who had an unambiguous result on testing for HIV-antibodies (either 2 or 3 different test kits were used for blood samples from each individual), HIV-seropositive people were 16 times more likely to die over five years than HIV-seronegative people (see table). Among individuals ages 25 to 34, HIV-seropositive people were 27 times more likely to die than HIV-seronegative people. In another study in Uganda, 19,983 adults in the rural Rakai District were followed for 10 to 30 months (Sewankambo et al. AIDS 2000;14:2391). In this cohort, HIV-seropositive people were 20 times more likely to die than HIV-seronegative people during 31,432 person-years of observation. Similar findings have emerged from other studies (Boerma et al. AIDS 1998;12(suppl 1):S3); for example, * in Tanzania, HIV-seropositive people were 12.9 time more likely to die over two years than HIV-seronegative people (Borgdorff et al. Genitourin Med 1995;71:212) * in Malawi, mortality over three years among children who survived the first year of life was 9.5 times higher among HIV-seropositive children than among HIV-seronegative children (Taha et al. Pediatr Infect Dis J 1999;18:689) * in Rwanda, mortality was 21 times higher for HIV-seropositive children than for HIV-seronegative children after five years (Spira et al. Pediatrics 1999;14:e56). Among the mothers of these children, mortality was 9 times higher among HIV-seropositive women than among HIV-seronegative women in four years of follow-up (Leroy et al. J Acquir Immune Defic Syndr Hum Retrovirol 1995;9:415). * in Cote d'Ivoire, HIV-seropositive individuals with pulmonary tuberculosis (TB) were 17 times more likely to die within six months than HIV-seronegative individuals with pulmonary TB (Ackah et al. Lancet 1995; 345:607). * in the former Zaire (now the Democratic Republic of Congo), HIV-infected infants were 11 times more likely to die from diarrhea than uninfected infants (Thea et al. NEJM 1993;329:1696). * in South Africa, the death rate for children hospitalized with severe lower respiratory tract infections was 6.5 times higher for HIV-infected infants than for uninfected children (Madhi et al. Clin Infect Dis 2000;31:170). Kilmarx and colleagues (Lancet 2000; 356:770) recently reported data on HIV infection and mortality in a cohort of female commercial sex workers in Chiang Rai, Thailand. Among 500 women enrolled in the study between 1991 and 1994, the mortality rate through October 1998 among women who were HIV-infected at enrollment (59 deaths among 160 HIV-infected women) was 52.7 times higher than among women who remained uninfected with HIV (2 deaths among 306 uninfected women). The mortality rate among women who became infected during the study (7 deaths among 34 seroconverting women) was 22.5 higher than among persistently uninfected women. Among the HIV-infected women, only 3 of whom received antiretroviral medications, all reported causes of death were associated with immunosuppression, whereas the reported causes of death of the two uninfected women were postpartum amniotic embolism and gunshot wound. Excess mortality among HIV-seropositive people also has been repeatedly observed in studies in developed countries, perhaps most dramatically among hemophiliacs. For example, Darby et al. (Nature 1995;377:79) studied 6,278 hemophiliacs living in the United Kingdom during the period 1977-91. Among 2,448 individuals with severe hemophilia, the annual death rate was stable at 8 per 1,000 during 1977-84. While death rates remained stable at 8 per 1,000 from 1985-1992 among HIV-seronegative persons with severe hemophilia, deaths rose steeply among those who had become HIV-seropositive following HIV-tainted transfusions during 1979-1986, reaching 81 per 1,000 in 1991-92. Among 3,830 individuals with mild or moderate hemophilia, the pattern was similar, with an initial death rate of 4 per 1,000 in 1977-84 that remained stable among HIV-seronegative individuals but rose to 85 per 1,000 in 1991-92 among seropositive individuals. Similar data have emerged from the Multicenter Hemophilia Cohort Study. Among 1,028 hemophiliacs followed for a median of 10.3 years, HIV-infected individuals (n=321) were 11 times more likely to die than HIV-negative subjects (n=707), with the dose of Factor VIII having no effect on survival in either group (Goedert. Lancet 1995;346:1425). In the Multicenter AIDS Cohort Study (MACS), a 16-year study of 5,622 homosexual and bisexual men, 1,668 of 2,761 HIV-seropositive men have died (60 percent), 1,547 after a diagnosis of AIDS. In contrast, among 2,861 HIV-seronegative participants, only 66 men (2.3 percent) have died (A. Munoz, MACS, personal communication). HIV can be detected in virtually everyone with AIDS. Recently developed sensitive testing methods, including the polymerase chain reaction (PCR) and improved culture techniques, have enabled researchers to find HIV in patients with AIDS with few exceptions. HIV has been repeatedly isolated from the blood, semen and vaginal secretions of patients with AIDS, findings consistent with the epidemiologic data demonstrating AIDS transmission via sexual activity and contact with infected blood (Hammer et al. J Clin Microbiol 1993;31:2557; Jackson et al. J Clin Microbiol 1990;28:16). Numerous studies of HIV-infected people have shown that high levels of infectious HIV, viral antigens, and HIV nucleic acids (DNA and RNA) in the body predict immune system deterioration and an increased risk for developing AIDS. Conversely, patients with low levels of virus have a much lower risk of developing AIDS. For example, in an anlysis of 1,604 HIV-infected men in the Multicenter AIDS Cohort Study (MACS), the risk of a patient developing AIDS with six years was strongly associated with levels of HIV RNA in the plasma as measured by a sensitive test known as the branched-DNA signal-amplification assay (bDNA): Plasma RNA concentration (copies/mL of blood) Proportion of patients developing AIDS within six years 30,000 5.4% 16.6% 31.7% 55.2% 80.0% (Source: Mellors et al. Ann Intern Med 1997;126:946) Similar associations between increasing HIV RNA levels and a greater risk of disease progression have been observed in HIV-infected children in both developed and developing countries (Palumbo et al. JAMA 1998;279:756; Taha et al. AIDS 2000;14:453). In the very small proportion of untreated HIV-infected individuals whose disease progresses very slowly, the amount of HIV in the blood and lymph nodes is significantly lower than in HIV-infected people whose disease progression is more typical (Pantaleo et al. NEJM 1995;332:209; Cao et al. NEJM 1995;332:201; Barker et al. Blood 1998;92:3105). The availability of potent combinations of drugs that specifically block HIV replication has dramatically improved the prognosis for HIV-infected individuals. Such an effect would not be seen if HIV did not have a central role in causing AIDS. Clinical trials have shown that potent three-drug combinations of anti-HIV drugs, known as highly active antiretroviral therapy (HAART), can significantly reduce the incidence of