Posted on 01/09/2008 6:19:16 PM PST by GodGunsGuts
MBARARA, Uganda — At the AIDS clinic here, the stories are brutal. A young cattle herder, infected with H.I.V. along with his wife, tells me that all four of their children died before turning 3.
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And most patients I meet say they and their families scramble to survive from meal to meal, never far from the edge of starvation. Many say their H.I.V. drugs have drastically increased their appetites and made them crave food even more.
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“Sometimes I am so hungry,” a 44-year-old widow says. “It’s intense. My whole body is shivering from hunger. Even when I have just finished eating, I am hungry again minutes later. It’s such a problem, because I don’t always have food.”
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As a journalist turned graduate student in public health, I am in Uganda for five weeks as part of a research team investigating whether “food insecurity” — a persistent difficulty in finding enough to eat — undermines the effectiveness of H.I.V. treatment.
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I wonder sometimes what is the point of researching this? Why not just give food to people so obviously in need? But international donors demand data and documentation. They want proof that an intervention will reduce the total misery index before they will shell out millions of euros for new programs, even if the need appears self-evident.
(Excerpt) Read more at nytimes.com ...
FATHER Angelo d'Agostino is puzzled. He sits at the heart of Africa's alleged AIDS epidemic with a hospital full of HIV-positive children who, health experts say, are condemned to die. Except that they are very much alive.
As a result, d'Agostini, in common with growing numbers of scientists and doctors around the world, is beginning to question whether HIV really is the killer it has been made out to be. He, like them, suspects that many "AIDS" cases are really old diseases given a new name and that people who test HIV-positive are not, as most have been led to believe, the victims of a new, inevitably lethal disease.
As founder of the Nyumbani hospice for abandoned and orphaned HIV-positive children in Nairobi, Kenya, he had expected to see much disease and death. But his so-called "AIDS babies" are confounding all predictions.
A year has passed since the home opened and only one of his first 45 children has been lost an ailing six-week-old infant who had to return to hospital almost immediately and died two weeks later. The rest, who are aged up to six years, are thriving and Nyumbani, which means "at home", teems with life and laughter.
Yet elsewhere in Kenya and across sub-Saharan Africa, according to the World Health Organisation (WHO), tens of thousands of children are dying because of HIV, usually in their first year. Its regional office in Brazzaville says infant mortality has increased so much because of AIDS that gains made in child-survival programmes of recent years are being eroded. WHO says the virus has infected 8m Africans and will be killing 500,000 a year by the end of the century.
But if HIV is causing such havoc elsewhere, why is it apparently proving so innocent in the children of Nyumbani?
D'Agostino, 67, is a former surgeon who trained as a Jesuit priest and became a professor of psychiatry in Washington before going to Africa 10 years ago. "I'm a physician and I bought the theory that HIV is the cause of AIDS," he said. Now he is surrounded by smiling faces that cast huge doubts over it.
"It is surprising. We expected more deaths, and a lot more serious illness. According to most predictions, the children should have died within two to three months of coming to us. Instead, we have now had to set up a nursery school and I'm planning to negotiate their entry into primary school.
"I had also been preparing to establish group therapy for the mothers to deal with their grief at the loss of the children. Instead, the only losses the hospice has are happy ones: some of the children become HIV-negative, and are taken back by relatives or ordinary children's homes."
Even those who persistently test positive are staying well. "I don't have any explanation for it," d'Agostino said. "Will they be alive this time next year? I have no reason to doubt it; they are healthy."
What d'Agostini's hospice provides is very basic care. "They are very sick when they come to us. But as a result of their care here they put on weight, recover from their infections and thrive. Hygiene is excellent. Nutrition is very good. They are really flourishing."
All this is in contrast to the way most children diagnosed as HIV-positive are treated. "People think a positive test means no hope, so the children are relegated to the back wards of hospitals," d'Agostino said. Abandoned by their HIV-positive mothers, the children are killed by multiple infections, malnutrition and misery rather than by AIDS.
At Nyumbani, most of the hands-on work with the children is done by women, usually single mothers, who are quick to bond with the babies in their care. "They have no money and no husband, but they have been mothers that is their big advantage."
Most important to the babies' survival, according to Sister Mary Owens, d'Agostino's assistant, is a big dose of "TLC" tender loving care. "Their whole experience in the home is one that makes them happy children."
Some of the babies become HIV-negative after a few months. The usual explanation for this is that they were never truly virus-infected, but instead inherited their mother's antibodies to HIV, which fade with time. But mothers, too, are being misdiagnosed.
D'Agostino tells of one woman who turned up with her sick baby, begging to be allowed to work for the hospice in return for care for the child. "She had been to hospital seeking treatment for the baby, and they found among other things that it was HIV-positive as well. The baby's grandmother threw both of them out of her house.
