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Debunkiamo un po'?
Da Hara2 Lun 3 Nov 2014 - 13:05
Hara2 ha scritto:
Nel web, nessun luogo escluso, è un proliferare di bufale, spesso vecchie e che a forza di venire rimpallate da un luogo all'altro acquistano maggior vigore e oltretutto aumentano così i "riferimenti" su Google, qualche volta anche grazie a organi d'informazione che ci cascano di mani e di piedi.
Qualche volta partono da errate teorie di personaggi riconosciuti , altre da non si sa dove. Poi, micidiali, le semibufale presentano anche maggiori difficoltà.
E fare debunking non è roba facile
Occorrono specialisti diversi a seconda della bufala o affidarsi a siti specializzati (che capita che a loro volta siano dubbi) e spenderci comunque un sacco di tempo
Spesso le bufale si basano su precedenti bufale e richiedono conoscenze in diverse discipline
D'altra parte le bufale spesso sono pericolose, esempio quelle di medicina, diffondono ignoranza e poi può essere divertente smontarle.
Quasi quasi un meta3D con almeno le bufale che vengono qui postate, che mi sembrano essere in deciso aumento, ci starebbe.
Uè, nessuna critica a nessuno, può capitare a chiunque (forse)
Inizio con una sciocchezza marginale nella quale sono incappato ultimamente
Testata: Libero
Data: 03 settembre 2014
Pagina: 5
Autore: Michael Sfaradi
Titolo: «La Norvegia ha superato addirittura i nazisti: gli islamici impongono la cacciata degli ebrei»
Gli ultimi 819 ebrei norvegesi stanno per lasciare il Paese, ancora non è deciso il periodo della partenza che probabilmente non sarà di massa ma a scaglioni. La Norvegia sarà così la prima nazione europea dove gli ebrei, di fatto, non potranno più vivere, al loro posto ci saranno le sempre più numerose e agguerrite comunità islamiche che
- Spoiler:
- secondo l'andamento delle nascite nel giro di pochi anni saranno la maggioranza della popolazione. Non è difficile capire che le regole democratiche, alla fine, consegneranno la nazione intera in mano a persone che non hanno radici nella penisola scandinava e che seguendo le loro tradizioni politiche e sociali la stravolgeranno completamente. Gli ebrei lasciano il Paese perché in Norvegia la forte presenza musulmana, con l'odio insito nei confronti degli infedeli, con la complicità delle istituzioni che non hanno mai preso provvedimenti al fine di proteggere le persone e i luoghi di culto martellati da continui attacchi antisemiti, è riuscita nel giro di pochi anni a rendere impossibile la vita alle piccole comunità ebraiche. L'appello più accorato è stato di Anne Sender, esponente dell'ebraismo locale, scrittrice e vincitrice del premio «Libertà di espressione», sul quotidiano Aftenposten nel febbraio 2013, dove preannunciava l'abbandono della Norvegia da parte di tutti gli ebrei. La Sender era stata pesantemente criticata dalla stampa norvegese che l'aveva definita una «Cassandra» e a poco più di un anno di distanza scopriamo che Cassandra aveva ragione. In questo pezzo d'Europa si sta realizzando lo Stato «Judenrein» il sogno del vecchio Führer: un'Europa senza ebrei, e a riuscire nell'impresa dove fallì il nazismo è l'Islam estremista che strumentalizza la situazione in Medioriente per giustificare, davanti al complice silenzio di un continente intero, atti che fino a poco tempo fa erano considerati inaccettabili. Durante l'operazione israeliana "Margine Protettivo" nella Striscia di Gaza, ci sono state in Norvegia manifestazioni oceaniche contro Israele dove gli slogan antisemiti sono stati urlati senza sosta, mentre le tre manifestazioni di sostegno al governo israeliano, organizzate dalle comunità ebraiche e dalle associazioni di amicizia con Israele, si sono potute tenere unicamente grazie alla presenza delle forze dell'ordine schierate a protezione dei manifestanti. La Norvegia non sarà solo la prima nazione europea senza ebrei, ma visto l'andamento potrebbe avere anche il primato dell'introduzione democratica della Sharia come legge dello Stato, sia dal punto di vista civile che penale. Si tratta però del primo tassello di un domino che in breve tempo coinvolgerà tutto il vecchio continente, i dati sono agghiaccianti. Dopo la Norvegia sono la Svezia e la Finlandia, infatti, le prossime candidate.