AIDS and death among HIV-infected individuals as compared to previously available HIV treatment regimens (Hammer et al. NEJM 1997;337:725; Cameron et al. Lancet 1998;351:543). Use of these 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, among both adults and children (Figure 1; CDC. HIV AIDS Surveillance Report 1999;11[2]:1; Palella et al. NEJM 1998;338:853; Mocroft et al. Lancet 1998;352:1725; Mocroft et al. Lancet 2000;356:291; Vittinghoff et al. J Infect Dis 1999;179:717; Detels et al. JAMA 1998;280:1497; de Martino et al. JAMA 2000;284:190; CASCADE Collaboration. Lancet 2000;355:1158; Hogg et al. CMAJ 1999;160:659; Schwarcz et al. Am J Epidemiol 2000;152:178; Kaplan et al. Clin Infect Dis 2000;30:S5; McNaghten et al. AIDS 1999;13:1687;). For example, in a prospective study of more than 7,300 HIV-infected patients in 52 European outpatient clinics, the incidence of new AIDS-defining illnesses declined from 30.7 per 100 patient-years of observation in 1994 (before the availability of HAART) to 2.5 per 100 patient years in 1998, when the majority of patients received HAART (Mocroft et al. Lancet 2000;356:291). Among HIV-infected patients who receive anti-HIV therapy, those whose viral loads are driven to low levels are much less likely to develop AIDS or die than patients who do not respond to therapy. Such an effect would not be seen if HIV did not have a central role in causing AIDS. Clinical trials in both HIV-infected children and adults have demonstrated a link between a good virologic response to therapy (i.e. much less virus in the body) and a reduced risk of developing AIDS or dying (Montaner et al. AIDS 1998;12:F23; Palumbo et al. JAMA 1998;279:756; O'Brien et al. NEJM 1996;334:426; Katzenstein et al. NEJM 1996;335:1091; Marschner et al. J Infect Dis 1998;177:40; Hammer et al. NEJM 1997;337:725; Cameron et al. Lancet 1998;351:543). This effect has also been seen in routine clinical practice. For example, in an analysis of 2,674 HIV-infected patients who started highly active antiretroviral therapy (HAART) in 1995-1998, 6.6 percent of patients who achieved and maintained undetectable viral loads (<400 copies/mL of blood) developed AIDS or died within 30 months, compared with 20.1 percent of patients who never achieved undetectable concentrations (Ledergerber et al. Lancet 1999;353:863). Nearly everyone with AIDS has antibodies to HIV. A survey of 230,179 AIDS patients in the United States revealed only 299 HIV-seronegative individuals. An evaluation of 172 of these 299 patients found 131 actually to be seropositive; an additional 34 died before their serostatus could be confirmed (Smith et al. N Engl J Med 1993;328:373). Numerous serosurveys show that AIDS is common in populations where many individuals have HIV antibodies. Conversely, in populations with low seroprevalence of HIV antibodies, AIDS is extremely rare. For example, in the southern African country of Zimbabwe (population 11.4 million), more than 25 percent of adults ages 15 to 49 are estimated to be HIV antibody-positive, based on numerous studies. As of November 1999, more than 74,000 cases of AIDS in Zimbabwe had been reported to the World Health Organization (WHO). In contrast, Madagascar, an island country off the southeast coast of Africa (population 15.1 million) with a very low HIV seroprevalence rate, reported only 37 cases of AIDS to WHO through November 1999. Yet, other sexually transmitted diseases, notably syphilis, are common in Madagascar, suggesting that conditions are ripe for the spread of HIV and AIDS if the virus becomes entrenched in that country (U.S. Census Bureau; UNAIDS, 2000; WHO. Wkly Epidemiol Rec 1999;74:1; Behets et al. Lancet 1996;347:831). The specific immunologic profile that typifies AIDS - a persistently low CD4+ T-cell count - is extraordinarily rare in the absence of HIV infection or other known cause of immunosuppression. For example, in the NIAID-supported Multicenter AIDS Cohort Study (MACS), 22,643 CD4+ T-cell determinations in 2,713 HIV-seronegative homosexual and bisexual men revealed only one individual with a CD4+ T-cell count persistently lower than 300 cells/mm3 of blood, and this individual was receiving immunosuppressive therapy. Similar results have been reported from other studies (Vermund et al. NEJM 1993;328:442; NIAID, 1995). Newborn infants have no behavioral risk factors for AIDS, yet many children born to HIV-infected mothers have developed AIDS and died. Only newborns who become HIV-infected before or during birth, during breastfeeding, or (rarely) following exposure to HIV-tainted blood or blood products after birth, go on to develop the profound immunosuppression that leads to AIDS. Babies who are not HIV-infected do not develop AIDS. In the United States, 8,718 cases of AIDS among children younger than age 13 had been reported to the CDC as of December 31, 1999. Cumulative U.S. AIDS deaths among individuals younger than age 15 numbered 5,044 through December 31, 1999. Globally, UNAIDS estimates that 480,000 child deaths due to AIDS occurred in 1999 alone (CDC. HIV/AIDS Surveillance Report 1999;11[2]:1; UNAIDS. AIDS epidemic update: June 2000). Because many HIV-infected mothers abuse recreational drugs, some have argued that maternal drug use itself causes pediatric AIDS. However, studies have consistently shown that babies who are not HIV-infected do not develop AIDS, regardless of their mothers' drug use (European Collaborative Study. Lancet 1991;337:253; European Collaborative Study. Pediatr Infect Dis J 1997;16:1151; Abrams et al. Pediatrics 1995;96:451). For example, a majority of the HIV-infected, pregnant women enrolled in the European Collaborative Study are current or former injection drug users. In this ongoing study, mothers and their babies are followed from birth in 10 centers in Europe. In a paper in Lancet, study investigators reported that none of 343 HIV-seronegative children born to HIV-seropositive mothers had developed AIDS or persistent immune deficiency. In contrast, among 64 seropositive children, 30 percent presented with AIDS within 6 months of age or with oral candidiasis followed rapidly by the onset of AIDS. By their first birthday, 17 percent died of HIV-related diseases (European Collaborative Study. Lancet 1991;337:253). In a study in New York, investigators followed 84 HIV-infected and 248 HIV-uninfected infants, all born to HIV-seropositive mothers. The mothers of the two groups of infants were equally likely to be injection drug users (47 percent vs. 50 percent), and had similar rates of alcohol, tobacco, cocaine, heroin and methadone use. Of the 84 HIV-infected children, 22 died during a median follow-up period of 27.6 months, including 20 infants who died before their second birthday. Twenty-one of these deaths were classified as AIDS-related. Among the 248 uninfected children, only one death (due to child abuse) was reported during a median follow-up period of 26.1 months (Abrams et al. Pediatrics 1995;96:451). The HIV-infected twin develops AIDS while the uninfected twin does not. Because twins share an in