"We took them in, and three to four months later sent the baby for another test. It was negative. The mother was delighted. The grandmother took them back. The mother kept working for us and some months later, when she was assigned to go with another child who was to be tested, she asked if she could have a test at the same time and lo and behold, she was negative too."
The experience at Nyumbani flies in the face of the coventional theories about the history of AIDS in Africa. Dr Robert Gallo announced in 1984 that HIV, a newly discovered virus, had been identified as the cause of the immune system breakdown devastating homosexual communities in the United States and Europe. Western doctors invaded Africa with HIV testing kits and computers to map the extent to which people were infected there.
Virus-hunters did succeed in finding large numbers of positive test results, and as far back as 1986 there were said to be 5m HIV-infected people on the continent. Lurid predictions followed, such as one newspaper claim that within 10 years AIDS would leave "vast areas of now-populated land devoid of a single living person".
The tests that led to those estimates are now admitted to have been unreliable, producing a high proportion of false positive results. Newer tests are said to be more accurate, but according to a recent review in the journal Bio/Technology, none has yet been scientifically validated.
The article showed that multiple, non-specific assaults on the immune system, which are extremely common in Africa as a result of poverty, prostitution and the breakdown of medical and social services, may be causing millions to test positive when they are not infected with HIV.
Encouraged by WHO-funded units and numerous non-governmental organisations involved in the fight against AIDS in Africa, doctors are reporting growing numbers of AIDS cases. But researchers have not established the extent to which these are genuinely the result of a new virus, as opposed to a consequence of an intensification in long-established threats to health.
Observers say poverty has driven millions of women into prostitution. Young African males have also been drawn into the trade. "AIDS" deaths are common among these prostitutes, especially when treatment of the resulting repeated infections is either absent or inadequate. Those whose immune systems collapse, as well as those who harbour a cocktail of infections, can become lethally infective.
However, a huge gap remains between this widely acknowledged increase in threats to health associated with prostitutes and their contacts, and the apocalyptic vision of Africa's future espoused by WHO on the basis of its HIV statistics.
As well as using a test that may be useless, these statistics are based on small and often inadequate population samples. Dr Hedvig Pelle, WHO co-ordinator for the Kenya National AIDS Control Programme, said: "AIDS is there. No doubt about it. And it is widespread and increasing. My colleagues in the other countries can tell you the same." But she added: "If you come with this postulate that there are a lot of false HIV-positives, it is very difficult to tell."
Political factors appear to play a part in determining whether a country has a major AIDS problem or not. Kenya lost an estimated Pounds 200m in desperately needed foreign currency in November 1991, when the industrialised world decided to try to force political and economic reform on the country by cutting aid. A recent crisis announcement on AIDS by the country's health minister is seen within the international aid community as an attempt to win back donor sympathy and funds, according to the journal Africa Confidential.
The announcement followed a warning by WHO-sponsored researchers that Kenya alone has an estimated 1m HIV-positive cases, and a cumulative total of 120,000 AIDS victims since the first case was diagnosed in 1985. "A far-from-veiled theory in circulation says figures which show AIDS spiralling out of control have been massaged to extract sympathy," the journal said.
If the HIV theory of AIDS turns out to be flawed, scientists may prove to have done Africans, more than any other people, a huge injustice. Propaganda on the spread of AIDS has discouraged investment, increased poverty and cast a new shadow of fear into the hearts of a people long besieged by health and social problems. *
Interesting, in Malawi, gov’t workers with HIV are getting a pay raise.
http://news.bbc.co.uk/2/hi/africa/7176483.stm
If the HIV theory of AIDS turns out to be flawed, scientists may prove to have done Africans, more than any other people, a huge injustice. Propaganda on the spread of AIDS has discouraged investment, increased poverty and cast a new shadow of fear into the hearts of a people long besieged by health and social problems. *
“Why not just give food to people so obviously in need”
Giving anyone anything never solves the problem. They eat for free, do no work, take drugs and have sex all day leading to HIV-AIDS and overpopulation.
It is what caused the problem in the first place.
DRUGS OR FOOD?
25 December 2007
Thanks for the reply. It’s nice to see FReepers who actually “get it.”
Why AIDS remains a very important POLITICAL ISSUE for the CONSERVATIVE movement:
The Hidden Agenda behind HIV
Rethinking AIDS, 1994
Despite all assurances to the contrary, the AIDS establishment continues to fund only research on HIV. Peter Duesberg inadvertently proved this blackout on all alternative research when he recently submitted a grant proposal to the National Institute on Drug Abuse. The Institute’s clinical director of AIDS research had personally invited the proposal, which outlined a plan to test the long-term effects of nitrite inhalants, or “poppers,” on the immune systems of mice. The answer came back in December: The anonymous referees had not only turned it down, but had refused even to review the proposal.