Vecchia bufala già più volte smentita, ricicciata fuori e rilanciata immediatamente in mille diversi luoghi telematici (con relativi commenti tipo "Io vorrei solo sapere cosa gli abbiamo fatto di male." oppure "era l'ora")
Anti-defamation legue
Alarmist E-Mail Claims Norway is 'Judenrein'
November 6, 2012
An e-mail rumor, with a subject line "Europe again becoming 'Judenfrei' and soon 'Judenrein,'" claims that "the last 819 Jews still living in Norway are now leaving the country due to the rise of anti-Semitism."
The e-mail goes on to cite a litany of attacks by Muslims against Jewish communities in Norway and elsewhere in Europe, and warns that "history is repeating itself."
Much of the information in this e-mail message is alarmist and outright false.
ADL is in close contact with the leadership of the Norwegian Jewish community. The community has assured us there is absolutely no truth to the claim that all 819 Norwegian Jews have left. The Jewish population of Norway is approximately 1,700 and there has not been any significant emigration.
Nota
Mi presi la briga di scrivere a un sito che ripubblicava senza alcun commentò la notizia, dicendogli che non era il caso di contribuire a diffondere idiozie, la loro risposta:
..le bufale non si smentiscono, è chi le diffonde che deve provarle. se poi dei minchioni ci cascano, pazienza...
IC redazione
IC sta per ...
Ultima modifica di Hara2 il Lun 3 Nov 2014 - 13:09 - modificato 1 volta.
Hara2- -----------
- Numero di messaggi : 1760
SCALA DI DAWKINS :
Data d'iscrizione : 10.01.14
Re: Debunkiamo un po'?
Da Justine Lun 3 Nov 2014 - 13:08
Qui bisognerebbe dumpare tutti i contenuti del forum di Nibiru. Peccato che da smartphone non riesca, ci pensi tu?
___________________
Smettetela di bistrattare e misinterpretare la Scienza per fingere di dare plausibilità alle vostre troiate
Grazie
Justine- ----------
-
Numero di messaggi : 15532
Occupazione/Hobby : Qui è l'una antenna
SCALA DI DAWKINS :
Data d'iscrizione : 24.05.14
Re: Debunkiamo un po'?
Da Hara2 Lun 3 Nov 2014 - 16:16
SauroClaudio ha scritto:
Volevo solo mostrare ad Hara coso c'è scritto su Wikipedia, estremamente obiettiva nella diagnosi ed anche nel riportare un fatto:
http://it.wikipedia.org/wiki/Aids._Il_virus_inventato
Aids il virus inventato è il titolo di un saggio scritto dal microbiologo Peter Duesberg.
Duesberg sostiene che, a suo dire, l'HIV che, non essendo mai stato isolato ufficialmente, non provocherebbe l'AIDS, che l'infezione non si trasmetterebbe per via sessuale e ancora, che l'AZT peggiorerebbe le condizioni del paziente.
Tali sue posizioni soggettive sono in contrasto con i dati oggettivi, clinici e scientifici, condivisi in merito dalla comunità scientifica internazionale. Tuttavia il virus HIV al 2013 non è stato ancora isolato .[/color][/size]
disclaimer wiki ha scritto:Le pratiche descritte non sono accettate dalla medicina, non sono state sottoposte a verifiche sperimentali condotte con metodo scientifico o non le hanno superate.
E non è riportata alcuna fonte autorevole
Comunque vediamo
Isolation: the suspected pathogen can be isolated - and propagated - outside the host.
- Spoiler:
- 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.
Transmission pathogenesis: transfer of the suspected pathogen to an uninfected host, man or animal, produces the disease in that host.
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, 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'NeilExternal Web Site Policy 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).