utero environment and genetic relationships, similarities and differences between them can provide important insight into infectious diseases, including AIDS (Goedert. Acta Paediatr Supp 1997;421:56). Researchers have documented cases of HIV-infected mothers who have given birth to twins, one of whom is HIV-infected and the other not. The HIV-infected children developed AIDS, while the other children remained clinically and immunologically normal (Park et al. J Clin Microbiol 1987;25:1119; Menez-Bautista et al. Am J Dis Child 1986;140:678; Thomas et al. Pediatrics 1990;86:774; Young et al. Pediatr Infect Dis J 1990;9:454; Barlow and Mok. Arch Dis Child 1993;68:507; Guerrero Vazquez et al. An Esp Pediatr 1993;39:445). Studies of transfusion-acquired AIDS cases have repeatedly led to the discovery of HIV in the patient as well as in the blood donor. Numerous studies have shown an almost perfect correlation between the occurrence of AIDS in a blood recipient and donor, and evidence of homologous HIV strains in both the recipient and the donor (NIAID, 1995). HIV is similar in genetic structure and morphology to other lentiviruses that often cause immunodeficiency in their animal hosts in addition to slow, progressive wasting disorders, neurodegeneration and death. Like HIV in humans, animal viruses such as feline immunodeficiency virus (FIV) in cats, visna virus in sheep and simian immunodeficiency virus (SIV) in monkeys primarily infect cells of the immune system such as T cells and macrophages. For example, visna virus infects macrophages and causes a slowly progressive neurologic disease (Haase. Nature 1986;322:130). HIV causes the death and dysfunction of CD4+ T lymphocytes in vitro and in vivo. CD4+ T cell dysfunction and depletion are hallmarks of HIV disease. The recognition that HIV infects and destroys CD4+ T cells in vitro strongly suggests a direct link between HIV infection, CD4+ T cell depletion, and development of AIDS. A variety of mechanisms, both directly and indirectly related to HIV infection of CD4+ T cells, are likely responsible for the defects in CD4+ T cell function observed in HIV-infected people. Not only can HIV enter and kill CD4+ T cells directly, but several HIV gene products may interfere with the function of uninfected cells (NIAID, 1995; Pantaleo et al. NEJM 1993;328:327). ANSWERING THE SKEPTICS: RESPONSES TO ARGUMENTS THAT HIV DOES NOT CAUSE AIDS MYTH: HIV antibody testing is unreliable. FACT: Diagnosis of infection using antibody testing is one of the best-established concepts in medicine. HIV antibody tests exceed the performance of most other infectious disease tests in both sensitivity (the ability of the screening test to give a positive finding when the person tested truly has the disease ) and specificity (the ability of the test to give a negative finding when the subjects tested are free of the disease under study). Current HIV antibody tests have sensitivity and specificity in excess of 98% and are therefore extremely reliable (WHO, 1998; Sloand et al. JAMA 1991;266:2861). Progress in testing methodology has also enabled detection of viral genetic material, antigens and the virus itself in body fluids and cells. While not widely used for routine testing due to high cost and requirements in laboratory equipment, these direct testing techniques have confirmed the validity of the antibody tests (Jackson et al. J Clin Microbiol 1990;28:16; Busch et al. NEJM 1991;325:1; Silvester et al. J Acquir Immune Defic Syndr Hum Retrovirol 1995;8:411; Urassa et al. J Clin Virol 1999;14:25; Nkengasong et al. AIDS 1999;13:109; Samdal et al. Clin Diagn Virol 1996;7:55. MYTH: There is no AIDS in Africa. AIDS is nothing more than a new name for old diseases. FACT: The diseases that have come to be associated with AIDS in Africa - such as wasting syndrome, diarrheal diseases and TB - have long been severe burdens there. However, high rates of mortality from these diseases, formerly confined to the elderly and malnourished, are now common among HIV-infected young and middle-aged people, including well-educated members of the middle class (UNAIDS, 2000). For example, in a study in Cote d'Ivoire, HIV-seropositive individuals with pulmonary tuberculosis (TB) were 17 times more likely to die within six months than HIV-seronegative individuals with pulmonary TB (Ackah et al. Lancet 1995; 345:607). In Malawi, mortality over three years among children who had received recommended childhood immunizations and who survived the first year of life was 9.5 times higher among HIV-seropositive children than among HIV-seronegative children. The leading causes of death were wasting and respiratory conditions (Taha et al. Pediatr Infect Dis J 1999;18:689). Elsewhere in Africa, findings are similar. MYTH: HIV cannot be the cause of AIDS because researchers are unable to explain precisely how HIV destroys the immune system. FACT: 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. The critics' reasoning would lead to the conclusion that M. tuberculosis is not the cause of tuberculosis or that hepatitis B virus is not a cause of liver disease (Evans. Yale J Biol Med 1982;55:193). MYTH: AZT and other antiretroviral drugs, not HIV, cause AIDS. FACT: The vast majority of people with AIDS never received antiretroviral drugs, including those in developed countries prior to the licensure of AZT in 1987, and people in developing countries today where very few individuals have access to these medications (UNAIDS, 2000). As with medications for any serious diseases, antiretroviral drugs can have toxic side effects. However, there is no evidence that antiretroviral drugs cause the severe immunosuppression that typifies AIDS, and abundant evidence that antiretroviral therapy, when used according to established guidelines, can improve the length and quality of life of HIV-infected individuals. In the 1980s, clinical trials enrolling patients with AIDS found that AZT given as single-drug therapy conferred a modest (and short-lived) survival advantage compared to placebo. Among HIV-infected patients who had not yet developed AIDS, placebo-controlled trials found that AZT given as single-drug therapy delayed, for a year or two, the onset of AIDS-related illnesses. Significantly, long-term follow-up of these trials did not show a prolonged benefit of AZT, but also never indicated that the drug increased disease progression or mortality. 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 (NIAID, 1995). Subsequent clinical trials found that patients receiving two-drug combinations had up to 50 percent 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 percent to 80 percent improvements in progression to AIDS and in survival when compared to two-drug regimens in clinical trials (HHS, 2004). 