Why does such a political correctness continue to dominate the War on AIDS? After all, public health officials cannot yet demonstrate they have saved any lives from the syndrome, while its death toll rises steadily. The scientific predictions have also failed miserably. In contrast to the predicted spread of AIDS in the United States, the epidemic has remained strictly confined to risk groups; nine of every ten AIDS cases have been male, and ninety percent of all AIDS victims have been linked to heavy drug use, whether intravenously or as “fast track” homosexuals. Indeed, epidemiologists have yet to establish that any epidemic at all has struck among blood transfusion recipients. Even individual AIDS diseases prefer specific risk groups, such as Kaposi’s sarcoma among homosexuals and the near-absence of Pneumocystis carinii pneumonia among Africans, whose lungs all contain the microbe. And some thirty-nine percent of AIDS diseases in America have nothing at all to do with immune deficiency — witness Kaposi’s sarcoma, various lymphomas, wasting disease, and dementia, for example. In short, AIDS is not an infectious disease.
The obsession with an “AIDS virus” has little to do with science or medicine. Writing in Nature in 1991 (June 21), British HIV researcher Robin Weiss and American CDC official Harold Jaffe hinted at the real purpose in an attack on Peter Duesberg: “But if he and his supporters belittle ‘safe sex,’ would have us abandon HIV screening of blood donations, and curtail research into anti-HIV drugs and vaccines, then their message is perilous.” To whom? If AIDS is not infectious, such recommendations would simply save the taxpayer money and anxiety.
But perhaps this is the point. A 1989 report by the National Research Council more explicitly revealed the hidden agenda. Originally sponsored by the Rockefeller and Russel Sage Foundations and then funded by the Public Health Service, AIDS: Sexual Behavior and Intravenous Drug Use laid out a plan for social engineering on a massive scale — using AIDS as the excuse. “The devastating effect of an epidemic on a community can evoke strong political and social responses,” the committee duly noted. “An epidemic necessitates the rapid mobilization of the community to counter the spread of illness and death” (p. 373). The power of such a method to force changes in cultural values is based on careful manipulation of fear. “Ideally, health promotion messages should heighten an individual’s perceptions of threat and his or her capacity to respond to that threat, thus modulating the level of fear.… What is not yet known is how to introduce fear in the right way in a particular message intended for a particular audience. Acquiring that knowledge will require planned variations of AIDS education programs that are carefully executed and then carefully evaluated,” stated the committee coolly (pp. 267-8).
The report then identified one of the major targets of change — Judaeo-Christian moral values. “Historically, there has been a strong social reluctance in the United States to speak or write about sexuality in explicit terms. Despite recent indications of greatly increased tolerance for sexual explicitness in the media and literature, that reluctance remains strong in much of the population; it is particularly strong in instances that involve the education of children and adolescents” (p. 379). The fear of a supposedly infectious AIDS epidemic, however, could be used to fix such problems. As the report declared, “The committee believes that, during an epidemic, politeness is a social virtue that must take second place to the protection of life” (p. 379).
Other public health officials have been even more forthright. As an officer of the Centers for Disease Control, Donald Francis had in 1984 drafted the CDC’s proposed AIDS strategy. In his 1992 retirement speech at the agency’s Atlanta, Georgia headquarters, Francis voiced the ambitions held by many of his fellow officers in describing “the opportunity that the HIV epidemic provides for public health” (JAMA, 9-16-92). He stated in no uncertain terms the radical nature of the plan:
“The cloistered caution of the past needs to be discarded. The climate and culture must be open ones where old ideas are challenged. Those who desire the status quo should seek employment elsewhere. The American HIV prevention program should be the place where the best and the brightest come, where the action is, where history is being made. This is the epidemic of the century, and every qualified person should want to have a piece of the action.”
The “action” described by Francis was a set of programs that would, as he fully recognized, need strong political protection from angry taxpayers and voters. For example, he bitterly attacked public opposition to condom distribution programs, and called for powerful legal measures to bypass parental discretion. “The ongoing controversies involving abstincence and condoms typify the morass into which schools can fall,” Francis complained. “If, in the opinion of those far more expert than I, schools cannot be expected to provide such programs, then health departments should take over, using as a justification their mandate to protect the public’s health.”
Francis also included proposals for dealing with the AIDS risk of intravenous drug use — including a call for “prescription of addicting drugs” with Federal government sponsorship. Even libertarians who advocate legalizing drugs would balk at such notions, which would ultimately create a massive bureaucracy encouraging drug use. “Following a more enlightened model for drug treatment, including prescribing heroin, would have dramatic effects on HIV and could eliminate many of the dangerous illegal activites surrounding drugs,” he insisted, knowing that only fear of the AIDS epidemic might make such proposals tolerable to the public. Ignoring the toxic, and possibly AIDS-inducing, effects of drugs, Francis emphasized that “In addition to treatment, safe injection [!] must be stressed both for those in treatment programs and those out of treatment. The provision of sterile injection equipment for drug users should be the standard of public health practice in the United States.”