Epidemiological association: the suspected cause must be strongly associated with the disease.
numerous studies from around the world show that virtually all AIDS patients are HIV-seropositive; that is they carry antibodies that indicate HIV infection
http://www.niaid.nih.gov/topics/HIVAIDS/Understanding/howHIVCausesAIDS/Pages/HIVcausesAIDS.aspx
Andiamo avanti:
http://it.wikipedia.org/wiki/AIDS (no disclaimer)
E ancora
NEW YORK (October 8, 2014) — Researchers at Weill Cornell Medical College have developed technologies that allow investigators, for the first time, to watch what they call the "dance" of HIV proteins on the virus’ surface, which may contribute to how it infects human immune cells. Their discovery is described in the Oct. 8 issue of Science, and is also a part of a study published the same day in Nature.
New studies in Nature and Science describe technology that reveals the motions of proteins on the surface of HIV that are key to the virus’s ability to infect human immune cells. This structure shows the two proteins (in red and gold) and sugars (in green) responsible for mediating HIV’s fusion with its host cells.
Image credit: Nature/Pancera et al.
- Spoiler:
The new technology platform opens new possibilities for devising an approach to prevent HIV infection, says Dr. Scott Blanchard, an associate professor of physiology and biophysics at Weill Cornell, and one of three co-lead authors on the Science study. He is also an author on the Nature paper that describes a three-dimensional structure of one of the shapes, or conformations of the HIV protein.
"Making the movements of HIV visible so that we can follow, in real time, how surface proteins on the virus behave will hopefully tell us what we need to know to prevent fusion with human cells — if you can prevent viral entry of HIV into immune cells, you have won," says Dr. Blanchard, who is also associate director of Weill Cornell's chemical biology program.- Spoiler:
- "What we have shown in the Science study is that we now have the means to obtain real-time images of processes happening on the surface of intact HIV particles, which we now plan to use to screen the impact of drugs and antibodies that can shut it down," he says.
"We desperately need solutions to prevent HIV infection, which, to date, has infected or killed more than 70 million people worldwide," Dr. Blanchard says.
If this technology proves useful in HIV management, it could potentially be used to decode infection processes for other viruses, he says.
USING LIGHT TO WATCH HIV DANCE
In the Science study, Dr. Blanchard worked with Dr. Walther Mothes, a HIV specialist at the Yale University School of Medicine, and with Dr. James Munro, who was Dr. Blanchard's first graduate student and who is now an assistant professor at Tufts University School of Medicine. Drs. Mothes and Munro are the two other co-lead investigators.
Dr. Blanchard adapted an imaging technique that uses fluorescence to measure distance on molecular scale — single-molecule fluorescence resonance energy transfer (smFRET) imaging — to study viral particles. His group developed fluorescent molecules (fluorophores) — which he dubs "beacons" — and the team inserted them into the virus's outer covering, known as the envelope. With two of these special beacons in place, smFRET imaging can be used to visualize how the molecules move over time, when the virus proteins change conformation. The approach provides a measure of distances, on the order of a billionth of an inch, between two beacons glowing in different colors, and this can be used to detect shape shifting as it occurs and the attached beacons move.
The team used the technology to study motions of proteins on the surface of the HIV virus (called envelope proteins) that are key to the virus's ability to infect human immune cells carrying CD4 receptor proteins. (CD4 receptor proteins help HIV bind to a cell.) The envelope consists of three gp120 and gp41 proteins positioned close together, and referred to as “trimers,” that open up like a flower in the presence of CD4, exposing the gp41 subunit that is essential for subsequent aspects of the mechanism that causes infection.
"There are 10-20 such envelope trimers on the surface of each HIV particle, and they mutate rapidly, thereby evading typical immune responses. This is why it is so difficult for humans to mount an effective immune response and why it is challenging for researchers to develop vaccines targeting the HIV envelope proteins," Dr. Blanchard says. The researchers were able to study proteins from two different strains of HIV, which contained beacons that did not alter the biology of the particles
Then they watched.
They saw that the gp120 proteins' virus particles changed shape constantly and that the timing and nature of their movements were both similar and distinct. "This answered the first big question of how opening of the envelope trimer is triggered," Dr. Blanchard says. "Many scientists believe that the particles remain in one conformation until they come across a CD4-positive cell. But we saw that the proteins dance when no CD4 was present — they change shape all the time."