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 clearly would not be seen if antiretroviral drugs caused AIDS (Figure 1; CDC. HIV AIDS Surveillance Report 1999;11[2]:1; Palella et al. NEJM 1998;338:853; Mocroft et al. Lancet 1998;352:1725; Mocroft et al. Lancet 2000;356:291; Vittinghoff et al. J Infect Dis 1999;179:717; Detels et al. JAMA 1998;280:1497; de Martino et al. JAMA 2000;284:190; CASCADE Collaboration. Lancet 2000;355:1158; Hogg et al. CMAJ 1999;160:659; Schwarcz et al. Am J Epidemiol 2000;152:178; Kaplan et al. Clin Infect Dis 2000;30:S5; McNaghten et al. AIDS 1999;13:1687). MYTH: Behavioral factors such as recreational drug use and multiple sexual partners account for AIDS. FACT: 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 (NIAID, 1995a; NIAID, 1995b). 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, 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 inhalable nitrites ("poppers") and other recreational drugs, and frequent receptive anal intercourse (Schechter et al. Lancet 1993;341:658). 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 cells - 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/mm3 of blood, and this individual was receiving immunosuppressive therapy (Vermund et al. NEJM 1993;328:442). 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/mm3 of blood. Only two individuals had two CD4+ T-cell measurements of less than 300/mm3 of blood, one of whom died with cardiac disease and non-Hodgkin's lymphoma listed as the cause of death (Des Jarlais et al. J Acquir Immune Defic Syndr 1993;6:820). MYTH: AIDS among transfusion recipients is due to underlying diseases that necessitated the transfusion, rather than to HIV. FACT: 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 transfusions for similar diseases. Approximately 3 years after the transfusion, the mean CD4+ T-cell count in 64 HIV-negative recipients was 850/mm3 of blood, while 111 HIV-seropositive individuals had average CD4+ T-cell counts of 375/mm3 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 (Donegan et al. Ann Intern Med 1990;113:733; Cohen. Science 1994;266:1645). MYTH: High usage of clotting factor concentrate, not HIV, leads to CD4+ T-cell depletion and AIDS in hemophiliacs. FACT: 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 (Hasset et al. Blood 1993;82:1351). In another report from the Transfusion Safety Study, no instances of AIDS-defining illnesses were seen among 402 HIV-seronegative hemophiliacs who had received factor therapy (Aledort et al. NEJM 1993;328:1128). In a cohort in the United Kingdom, researchers matched 17 HIV-seropositive hemophiliacs 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/mm3 lower in the HIV-seropositive patient (Sabin et al. BMJ 1996;312:207). 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 (Gjerset et al., Blood 1994;84:1666). Similarly, the Multicenter Hemophilia Cohort Study found no association between the cumulative dose of plasma concentrate and incidence of AIDS among HIV-infected hemophiliacs (Goedert et al. NEJM 1989;321:1141.). MYTH: 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. FACT: 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 homosexual men and injection-drug users, a majority of whom are male. Because HIV is spread primarily through sex or by the exchange of HIV-contaminated needles during injection-drug use, it is not surprising that a majority of U.S. AIDS cases have occurred in men (U.S. Census Bureau, 1999; UNAIDS, 2000). Increasingly, however, women in the United States are becoming HIV-infected, usually through the exchange of HIV-contaminated needles or sex with an HIV-infected male. The 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 percent 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 (NIAID Fact Sheet: HIV/AIDS Statistics). In Africa, HIV was first recognized in sexually active heterosexuals, 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 (U.S. Census Bureau, 1999; UNAIDS, 2000). MYTH: HIV cannot be the cause of AIDS because the body develops a vigorous antibody response to the virus. FACT: This reasoning ignores numerous examples of viruses other than HIV that can be pathogenic after evidence of immunity appears. Measles virus may persist for years in brain cells, eventually causing a chronic neurologic disease despite the presence of antibodies. Viruses such as cytomegalovirus, herpes simplex and varicella zoster may be activated after years of latency even in the presence of abundant antibodies. In animals, viral relatives of HIV with long and variable latency periods, such as visna virus in sheep, cause central nervous system damage even after the production of antibodies (NIAID, 1995). Also, HIV is well recognized as being able to mutate to avoid the ongoing immune response of the host (Levy. Microbiol Rev 1993;57:183). MYTH: Only a small number of CD4+ T cells are infected by HIV, not enough to damage the immune system. FACT: New techniques such as the polymerase chain reaction (PCR) have enabled scientists to demonstrate that a much larger proportion of CD4+ T cells are infected than previously realized, particularly in lymphoid tissues. Macrophages and other cell types are also infected with HIV and serve as reservoirs for the virus. Although the fraction of CD4+ T cells that is infected with HIV at any given time is never extremely high (only a small subset of activated cells serve as ideal targets of infection), several groups have shown that rapid cycles of death of infected cells and infection of new target cells occur throughout the course of disease (Richman J Clin Invest 2000;105:565). MYTH: HIV is not the cause of AIDS because many individuals with HIV have not developed AIDS. FACT: HIV disease has 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 (Alcabes et al. Epidemiol Rev 1993;15:303). 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 (Evans. Yale J Biol Med 1982;55:193; Levy. Microbiol Rev 1993;57:183; Fauci. Nature 1996;384:529). MYTH: Some people have many symptoms associated with AIDS but do not have HIV infection. FACT: Most AIDS symptoms result from the development of opportunistic infections and cancers associated with severe immunosuppression secondary to HIV. However, immunosuppression has many other potential causes. Individuals who take glucocorticoids and/or immunosuppressive drugs to prevent transplant rejection or for autoimmune diseases can have increased susceptibility to unusual infections, as do individuals with certain 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 staggering rise in cases of immunosuppression among individuals who share one characteristic: HIV infection (NIAID, 1995; UNAIDS, 2000). MYTH: The spectrum of AIDS-related infections seen in different populations proves that AIDS is actually many diseases not caused by HIV. FACT: The diseases associated with AIDS, such as PCP and 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 viral, fungal and bacterial infections common in the community. For example, HIV-infected people in certain midwestern and mid-Atlantic regions 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 different pathogens than is an individual in an American city. Children may be exposed to different infectious agents than adults (USPHS/IDSA, 2001). More information on this issue is available on the NIAID Focus On the HIV-AIDS Connection web page.