Most chillingly of all, Francis saw the possibilities in harnessing other epidemics to advance similar agendas. As he put it, “if we establish new mechanisms to handle the HIV epidemic, [these] can serve as models for other diseases.”
The common denominator of these and similar plans is that they originate with the Federal government’s Public Health Service, and especially from its frontline public health agency, the Centers for Disease Control. Public perceptions often paint the CDC as a minor office that gathers and publishes dull statistics on disease. The truth is shockingly different. A sophisticated $2 billion-per-year operation, the CDC employs a staff of thousands who see themselves as having an activist mandate. They view epidemics as opportunities for control and for imposing lifestyle changes on the population.
The CDC has traditionally specialized in contagious disease. Its initials, in fact, originally stood for the Communicable Disease Center, from its formation in 1946 until its name changed in 1970. And therein lies its bias, for it tends to interpret almost any epidemic as being infectious. Certainly the CDC has plenty of raw material with which to work; each year brings at least one thousand outbreaks, or “clusters,” of disease that strike in the United States — one every eight hours. These can range from flus and pneumonias to closely-occurring cancers, but most outbreaks involve no more than a handful of people each; since the polio epidemic, none have posed serious threats to the general public. However, by falsely labelling any arbitrarily chosen outbreak as infectious and blaming it on a virus or other microbe, the CDC can quickly generate public fear and political mobilization behind almost any agenda.
The CDC has actually engineered a number of false alarms or misdirected campaigns over the past four decades, neutralizing scientific dissent and calmer voices when necessary. AIDS, though not the first example, has now become the most successful epidemic by far. Two powerful weapons in the agency’s arsenal, both unknown to the public at large, have made this possible: a semi-secret wing of the CDC known as the Epidemic Intelligence Service (EIS), and a quiet “partnership” program with private organizations.
The Epidemic Intelligence Service
Among epidemiologists, it is often half-jokingly referred to as the “medical CIA.” Founded in 1951 by public health professor Alexander Langmuir, the EIS was first designed to act as an elite biological-warfare countermeasures unit of the CDC. Langmuir was hired because he also served as one of the select advisors to the Defense Department’s chemical and biological warfare program.
The first EIS class of 21 recent medical or biological graduates underwent several weeks of intense training at the CDC’s Atlanta headquarters, before being dispatched on their two-year assignments on loan to various state or local health departments around the country. They acted as the eyes and ears of the CDC, carefully monitoring for any possible outbreak of war-induced disease. While on their tours of duty, each EIS officer could be sent elsewhere in the country on a 24 hour-a-day basis. In case of war, the EIS would operate under any emergency powers granted the CDC — potentially including quarantines, mass immunizations, or other drastic measures.
In an article written for the American Journal of Public Health (March, 1952), Langmuir made clear that membership in the EIS did not end with the two year assignment, but was permanent. He wrote that, “As a result of their experience, many of these officers may well remain in full-time epidemiology or other public health pursuits at federal, state, or local levels. Some, no doubt, will return to civilian, academic, or clinical practice, but in the event of war they could be returned to active duty with the Public Health Service and assigned to strategic areas to fulfil the functions for which they were trained.”
Every year since 1951 has seen a new crop of EIS recruits, some classes over one hundred members in size. The nearly 2,000 alumni have gone on to high positions in society, though rarely advertising their affiliation. Indeed, the CDC has now made the EIS more secretive than ever, having suppressed the public availability of the membership directory since last year. Members can be found in the Surgeon General’s office and elsewhere in the Federal government, as well as in the World Health Organization, state and local health departments, universities, pharmaceutical companies, tax-exempt foundations, hospitals, and even as staff writers, editors, or news anchormen for major newspapers, scientific journals, and television news departments. In these positions, EIS alumni act not only as the CDC’s surveillance arm and emergency reserve, but also as seemingly “independent” advocates for CDC policies.
In time, the fear of artificial disease epidemics faded. But Langmuir and other top CDC officials had always held bigger plans for the EIS. Langmuir, for example, an apostle of Planned Parenthood founder Margaret Sanger, involved the EIS in the population control movement by the 1960s. The CDC has gained most, however, from EIS activities in natural disease epidemics, to which its “disease detectives” have turned their attention.
The flu, being truly an infectious disease, often proved itself most valuable to the CDC. Although the winter following the end of World War I was the last time a flu epidemic caused widespread death, the CDC has pushed annual flu vaccinations up to the present day. At times, the agency has even rung the alarm over an impending flu crisis, hoping to use memories of the 1918 epidemic to gain emergency powers and impose mass vaccinations. By using such tactics in 1957 over the Asian flu, the CDC managed to wrangle extra money out of Congress to expand the EIS and crash-produce a vaccine. But the flu season was already winding down by the time the vaccine was ready, and the flu itself turned out to have been as mild as in any other year.