The researchers were then able to watch how the viruses responded when synthetic CD4 was introduced. They also saw that antibodies known to exhibit some effectiveness acted to prevent gp120 from opening, and that these effects correlated with a decrease in the virus' ability to infect cells. Similar things happened when they introduced a small molecule now under development to prevent HIV infection.
"The practical outcome from this technology is that we can begin to understand how the biological system moves. So far we have detected three different conformations of the envelope trimer. We are working now to improve the technology to achieve the imaging precision we need to make broadly effective therapies," Blanchard says.
TECHNOLOGIES WORK HAND IN HAND
The Nature study, led by researchers at the National Institute of Allergy and Infectious Diseases, used X-ray crystallography to capture a three-dimensional structure of one of the conformations revealed in the Science paper. The protein constructs used in this investigation were originally developed by a team of researchers headed by Dr. John Moore, professor of microbiology and immunology at Weill Cornell.
"The antibodies used in the crystallography study are ones that we observed to stop the dance of the HIV envelope proteins, pushing the trimer assembly into a quiescent, ground state," Dr. Blanchard says.
"This concrete, atomic resolution picture of what the pre-fusion machinery looks like and where these antibodies bind provides an important step forward to understanding HIV's biology," he says.
"Dr. Blanchard believes both techniques — smFRET and X-ray crystallography — can work hand in hand to help scientists describe the functions of molecules from the perspective motion, including the other two distinct conformations identified in the smFRET study.
"The approach is really a breakthrough for science because most research is done in a test tube where billions of molecules are present, all behaving independently. It is very difficult to extract direct information about these types of movements from indirect observations," such as those that don't use imaging technology, he says. "The single-molecule approach allows practical, interpretable, real-time information to be obtained about molecular processes in complex biological systems."
This work was supported by NIH grants R21 AI100696, P01 56550, and R01 GM098859, by the Irvington Fellows Program of the Cancer Research Institute, a fellowship from the China Scholarship Council-Yale World Scholars, grants from the International AIDS Vaccine Initiative's (IAVI) Neutralizing Antibody Consortium, the NIH Intramural Research Program (Vaccine Research Center), the Bill & Melinda Gates Foundation and the United States Agency for International Development (USAID).
Support for the Nature study was provided by the Intramural Research Program of the Vaccine Research Center, National Institute of Allergy and Infectious Diseases (NIAID) at the National Institutes of Health, and by grants from the Division of AIDS, NIAID, National Institutes of Health for CHAVI and CHAVI-Immunogen Discovery Centers, from the National Institutes of General Medical Sciences, from the Irvington Fellows Program of the Cancer Research Program, and from the International AIDS Vaccine Initiative's Neutralizing Antibody Consortium. Use of sector 22 (Southeast Region Collaborative Access team) at the Advanced Photon Source was supported by the US Department of Energy, Basic Energy Sciences, Office of Science, under contract number W-31-109-Eng-38.
Contributing to the Science study were Xiaochu Ma (Yale University School of Medicine), Jason Gorman, Peter D. Kwong and James Arthos (National Institute of Allergy and Infectious Diseases), Zhou Zhou (Weill Cornell Medical College), Dennis R. Burton (The Scripps Research Institute), Wayne C. Koff (International AIDS Vaccine Initiative), Joel R. Courter and Amos B. Smith III (the University of Pennsylvania).
Co-authors of the Nature study are Peter D. Kwong, Marie Pancera, Tongqing Zhou, Aliaksandr Druz, Ivelin S. Georgiev, Cinque Soto, Jason Gorman, Priyamvada Acharya, Gwo-Yu Chuang, Gilad Ofek, Guillaume B. E. Stewart-Jones, Jonathan Stuckey, Robert T. Bailer, M. Gordon Joyce, Mark K. Louder, Yongping Yang, Baoshan Zhang, and John R. Mascola (National Institute of Allergy and Infectious Diseases), Jinghe Huang, Mark Connors, Nancy Tumba and Lynn Morris (National Institute of Allergy and Infectious Diseases), Myron S. Cohen (National Institute for Communicable Diseases of the National Health Laboratory Service, South Africa), Barton F. Haynes (Duke University), James B. Munro and Walther Mothes (Yale University School of Medicine).