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Nog vragen? Stel ze dan bij ons, dan geeft Wilhelm, die tenminste wel verstand heeft van virussen antwoord. ;)
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Nou, en welke van de 2 artikelen gebruikt degelijke bronvermeldingen denk je? Mag jij raden!
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Niet dat van jou...
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Dit zijn de mensen van rethinking AIDS. Dan heb je ook nog 3 Nobelprijswinnaren chemie die hetzelfde zeggen: AIDS is niet besmettelijk en wordt niet veroorzaakt door HIV. Allemaal nutcases zeker? Nobelprijs gekocht zeker? Etienne de Harven, MD Rethinking AIDS President Member and Professor in cell biology, Sloan Kettering Institute, New York, 1956-1981. Isolated and obtained the first electron microscopic studies of the murine Friend leukemia virus, and retroviral budding. Director of the Electron Microscopy Laboratory at the Banting Institute, Department of Pathology, University of Toronto. He is also a member of South Africa's Presidential AIDS Advisory Panel. etienne.deharven@rethinkingaids.com And, in alphabetical order (by last name): David Crowe Rethinking AIDS Treasurer HBSc Hons. Biology/Mathematics, 1978 (Lakehead University, Ontario). President, Alberta Reappraising AIDS Society. Treasurer, Green Party of Alberta. david.crowe@rethinkingaids.com Peter H. Duesberg, PhD Professor of molecular and cell biology at the University of California, Berkeley. In 1968-1970 he demonstrated that influenza virus has a segmented genome. This would explain its unique ability to form recombinants by reassortment of subgenomic segments. He isolated the first cancer gene through his work on retroviruses in 1970, and mapped the genetic structure of these viruses. This, and his subsequent work in the same field, resulted in his election to the National Academy of Sciences in 1986. He was also the recipient of a seven-year Outstanding Investigator Grant from the National Institutes of Health from 1985-1992. He is also a member of South Africa's Presidential AIDS Advisory Panel. peter.duesberg@rethinkingaids.com Charles L. Geshekter, PhD Professor of African history at California State University, Chico, recipient of grants from the Ford Foundation, Fulbright-Hayes, National Endowment for the Humanities and Social Science Research Council. From 1991-95, he chaired the History of Science Section of the AAAS and was a member of its Executive Council. He is also a member of South Africa's Presidential AIDS Advisory Panel. charles.geshekter@rethinkingaids.com Roberto Giraldo, MD (University of Antioquia, Colombia, specialty internal medicine) ; Master of Science in infectious and tropical diseases (U. of London, The London School of Hygiene and Tropical Medicine). Member of South Africa's Presidential AIDS Advisory Panel. roberto.giraldo@rethinkingaids.com Claus Koehnlein, MD Specialist in internal medicine, Dept. of Oncology, Univ. of Kiel, Germany (1983 -1993). Since 1993, in private practice increasingly treating HIV- positive people who decline antiviral drugs. Member of SA Presidential AIDS Advisory Panel. claus.koehnlein@rethinkingaids.com Robert Leppo BA, Stanford University (1965); MBA, Harvard Business School (1969). Historian, philanthropist, and investor. robert.leppo@rethinkingaids.com Frank Lusardi Professional software development. frank.lusardi@rethinkingaids.com Christine Maggiore Founder/director of Alive & Well AIDS Alternatives and author of the book What If Everything You Thought You Knew About AIDS Was Wrong? A former public speaker and educator for AIDS Project Los Angeles and founding board member of Women at Risk, Maggiore tested HIV positive in 1992 and lives in health without AIDS medications. christine.maggiore@rethinkingaids.com Bryan Owen Rethinking AIDS Webmaster Web application developer for several commercial and Department of Defense projects including workflow, document management, and business-to-business e-Commerce systems. bryan.owen@rethinkingaids.com David Rasnick, PhD Senior Researcher, Rath Health Foundation, Africa. Between 1978 and 1996, he worked as a pharmaceutical protein chemist at Abbott Laboratories, Enzyme Systems Products, Prototek, Inc., and Khepri Pharmaceuticals. He was a visiting scholar at the department of molecular and cell biology, UC Berkeley (1996-2005), where he worked in the Duesberg laboratory on the aneuploidy theory of cancer. He is also a member of South Africa's Presidential AIDS Advisory Panel. david.rasnick@rethinkingaids.com Gordon Stewart, MD Emeritus Professor of Public Health, Univ Glasgow, UK; Formerly professor of epidemiology, Univ. NC at Chapel Hill, NC; Watkins Chair of Epidemiologyepid and professor medicine, Tulane Univ., New Orleans, LAa; consultant, New York City Health Dept; WHO; Senior Visiting Fellow, US National Science Foundation; emeritus fellow, Infectious Diseases Soc. America. Member of South Africa's Presidential AIDS Advisory Panel. gordon.stewart@rethinkingaids.com
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"Niet dat van jou..." HAHAHAHA!! Dat is een AIDS-ontkennertje ten top. Het is het artikel waar de beweringen onderbouwd worden met werkelijke resultaten uit onderzoeken dus zeg je maar lekker dat dat geen goede bronvermeldingen zijn, in tegenstelling tot... ja hoor!