By 1976, CDC director David Sencer wanted to try again, though on a grander scale. After one soldier in Pennsylvania died of a flu-related pneumonia in January, Sencer predicted that a pig-borne human virus, nicknamed the “swine flu,” would soon devastate the United States. Panicked with visions of impending doom, Congress moved to authorize the CDC’s immunization plan for every man, woman, and child in the country. Unexpectedly, the legislation suddenly stalled when the insurance companies underwriting the vaccine discovered that it had seriously toxic side effects.
Sencer had to do something fast. He immediately set up a “War Room” in Auditorium A at the CDC headquarters, and put the EIS network on full alert to search for any disease outbreak that might resemble the flu. Within weeks, the War Room received word of a pneumonia cluster among men just returning home from the Philadelphia convention of the American Legion. Several Philadelphia-based EIS officers and alumni had detected the outbreak, and acted as a fifth column that not only helped arranged an invitation for the CDC to come in, but also took their orders from the arriving team of CDC and EIS officers. Even the New York Times staff writer sent to cover the story, Lawrence Altman, was himself an EIS alumnus.
The CDC team allowed media rumors to circulate that this Legionnaires’ disease was the beginning of the swine flu. Within days, Congress decided to pass the vaccine bill. Only later did the CDC admit that the legionnaires had not been infected by the flu virus, too late to stop the immunization program. Some 50 million Americans received the vaccine, leading to more than a thousand cases of nerve damage and paralysis, dozens of deaths, and lawsuits awarding almost $100 million in damages. In the ultimate irony, no swine flu epidemic ever materialized; the only destruction left behind by the phantom swine flu resulted from the CDC’s vaccine.
The agency later blamed Legionnaires’ disease on a common soil bacterium, one that clearly fails Koch’s postulates for causing the disease and is therefore actually harmless. The legionnaires’ deaths are not so hard to understand, since the pneumonias struck elderly men, many of whom had undergone kidney transplant operations, and who had become particularly drunk during the Bicentennial celebration — the classic risks for pneumonia. Thus “Legionnaires’ disease” is not an infectious condition, but merely a new name for old pneumonias.
Using its EIS network, the CDC has applied similar tactics to other outbreaks of disease. During the 1960s, for example, the EIS helped fuel the National Institute of Health’s growing Virus-Cancer Program by tracking down every small cluster of leukemia cases, trying to create the impression that some virus was responsible for the cancer. Robert Gallo became one of many scientists so impressed with the CDC investigations that he devoted the rest of his career to finding a human leukemia virus.
More recently, the CDC managed to have a team of EIS officers invited into New Mexico to investigate a cluster of pneumonia cases among Navajo Indians. By June of 1993, the CDC began insisting that the brief and relatively small outbreak was caused by a rat fecal virus, the Hantavirus. But as a letter in the January 1 issue of the Lancet pointed out, most of the affected Navajos actually tested negative for the virus. And unlike a contagious disease, this pneumonia never spread beyond the first few dozen victims. Again, the CDC’s “disease detectives” used a high-profile investigation to create media publicity and frighten the general population, rather than troubling themselves with the scientific method and its more boring answers.
Of all the epidemics mismanaged by the CDC, AIDS proved the most spectacular in achieving political success. By 1981, the EIS had so thoroughly penetrated the medical and public health institutions in the United States that it could now detect even the smallest and most loosely-connected “clusters” of diseases, no matter how far apart the victims were in time and space. The original AIDS cases were all found in homosexual men in the “fast track” lifestyle — those having hundreds or thousands of sexual contacts and using enormous amounts of hard drugs to make such promiscuous activity possible. For the CDC, the trick was to make the illness seem contagious; a simple drug-induced epidemic among homosexuals would hardly have frightened the public, nor have allowed the CDC to accomplish its radical public health agenda.
The epidemic officially began in 1980 after Michael Gottlieb, a new immunologist at the UCLA Medical Center in Los Angeles, decided to test the brand new T cell-counting technology. He put out an informal request to fellow physicians to refer cases of immune deficiency to him. Over the next several months, colleagues sent him four such cases, all male homosexuals with Pneumocystis carinii pneumonia. Sensing that the CDC might take an interest, Gottlieb called active EIS officer Wayne Shandera in the Los Angeles health department. Shandera had heard an isolated report of a fifth homosexual with the same problem, and compiled a report for the CDC.
Ordinarily, each of the five cases would have been seen by separate doctors, leaving nothing to suggest the word “epidemic” to anyone. But having a pre-positioned EIS agent like Shandera certainly helped the CDC gather such cases together as a potential cluster. Shandera’s report fell on the desk of James Curran, an official in the CDC’s venereal diseases division; the 1987 book And the Band Played On records that Curran wrote “Hot stuff. Hot stuff.” on the report (p. 67). He had the agency publish it immediately.