E ancora
Duesberg has recently got an article called “AIDS since 1984: No evidence for a new, viral epidemic – not even in Africa” published in the obscure Italian Journal of Anatomy and Embryology. This is after getting rejected from four other journals and having gotten a previous version of the article pulled from the journal Medical Hypotheses, itself a crank journal.
One of the co-authors is Henry Bauer. He is a homophobic professor emeritus in chemistry and science studies at Virgina Tech. He is also, apparently, a world-renowned proponent of the existence of the Loch Ness monster. I kid you not. He was also an editor of the woo-woo journal Journal of Scientific Exploration. All of these three journals mentioned have an impact factor well below 1, making them shoddy and unreliable at best.
- Spoiler:
- The Duesberg et. al. (2011) paper itself is just a rehashing of the same old falsehoods that HIV/AIDS denialists have peddled for many decades, this time, yet again, published in an obscure and unimportant journal. Other commentators have already started picking the “paper” apart, but there are additional things that should be added, so the following is a combination of criticism so far, with my own contributions and expansions.
The Spread of Plague is not analogous to HIV/AIDS
–> Duesberg et. al. (2011) tries to compare the spread of infectious diseases such as plague caused by Y. pestis with HIV and concludes that since the spread of HIV and incidence of AIDS does not match that of the typical infectious diseases, this means that HIV cannot be the cause of AIDS or of an infectious epidemic. This is a flawed analogy, because unlike plague, HIV does not spread through casual, non-sexual contact as Y. pestis can and HIV/AIDS can take several years to be clinically obvious, rather than having an incubation time of a couple of days (Hoofnagle, 2011).
Data on population growth does not refute the severe impact of HIV/AIDS
–> Duesberg et. al. (2011) then claims that there cannot be an HIV/AIDS epidemic, since the population growth of the countries hit by HIV/AIDS the hardest, such as South Africa, is still positive.
–> Hoofnagle (2011) points out that even if we accept that, it does not necessarily support the conclusion made, since HIV/AIDS is attached to a strong social stigma, and South Africa use an entire government infested by HIV/AIDS denialism.
–> Also, population growth is not a good measure of the impact of HIV/AIDS, because the birth rates are quite high, thereby masking the effect. Kalichman (2009, pp. 77-78) points out that countries in southern Africa, including South Africa, have seen a massive decrease in life expectancy over the years that correspond to the occurrence of AIDS pandemic. He writes that: “Life expectancy in many countries that were improving during the post-colonial years of the 1960s and 1907s began to erode in the 1980s and 1990s, and life expectancy in many countries is now worse than even during the 1950s, the last full decade of colonialism. The reason why some countries afflicted by AIDS sustain positive population growth is simply due to high birth rates.” This shows the effects of the AIDS pandemic.
–> In a paper published in PNAS, Gregson et. al. (2007), the authors make a similar point about Zimbabwe.
–> Researchers at Harvard School of Public Health concludes in Chigwedere et. al. (2008) that over 330000 individuals with HIV/AIDS died earlier than needed because the previous President of South Africa, Thabo Mbeki, and his government refused to let his people have access to antiretrovirals. They believed that it was just a western pharmaceutical plot to destroy the future of the country and instead, he suggested garlic and lemon as treatment (Kalichman, 2009). We can easily see what horrible results that led to.
Duesberg false claims about antiretrovirals (ARVs)
–> Duesberg et. al. (2010) tries to use the Concorde Study (Concorde Coordinating Committee, 1994) to show that AZT is useless as treatment for HIV/AIDS. However, Hoofnagle (2011) convincingly demonstrate that Duesberg incorrectly characterize the paper by claiming that the study was about an experimental group and a placebo group, when in fact, it had two experimental groups, one before the onset of AIDS and the other after. All the subjects where treated with AZT. The study did not show that treatment was useless, only that there was no point in treating patients with a single drug before the condition had progressed to AIDS.
–> Duesberg does not seem to understand that because of the evolution of drug resistance, treatment with a single drug is no longer the standard of care for HIV/AIDS. The so called HAART treatment uses multiple combined drugs to reduce the risk of resistance, as even if some virus particles become resistant to one of the drugs, the other drugs in the regiment can destroy them and prevent the resistance from spreading. Duesberg therefore attacks a straw man.