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"Dit zijn de mensen van rethinking AIDS. Dan heb je ook nog 3 Nobelprijswinnaren chemie die hetzelfde zeggen: AIDS is niet besmettelijk en wordt niet veroorzaakt door HIV. Allemaal nutcases zeker? Nobelprijs gekocht zeker? " Waarvan een dus Peter Duesberg is die in 1997 al de vloer aanveegde met de claims van de Perth Group dat het bestaan van HIV nooit is aangetoond. Waarom kies je er toch voor om dat steeds te vergeten? O laat maar, ik weet het al. En inderdaad, die Duesberg en Mullis zijn ergens ontspoord. Maar als je zo hecht aan Nobelprijswinnaars waarom heb je het dan niet over die ZEVEN nobelprijswinnaars die de Durban declaratie ondertekend hebben? Toch raar dat je zo op die titels staat terwijl je tegelijkertijd de hele "orthodoxie" veroordeelt. Het is typisch AIDS-ontkennertjesgedrag.
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Maar de stand van zaken op Zapruder is dus dit. We hebben: de schrijvers: -een fotograaf/software-ontwerper -een biochemicus die sinds de 2e helft van de jaren 70 niets meer heeft gepubliceerd het publiek: -een stuk of 7 HIV-geinfecteerden die eerder al op het forum van bovenstaande biochemicus kwamen. -de vaste zapruderkliek de inhoud: -herkauwen van de oude claims van de "aids-dissidenten" -vertellen wat de aids-dissidenten denken wat er in de echte onderzoeken staat. Wat ontbreekt er? -informatie over wat nu de werkelijke stand van zaken is in AIDS-onderzoek. -acceptatie van de feiten zoals ie er zijn. (bv. dat je in NL tegenwoordig heel oud kan worden met HIV) En waar verwijst Zapruder/Patman steeds naar? Steeds naar z'n eigen site, waar dus het grootste deel van het verhaal ontbreekt, nl. de werkelijke stand van zaken van 25 jaar AIDS-onderzoek en alle bevindingen.
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hier trouwens nog een (nieuw) goed artikel over HIV/AIDS ontkenners: http://medicine.plosjournals.org/perlserv/?requ... en kijk nou! het is geschreven door twee medici, niet door een fotograaf en een gesjeesde ex-biochemicus.
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@Brum D Geef het toch op, jongen... Zappie is zo'n rechtgeaarde complotter... die zal van zijn leven niet toegeven dattie ongelijk heeft. Al is heel de wereld het met hem oneens. Nu ik dit heb geschreven krijg ik ook wel weer het verwijt dat ik dom ben en mijn kop in het zand steek.... Kom er maar in, Zappie!
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Brummetje je hebt best argumenten, maar die verkleinwoordjes en dat denigrerend toontje. Laat dat toch achterwege! Voegt nl niets toe.
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Waardevol slagveld van meningen en feiten. Bedankt Brum en Zapr voor de bijdragen!
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"Laat dat toch achterwege! Voegt nl niets toe." O nee? Voegt dat niks toe? Hoeveel (afrikaanse) vrienden heb jij moeten begraven dan? En hoeveel familie? En dan komt er zo'n klootzak van een Patman keer op keer weer de oude HIV/AIDS-ontkenners-clichés uit de kast halen ter meerdere glorie van 'm zelf (want met opkomen voor HIV/AIDS-patienten heeft het geen zak te maken, alleen met Patman's strijd tegen "de orthodoxie"). Reken maar dat die verkleinwoordjes en dat denigrerende toontje iets toevoegen! Namelijk mijn woede en minachting voor zo'n megalomane klootzak als Patman. Wil je weten wat realiteit is over HIV/AIDS, kijk dan hier: http://www.quackwatch.org/04ConsumerEducation/h... Wil je meer onderbouwing, volg dan de links.
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Kijk, en dat is nou typisch de reactie die al die orthodoxe wetenschappers laten horen. Een normale discussie is al 20 jaar onmogelijk. Er zijn heel erg veel gereputeerde wetenschappers die serieus twijfelen aan HIV maar die gaan zich echt niet mengen in dit soort discussies. Wetenschap is al 20 jaar geleden vaarwel gezegd in dit deel van de onderzoekswereld. Veel geld, daar gaat het om, heel veel geld. En een enorme inteelt. Toen ik onderzoek deed hiernaar heb ik ze allemaal aan de lijn gehad, van HIVnet tot die toko van Joep de Lange en HIVmonitoring. Behalve dat het allemaal door pharma gesponsorde bedrijven zijn, hebben ze ook allemaal zo;n grote bek als die Brum. Normaal praten kunnen ze niet. Bewijzen laten zien ook niet. Het enige dat ze kunnen is enorme onderzoeksbudgetten verbranden en Afrikanen aan dodelijke troep stoppen. Met dank aan discussiestoppers als Brum. Zo;n Braad (Brum) heeft maar 1 verhaal: hij begint je meteen holocaust ontkenner en weet ik wat allemaal te noemen. Argumenten heeft hij niet behalve de napraterij van quasie-wetenschappers die hun geld verdienen aan AIDS en HIV.