By the time the report appeared on June 5, 1981, Curran was already organizing a special Kaposi’s Sarcoma and Opportunistic Infections (KSOI) task force to lead an investigation of the five-victim epidemic. EIS members Harold Jaffe and Mary Guinan, also from the venereal diseases division, helped run the task force. The first order of business was to find as many similar patients as possible, thereby causing the epidemic to “grow.” Next was to explain the syndrome; to the CDC, this meant trying to find an infectious agent. This would be no simple task, since essentially all of the first fifty cases admitted to heavy use of poppers, a drug preferred by homosexuals as a means of facilitating anal intercourse. Even if this toxic drug presented itself as the obvious explanation, the CDC investigators had no intention of letting the evidence interfere. Accordinng to historian Elizabeth Etheridge, “While many of the patients were routine users of amyl nitrites or ‘poppers,’ no one in the KSOI task force believed the disease was a toxicological problem” (Sentinel for Health, 1992, p. 326).
So the EIS was activated to prove AIDS infectious. EIS officer David Auerbach and others confirmed that these extremely promiscuous homosexuals were often linked to one another through long chains of sexual encounters. To prove that AIDS was “spreading” to other people, other officers scoured hospitals to find heroin addicts with opportunistic infections, and blamed their needle-sharing rather than the heroin use, itself a classic risk factor for pneumonias and other illnesses. Bruce Evatt and Dale Lawrence, both members of the EIS, discovered one hemophiliac in Colorado with an opportunistic pneumonia as a side effect of internal bleeding, but rediagnosed the patient as an AIDS case. Even Haitians in Florida and Haiti were interviewed by EIS officer Harry Haverkos, who renamed their endemic tuberculosis as AIDS.
Not understanding the loaded nature of such investigations, the outside world completely bought the CDC line. Soon the race was on for scientific researchers to find the guilty virus. But this search, too, had been rigged. Donald Francis, an EIS member himself since 1971, decided just eleven days after the original Shandera report that the syndrome should be blamed on a retrovirus — with a latent period, no less. Using his various contacts in the retrovirus field, Francis spent the next two years pushing Robert Gallo to isolate a new retrovirus. Eventually Gallo did take an interest, and claimed credit for finding HIV.
With his April 23, 1984, press conference, Gallo completed the crusade begun by the CDC and its EIS. As the cameras rolled and the cameras flashed, Gallo and Health and Human Services Secretary Margaret Heckler launched the nation into a War on AIDS. Few people knew the true story behind that announcement, or of the political agenda that Don Francis and others were preparing to foist on the American people.
The Partnership Program
The CDC’s second major weapon for mobilizing public support lay in its assistance programs for private organizations. By funding or otherwise supporting groups not affiliated with the CDC, the agency could create apparently spontaneous mass movements. Spokesmen claiming to represent various communities could all simultaneously advocate policies identical to those of the CDC, while allowing the agency to remain quietly in the background and avoid direct criticism.
In 1984, the CDC began forming “partnerships,” based on “cooperative agreements,” with large numbers of “community-based organizations,” for the purpose of AIDS “education” [read: indoctrination]. At first the funding was channeled through the United States Conference of Mayors, which dispersed the money to a growing network of AIDS activist groups. By 1985, the CDC was giving over $1 million to state governments, influencing their response to AIDS.
After 1986, the money began flowing freely, and the CDC’s corresponding influence expanded quickly. The American Red Cross alone received over $19 million from 1988 to 1991, cementing CDC control among medical institutions. Millions more were targeted to such groups as the American Medical Association, the National Association of People with AIDS (which operates as a coordinating center for much of the AIDS activist and gay rights movements), Americans for a Sound AIDS Policy (which generates CDC-approved materials for evangelical Christians), the National Education Association (the major teachers’ union), the National PTA, the National Association of Broadcasters (which represents most television and radio stations and their networks), the National Conference of State Legislatures, and dozens of others. Even such groups as the National Urban League, the National Council of La Raza, and the Center for Population Options receive CDC grants and other technical aid. Many specifically AIDS-related groups actually depend on CDC money for their very existence.
Naturally, the CDC has established mechanisms for ensuring that its money and other aid are used for the intended purposes. Organizations wishing to receive grants must not only file applications, but are pre-screened by having to send representatives to CDC workshops on how to apply. These meetings allow the CDC to meet and judge applicants directly. Furthermore, any organization receiving aid winds up having CDC supervision of its AIDS-related “educational” activities.
It is little wonder there is so much political pressure, from all sides, to defend both the virus-AIDS hypothesis and the CDC’s public health agenda.