–> Overall, Duesberg et. al. (2011) promotes an irrational analysis of risk, overemphasizing risks with treatments, while vastly underestimating the risk of not being treated. These, and other factors, must be viewed against each other. They even criticize the process of trying to prevent mother-to-child preventing in the same manner: overstating the risks, ignoring the benefits.
Conclusion
The Duesberg et. al. (2011) article makes the same flawed claims as HIV/AIDS denialists usually do and it is not worth taking any of them seriously. Not all infectious diseases are equivalent. It is more reasonable to look at life expectancy rather than population growth when trying to find the severe impact of HIV/AIDS on countries in Southern Africa, because a high birth rate masks changes in population. Duesberg incorrectly characterizes the research of other scientists in his attempt to make ARVs look like ineffective poisons and performs multiple, irrational analysis of risk when he ignores benefits and focus on risks instead.
It is not a scientific paper, just rehashing of the same old denialists falsehoods about HIV and AIDS that has been debunked over and over again many times before.
References and Further Reading:
Chigwedere, P., Seage, G.R., III, Gruskin, S., Lee, T.-H., and Essex, M. Estimating the Lost Benefits of Antiretroviral Drug Use in South Africa. J. Acquir. Immune Defic. Syndr. 49:410–415 (2008).
Concorde Coordinating Committee. (1994) Concorde: MRC/ANRS randomised double-blind controlled trial of immediate and deferred zidovudine in symptom-free HIV infection. Concorde Coordinating Committee. Lancet. 343(8902):871-81.
Corbyn, Zoë. (2011). Paper denying HIV–AIDS link secures publication: Work by infamous AIDS contrarian passes peer review. Nature News. Accessed: 2010-01-06.
Gregson S; Nyamukapa C; Lopman B; Mushati P; Garnett G.P; Chandiwana S.K; Anderson R. M. (2007). Critique of early models of the demographic impact of HIV/AIDS in sub-Saharan Africa based on contemporary empirical data from Zimbabwe. Proc Natl Acad Sci. 104:14586-14591.
Hoofnagle, M. (2011). Duesberg Strikes a blow for HIV/AIDS denialism. Denialism blog. Accessed: 2012-01-06.
Kalichman, S. (2009). Denying AIDS: Conspiracy Theories, Pseudoscience and Human Tragedy. New York: Copernicus Books.
E ancora
The Evidence That HIV Causes AIDS
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
- Spoiler:
- 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:
Epidemiological association: the suspected cause must be strongly associated with the disease.
Isolation: the suspected pathogen can be isolated - and propagated - outside the host.
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).
(Continua)
Ultima modifica di Hara2 il Lun 3 Nov 2014 - 16:23 - modificato 1 volta.
Hara2- -----------
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Data d'iscrizione : 10.01.14
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Da Hara2 Lun 3 Nov 2014 - 16:21
- Spoiler:
- 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
<500
501 - 3,000
3,001 - 10,000
10,001 - 30,000
>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).
Leggere almeno questo
ANSWERING THE SKEPTICS:
RESPONSES TO ARGUMENTS THAT HIV DOES NOT CAUSE AIDS
- Spoiler:
MYTH: HIV antibody testing is unreliable.- Spoiler:
- 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.
NIAID is a component of the National Institutes of Health (NIH), which is an agency of the Department of Health and Human Services. NIAID supports basic and applied research to prevent, diagnose, and treat infectious and immune-mediated illnesses, including HIV/AIDS and other sexually transmitted diseases, illness from potential agents of bioterrorism, tuberculosis, malaria, autoimmune disorders, asthma and allergies.
News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov.
Prepared by:
Office of Communications and Public Liaison
National Institute of Allergy and Infectious Diseases
National Institutes of Health
Bethesda, MD 20892
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Posso andare avanti per 1000mila pagine il punto è sempre quello. Vi è ogni evidenza scientifica contro la "tesi" di Duesberg.
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Re: Debunkiamo un po'?
Da Rasputin Lun 3 Nov 2014 - 22:26
O'Hara ha scritto:Inizio con una sciocchezza marginale nella quale sono incappato ultimamente
Guarda caso, riguarda gli ebrei
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