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"Er zijn heel erg veel gereputeerde wetenschappers die serieus twijfelen aan HIV maar die gaan zich echt niet mengen in dit soort discussies." Nee, er zijn een paar handenvol roepers die achterhaalde argumenten van de AIDS-ontkenners blijven herkauwen. "Bewijzen laten zien ook niet. " hahaha! http://www.quackwatch.org/04ConsumerEducation/h... Voor de honderdste keer: er staan talloze bronverwijzingen in die links. Daar heb je je overvloed aan bewijzen. "hij begint je meteen holocaust ontkenner en weet ik wat allemaal te noemen." ach jongen toch. Wijs dat eens aan waar ik dat gezegd heb? "rgumenten heeft hij niet behalve de napraterij van quasie-wetenschappers die hun geld verdienen aan AIDS en HIV." Quasi-wetenschapper is een term die je op iemand als Godschalk kan toepassen, die al uit de wetenschappelijke wereld is gestapt nog vóór de jaren 80, toen AIDS voor het eerst beschreven werd. Typisch aan Patman is dat ie wel keer op keer loopt te schermen met z'n "3 nobelprijswinnaars", maar dat ie alle wetenschappers "quasi-wetenschappers" noemt omdat ze niet meegaan met z'n fantasietjes. En nog een keer: het probleem in Afrika is juist dat AIDS-remmers afwezig zijn (want te duur). In landen waar ze WEL aanwezig zijn sterven er nog maar weinig mensen aan AIDS. En dat keiharde feit verstoort Patman's fantasietje zo erg dat ie het maar blijft ontkennen. Weet je wat een discussiestopper is? Als je steeds alleen maar verwijst naar je eigen, volstrekt eenzijdige, artikelenreeks en steeds wegloopt als je geconfronteerd wordt met realiteit. Je hebt geen idee wat de werkelijke stand van zaken is, welke bewijzen en aanwijzingen er zijn, omdat je enkel en alleen luistert naar wat HIV/AIDS-ontkenners je vertellen wat de stand van zaken is. En dan krijg je dus die eeuwig herhalende onzin over "de klassieke manier om een virus te isoleren" die simpelweg zelf verzonnen is door de Perth Group; dat is al bekend sinds 1996, maar mensen als Patman, Godschalk en het kleine AIDS-ontkennerskliekje op Zapruder blijven het maar herhalen. En dan vinden ze het nog gek dat niemand met ze in discussie wil.. nou DAAROM! Je luistert niet naar feiten, maar herkauwt steeds je achterhaalde mantra's.
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Je hebt sowieso geen enkele intentie om te discussieren, Patman, maar je wil alleen maar evangeliseren. Zodra je de tegenargumenten boven het hoofd groeien, loop je weer laf weg, om het de volgende keer te proberen in de hoop dat het dan wel lukt zonder kritiek te krijgen. Het gaat je niet om de HIV/AIDS of om het lot van de miljoenen die ermee te maken hebben, maar alleen om je eigen messiaanse rol als Don Quichotte tegen "de orthodoxie". Het gaat je niet om de feiten (die je simpelweg ontkent), maar om het verspreiden van je boodschap. Moet ik dat nog eens opzoeken, dat comment op Zapruder waarin je toegeeft dat je "een missie" hebt met Zapruder en dat de comments in lijn met die missie moeten zijn? Dat was tenminste voor een keer een eerlijk comment.
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en vertel eens Patman, hoe kan het dat dit artikel na drie en een half uur nog maar 2 stemmen heeft ipv de gebruikelijke 20-30 stemmen van de zapruder spamdienst? Toch een beetje moeite met je eigen klapvee te overtuigen?
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24 jaar lang onderzoek, Enige resultaat: dodelijke medicijnen die al bestonden voordat HIV was bedacht en nu onder de naam AIDS-remmers iedereen opnieuw ziek en dood maken. Net als toen ze tegen de kanker werden gebruikt. Even succesvol. Duidelijk verhaal. Keep up the good work. Over nog eens 24 jaar zullen de laatsten die de preventieve AIDS-kuur hebben overleefd (daar is nu serieus sprake van) nog een aan je denken ;) Afrika helpen doe je door ze goed te eten geven, goede normale medicijnen en vooral dat AIDS te vergeten.
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"24 jaar lang onderzoek, Enige resultaat: dodelijke medicijnen die al bestonden voordat HIV was bedacht en nu onder de naam AIDS-remmers iedereen opnieuw ziek en dood maken." En de oogkleppen blijven gewoon op. Nee, de AIDS-remmerscocktails bestonden NIET voordat er aidsonderzoek bestond; dat is gewoon onnozel. Feit: de levensverwachting van HIV-patienten is sterk toegenomen met de komst van steeds betere cocktails. Ontkennen is gewoon onnozel omdat iedereen de cijfers kan zien: van de ~13000 HIV-patienten in NL sterven er per jaar minder dan 100. Zo simpel is het. Eenduidige conclusie: mensen gaan dus NIET massaal dood aan AIDS-remmers. "Afrika helpen doe je door ze goed te eten geven, goede normale medicijnen en vooral dat AIDS te vergeten." Dit is werkelijk om te kotsen. Vertel dat tegen m'n dode vrienden. Het bevestigt wederom dat je geen zier geeft om HIV/AIDS-patienten maar deze hele campagne ter glorie van jezelf voert. Nog steeds heb je niet door dat die afrikaanse AIDS-doden al decennia sterven ZONDER dat er AIDS-remmers voorhanden zijn. "24 jaar onderzoek, en langzaam, beetje bij beetje, weten we steeds meer over HIV en wie weet, vinden we ooit een vaccin." Is kanker ook een complot? En MS? Waar staat dat toch geschreven die wet dat als je veel geld in een onderzoek stopt dat je een garantie hebt om een vaccin te vinden? Tis geen film waar het tegengif altijd net op tijd gevonden wordt, het is 'the real world' waar zaken altijd net wat complexer zijn dan je zou willen. Kan je jammer vinden, maar helaas. Als je wil weten welke resultaten er zijn geboekt zal je ze toch eens op moeten zoeken. En die vind je dus op sites die informatie geven op AIDS, en NIET op sites die HIV/AIDS ontkennen. Dus als je alleen je informatie van dat soort sites afhaalt dan krijg je dat vertekende beeld van je. Maar zoals gezegd, AIDS interesseert je geen drol, maar je kruistocht tegen "de orthodoxie". En ach, het is zo lekker controversieel om te zeggen dat "HIV nooit is aangetoond", ook al is die absurde stelling al meer dan 10 jaar ontkracht, onder andere door de man die je steeds maar aanhaalt als "een nobelprijswinnaar", Peter Duesberg.