As with so many non-contagious diseases in the past, the CDC has persuaded the public that AIDS is infectious. Thus the taxpayer is manipulated with fear to acquiesce to the radical measures being pushed by the agency. Where “safe sex” programs, sterile needle exchanges, Federal subsidies of drug addiction, and other CDC proposals would normally be thrown out — along with the officials who proposed them — many Americans suspend judgment.
Most people do not yet realize that the entire campaign has been orchestrated mostly by a single agency of the Federal government, rather than being a spontaneous decision by independent experts and activists. As intended, the CDC has been able to mobilize the scientists, the medical institutions, political bodies, the news media, and a bewildering array of AIDS organizations behind its hidden agenda. All such groups will lose their credibility once the public discovers the real source of the campaign, and honest skepticism will spread faster than AIDS itself.
Signs of imminent change are appearing. The CDC’s public health measures — condoms, sterile needles, contact tracing, and the like — have failed to prevent the steady growth of AIDS. As this bad advice is recognized for what it is, more voices are joining the chorus of dissent against the HIV-AIDS hypothesis. The CDC may soon have to hold HIV research meetings all by itself.
That is, if Congress doesn’t abolish the CDC first.
What a fraud! After the Oil for Food scandal in Iraq, why would any intelligent government believe UN statistics on AIDS cases in Africa? Unfortunately, our President poured $18,000,000,000 additional tax dollars down this rat hole run by charlatans who enrich themselves out of our pay checks.
Quite true. But I think you are missing the point of the post. Read the first couple of replies, and then you will get the gist of what I’m trying to get across.
PS There’s nothing wrong with private charity. It’s when the government gets involved that things go south.
They are getting a raise to buy food, now there’s an interesting solution. Peter Duesberg has often quipped that if they just opened a massive chain of Burger Kings across the poor areas of Afica, African AIDS would be solved practicly overnight.
http://www.globalaging.org/health/world/vaccine.htm
http://query.nytimes.com/gst/fullpage.html?sec=health&res=9801E1D9123FF930A35751C0A9669C8B63
Do you ever post about anything else? :p
LOL
Culture incentives are totally f’ed if a man and his wife “near starvation” choose to have four children.
Giving these weak, malnourished people ‘HIV’ drugs is a cruel punishment. What little chance they have of surviving is destroyed by the drugs; why not just gas them like the NAZIs did? They wouldn’t suffer as much that way. Genocide is nasty business.
You need to read this. I know it is dated, and I could easily give you something much more recent, but it is a great place to start. Then, if you really want your blood to boil, go back and read post #7 (in that order). If you want to pursue it further by reading/watching more up-to-date articles/papers/videos, ping me and I’d be glad to send them along.
From Policy Review (conservative think tank, Hoover Inst.)
http://www.duesberg.com/about/pdpolicy.html
If you haven’t noticed, I cycle through issues. I stick with something for a while and then move on. It’s the way my mind works. Different strokes for different folks.
You're right - someone benefits from these perverse incentives -- incentives that encourage half starving disease ridden people to have four children.... or more. We're enabling this evil with our tax dollars. Stunningly stupid.
The difference between the AIDS establishment and the Nazis is intent. But just try and tell that to a poor African once the full extent of this medical/political scandal finally breaks into the mainstream!
Right about now, you'd have tough time selling me that idea. I believe that genocide is a big part of the motivation. Everything that the UN does appears to point to deliberate genocide in Africa.
Well, UN cerainly has given every indications that they want to turn Africa into something akin to a pan-communist continent. There’s no doubt about that. But I don’t think the average UN/WHO health worker has any clue about what’s going on with respect to AIDS. They are following what they think is the best medical advice and keep shoveling those AIDS drugs into their poor, hungry stomachs. And then when they get worse, they blame it on a harmless retrovirus and shovel even more drugs into their stomachs, until such time as they die of “AIDS.”
I get the impression that AIDS is doing to Africa what the Black Plague did to Europe — change the whole social structure. After the Plague had its run, Europe saw the beginning of an affluent culture because there were fewer people in society with more goods. And cleanliness/fastidiousness was the prevailing survival skill. With AIDS, maybe an after effect of affluence might happen, and the prevailing survival skill will be faithfulness.
Read post #15 and then read the article in post #7 (in that order) and then tell me what you think. All the best—GGG
I’ll need to bmflr, it’s too much to read right now.
I think I understood what you just said, but I have no idea what “bmflr” means. Whenever you get a chance give them a read. Trust me, you won’t regret it.
PS, according to the editors, the link in post #15 was considered one of the three or four most controversial, most talked about articles in Policy Review’s entire history.
Got it.
All the best—GGG
PS FR should have a contest to see who is most familiar with that list!
There was a political movement in the US to broaden the definition of HIV/AIDS to include symptoms like chronic fever / weight loss and even cervical cancer to count as AIDS when a series of positive tests wasn’t possible. The activists would rather have one positive test or even merely a collection of symptoms and thus a diagnosis. Adding poor Africans with malaria and untreated STDs makes much more sympathy and funding than drug-fazed gays.
Some of these HIV positive cases may also be people who are exposed and actually fight it off, contrary to popular wisdom. That, too, makes for poor fund and conciousness raising.
HIV probably causes AIDS, and is probably killing a couple million people. But is isn’t infecting a quarter of Africa, though SF’s bath houses may have that high a rate.
It would be ironic if the toxic drugs or lack of treatment for curable diseases is denied these “never really or no longer HIV positive” patients, leading to unnecessary deaths.
==HIV probably causes AIDS
Although I am convinced that HIV does not cause AIDS, I appreciate your attitude. If more people felt like you, perhaps we could finally set up the “simple set of tests” to settle Duesberg et al’s challenge to the HIV-AIDS hypothesis once and for all:
(Duesberg and Ellison on) HOW TO RESOLVE THE AIDS DEBATE
A relatively simple set of tests would quickly determine, once and for all, whether HIV (or any virus) causes AIDS:
1) The virus should be chemically active in more cells than the host can generate.
2) The symptoms of the disease should occur within weeks or months after infection.
3) The disease should spread relatively randomly among its potential hosts, rather than being confined to highly specific groups.
4) Antibodies produced by the immune system should be able to fight or completely neutralize the disease.
5) A controlled study, in which a group of people with the virus should be compared to a group without, to see whether those with the virus develop the sickness. The groups should be matched for all possible health risk factors: equivalent types and amounts of drug use, use of antibiotics, use of AZT, exposure to previous diseases, hemophilia, etc.
HIV, of course, already fails points (1) through (4), and we have little trouble anticipating the result of a controlled study.
http://www.duesberg.com/about/pdpolicy.html
Let me spell out the above for my limited understanding. Tell me if I get it right.
Viruses attack cells in host organisms. In this case the HIV virus supposedly attacks the "T-helper" cells which form a necessary part of humans' immune systems. This attack supposedly succeeds in AIDS victims, who become vulnerable to a variety of diseases because their immune systems, compromised by a shortage of T-helper cells, can't fight off the diseases.
For this to happen, HIV would have to invade a large enough percentage of damaged T-helper cells to account for the observed shortage of healthy T-helper cells.
But no one has shown HIV present in a large enough percentage of damaged T-helper cells to account for the observed shortage of healthy T-helper cells.
This argues powerfully against the HIV->AIDS theory.
Correct?
HIV has never been observed to “damage” any T-Cells. Go to page 390 of the following paper, and you will see what I mean. The section is entitled “Predictions vs. Facts”:
http://www.duesberg.com/papers/chemical-bases.html
Until recently, prevailing dogma said HIV causes AIDS by killing T-cells. Most people, including Robert Gallo, still adhere to this belief even though there is no evidence to support it. On the contrary, the wealth of evidence available clearly shows that HIV does not, in fact, kill T-cells. This is not surprising since the hallmark of retroviruses (HIV included) is that they do not kill cells [1, 2].
The discoverer of HIV, Luc Montagnier, heads [3] a list [4-6] of virologists who have confirmed that HIV does not kill T-cells in culture. Neither does it kill T-cells in human beings. Mario Roederer of Stanford University said in an editorial in 1998 [7] that the results of Pakker et al. [8] and Gorochov et al. [9] “provide the final nails in the coffin for models of T cell dynamics in which a major reason for changes in T cell numbers is the death of HIV-infected cells.”
Roederer went on to conclude that, “The facts (1) that HIV uses CD4 as it primary receptor, and (2) that CD4+ T cell numbers decline during AIDS, are only an unfortunate coincidence that have led us astray from understanding the immunopathogenesis of this disease.” See references [10, 11] for additional evidence that HIV does not kill T-cells in people.
The fact that HIV does not kill T-cells has caused a remarkable about-face in mainstream thinking. Commenting on a recent paper by Hellerstein et al. [12], Guido Silvestri and Mark Feinberg summarized in 2003 the latest speculation that HIV causes AIDS not by killing T-cells but by over-stimulating the immune system [13]. Silvestri and Feinberg inform us that, “Prevailing views…have shifted from models that focus primarily on direct HIV-mediated killing of CD4+ T cells to models that emphasize the pathogenic role of generalized immune system activation.” In other words, HIV no longer causes AIDS by killing our immune cells, as Gallo contends, but by boosting our immune system.
http://www.rethinkingaids.com/GalloRebuttal/Farber-Gallo-50.html
*Created November 1994. Last updated February 27, 2003.
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.
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:
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.
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,
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):
|
(copies/mL of blood) |
developing AIDS within six years |
|---|---|
|
501 - 3,000 3,001 - 10,000 10,001 - 30,000 >30,000 |
16.6% 31.7% 55.2% 80.0% |
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).
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. 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;