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Hey Bram/Brum/Braad, gaat 'ie lekker? Pas maar op, straks wordt schuimbekken nog als nieuw symptoom aangemerkt voor seropositiviteit ;-)
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"Nog steeds heb je niet door dat die afrikaanse AIDS-doden al decennia sterven ZONDER dat er AIDS-remmers voorhanden zijn." Iedereen komt te sterven jongen. Als je zo ziek bent als de gemiddelde Afrikaanse AIDS patient en je doet er niks aan dan gaat het toch vanzelf fout? Wat is er toch mis met het geven van schoon drinkwater, vitaminen, eiwitten en antibiotica aan AIDS patienten. Waarom ligt die focus toch op AIDS remmers? Als mijn imuunsysteem op apegapen ligt dan ben ik erbij gebaat om vitaminen en mineralen tot me te nemen. Als ik dan wat aangesterkt ben kan ik de medicijnen tegen de ziektes die ik opgelopen heb beter verwerken. Maar op het moment dat ik in die toestand seropositief wordt bevonden dan krijg ik meteen zware medicijnen voorgeschreven. Kun je me net zo goed van het dak af gooien. Waar blijft de menselijkheid in dit hele verhaal? Die vervliegt blijkbaar spontaan als de hypotheek moet worden betaald..
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"Wat is er toch mis met het geven van schoon drinkwater, vitaminen, eiwitten en antibiotica aan AIDS patienten. Waarom ligt die focus toch op AIDS remmers?" Er is helemaal NIKS mis met het geven van schoon drinkwater etc. aan ALLE mensen op aarde (daar was ik dan ook voor in Afrika), maar daar rem je het HIV niet mee. Het is heel makkelijk: AIDS-remmers beschikbaar -> AIDS een chronische ziekte waar je oud mee kan worden AIDS-remmers NIET beschikbaar -> AIDS een dodelijke ziekte waar het gros binnen ~15 jaar aan overlijdt. En ja, AIDS-remmers hebben bijwerkingen, zoala ALLE werkende medicijnen. En heftige medicijnen hebben vaak heftige bijwerkingen. Het is dan ook bepaald geen pretje ze dagelijks te moeten slikken en de een reageert er heftiger op dan de ander (zoals bij ALLE werkende medicijnen), maar het punt is dat ze ervoor zorgen dat het HIV-virus hanteerbaar is en dat je er oud mee kan worden. Alle cijfers tonen dat eenduidig aan; van de ~13000 HIV-besmetten in NL sterven er jaarlijks ong. 85; dat is 0.65% Je hoeft geen rekenwonder te zijn om dan in te zien dat de overgrote meerderheid nog leeft na een jaar of 15.
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En het gemiddelde sterftecijfer in Nederland is 8,7 (= 8,7 doden per 1000 Nederlanders per jaar) Je hoeft dus geen rekenwonder te zijn om op te merken dat bovenstaande bereking er niet veel toe doet. Tenzij hiv-patienten langer leven dan de gemiddelde Nederlander natuurlijk...
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Correctie: blijkbaar heb je dus toch enig wiskundig inzicht nodig om in te zien dat bovenstaande berekening er alles toe doet. Nee natuurlijk leven HIV-patienten niet langer dan de gemiddelde nederlander; de gemiddelde HIV-patient is dan ook geen 80 jaar oud. Waar het om gaat is dat het jaarlijkse sterfpercentage ver beneden de 1% ligt.
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Bram, vind jij dan helemaal niets verdacht aan het feit dat AZT in eerste instantie was afgekeurd als chemokuur voor kanker? Dat de FDA het te gevaarlijk -lees:te giftig- vond om verantwoord te gebruiken? Los van het feit of je de argumenten van Patman wilt geloven moet je toch toegeven dat er een smerig kantje aan zit. De kuren zijn misschien dan wel minder dodelijk geworden, maar nog steeds hakt men in wezen met dezelfde botte chemobijl van een paar decennia terug. Je vergeet in al je boosheid dat Patman stelt dat de mensen die de diagnose HIV krijgen worden genept door de doktoren en pharmabedrijven, hen treft geen blaam. Zijn zijn slachtoffer van wat misschien wel op z'n minst een vreselijke vergissing is.
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"De kuren zijn misschien dan wel minder dodelijk geworden, maar nog steeds hakt men in wezen met dezelfde botte chemobijl van een paar decennia terug. " Ja duh! Wat is je punt nu? Er is NIEMAND die beweert heeft dat AZT (wat sinds jaren overigens maar EEN VAN DE aidsremmers, ook al zoiets wat gemakshalve maar steeds vergeten wordt door de aids-ontkenners) een pretje is. Waar het om gaat is dat bewezen is dat patienten die AZT kregen toegediend toen het op de markt kwam een hogere levensverwachting hadden dan patienten die het niet kregen. Pure AZT is niet al te best (zoals chemokuren voor kankerpatienten ook niet bepaald een pretje zijn), maar inmiddels zijn er allerlei cocktails voorhanden (inderdaad: ontwikkelingen dankzij onderzoek). Maar de ontkenners willen dat niet horen; die staren zich blind op de giftige eigenschappen van AZT zonder naar het totaal-plaatje te kijken waaruit blijkt dat mensen ermee gebaat zijn. Los daarvan, dit argument staat natuurlijk helemaal los van de stupide lang ontkrachte claim dat "HIV nooit is aangetoond" volgens een clubje nitwits, noch dat al lang op honderden manieren bewezen is dat HIV de oorzaak is van AIDS.
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