Slow Viruses: The Original Sin Against the Laws of Virology

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http://www.mercola.com/2000/dec/31/slow_virus.htm

Slow Viruses: The Original Sin Against the Laws of Virology

By H. Duesberg and J. Ellison

from " INVENTING THE AIDS VIRUS " , Regnery publishing, 1996

Reprinted from Health, Education, AIDS Liaison (HEAL), Toronto

From the discovery of tobacco mosaic virus through the polio epidemic,

scientists have found and legitimately blamed many viruses for a variety of

diseases, each having passed the acid test of Koch's postulates. But for

every truly dangerous virus, many more perfectly harmless passenger viruses

can be found in humans and animals.

NIH-sponsored polio research during the late 1950s proved the point.

Researchers trying to isolate new strains of poliovirus accidentally found

numerous closely related passenger viruses - -such as sackie and

echoviruses - that, like polio, infected the digestive system. Scientists

classified some of these viruses as " orphans " - viruses without

corresponding diseases.

The virus hunters could not bring themselves to believe microbes could exist

without being harmful and expected even these " orphan " viruses would someday

find appropriate sicknesses.

When trying to blame a passenger virus for a disease, however, one nagging

problem haunts the virus hunter: The laws of virology dictate that the

illness will strike the victim soon after infection. When microbes infect a

new host, they cause sickness within days or weeks at most. In order to

cause disease, viruses need to grow into sufficient numbers to take over the

body; otherwise, the host's immune defenses will neutralize the invader and

prevent disease altogether.

The rate-determining step of such fast, exponential growth is the generation

time of the virus. Since the generation time of all human viruses is between

eight and forty-eight hours, and since the infected cell produces one

hundred to one thousand viruses per day, viruses multiply exponentially,

increasing in numbers hundred- to thousand-fold per day. Within a week or

two, one hundred trillion (1014) cells can be produced - one for each of the

one hundred trillion cells in the human body.

Therefore, if scientists wish to convict an innocent virus, they must invent

a new property for it that allows the virus to violate the laws of virology.

For example, they can hypothesize a " latent period " of months or years

between the time the virus invades the body and the appearance of symptoms -

hence, a " slow " virus.

However, the slow virus concept has never been reconciled with the short

generation time of viruses and the immune system. Once the virus lies

totally dormant, an intact immune system will never allow any virus to be

reactivated to multiply into numbers that would threaten the host.

For a virus to be reactivated, the immune system first must be destroyed by

something else - the real cause of a disease. A reactivated virus would just

contribute an opportunistic infection. Thus, there are no slow viruses, only

slow virologists.

A conventional virus could, however, be slow acting in a defective immune

system.

Indeed, some exceptional victims suffer pre-existing health problems that

prevent their immune systems from reacting decisively against the virus,

allowing it to continue growing and damaging the host for a long period of

time. This can happen with virtually any type of virus, but it is extremely

rare. When such a chronic infection does occur, as with a small percentage

of hepatitis cases whose immune system is damaged by alcoholism or

intravenous drug addiction, the virus keeps growing abundantly in the body

and can easily be found by experimental tests.

Other germs, like herpes viruses, can hide out in some recess of the body,

breaking out periodically to strike again when the immune system passes a

seasonal low.In both examples, only the weakened immune system of the host

allows the infection to smolder or occasionally reappear from hibernation.

By contrast, a slow virus is an invention credited with the natural ability

to cause disease only years after infection - termed the " latent period " -

in previously healthy persons, regardless of the state of their immunity.

Such a concept allows scientists to blame a long-neutralized virus for any

disease that appears decades after infection. The slow virus is the original

sin against the laws of virology.

The slow-virus or latent-period concept, now used to connect HIV with AIDS,

can be traced back to the days of the war on polio. The researcher who

popularized this modern myth is today an authority for AIDS researchers and

one whose career epitomizes the evolution of the virus hunters over the past

three decades.

Dr. Carleton Gajdusek is a pediatrician who has worked as a virologist at

the NIH for decades. Having spent a great deal of time studying contagious

childhood diseases around the world, Gajdusek was sponsored by the NFIP and

sent to New Guinea in 1957.

There, a doctor with the local health department introduced him to a disease

called kuru, a mysterious ailment that attacked the brain, rendering the

victim increasingly spasmodic or paralyzed until death within months. The

syndrome existed only among the thirty-five thousand tribal villagers in one

set of valleys, mostly the Fore tribe.

Before Gajdusek's arrival, no outsider had ever described kuru, although the

Fore tribesmen told him the condition had begun appearing a few decades

earlier.

Gajdusek's initial study assumed the disease to be infectious. He reported

that the natives routinely cannibalized the brains of relatives for ritual

purposes, a practice that they told him had begun around the same time as

the arrival of kuru.

Gajdusek later explained to one interviewer that cannibalism " expressed love

for their dead relatives, " and that it also " provided a good source of

protein for a meat-starved community. "

Gajdusek decided that kuru was transmitted by the eating of deceased

victims' brains. Yet when he searched for a virus, he ran into a baffling

absence of evidence. None of the typical signs of infection could be found

in the patients. Their bodies showed no inflammation and no fever, no

changes were registered in their supposedly infected spinal fluid, their

immune systems failed to react as if any microbe had invaded the body, and

those people with suppressed immune defenses had no greater risk of catching

the disease.

Another scientific group soon arrived from Australia and concluded that kuru

might be genetically inherited.

Upon arriving back in the United States, Gajdusek was hired by the NIH to

work at its institute for studying neurological disease. While continuing to

monitor kuru incidence, he devoted his time to laboratory study of the

condition.

Word of his discovery of kuru meanwhile made its way to England, where

another virus hunter was investigating a sheep disease known as scrapie,

which involved symptoms of brain degeneration. The English researcher

suggested to Gajdusek that kuru might be caused by a slow virus, one with a

long latent period.

Gajdusek was immediately hooked by the revolutionary idea, despite his own

" misgivings " that genes, toxins, or nutritional deficiencies might be the

cause of kuru.

Again determined to find an elusive virus, he tried to transmit kuru from

victims to chimpanzees. But none of the animals became sick when injected

with blood, urine, or other bodily fluids from kuru patients, nor from the

cerebrospinal fluid that surrounds the brain, which should have been full of

the alleged brain-destroying virus. Indeed, the monkeys contracted no

disease even from eating kuru-affected brains - the authentic animal model

of cannibalism.

Only one bizarre experiment did work, in which the brains of kuru patients

were ground into a fine mush and injected directly into the brains of live

monkeys through holes drilled in their skulls. Ultimately, some of the

experimental monkeys suffered coordination and movement problems.

Surprisingly, though, even this extreme method could not transfer kuru to

dozens of other animal species. And no virus could be seen in the brain

tissue, even using the best electron microscopes.

At this point, one might expect Gajdusek would have suspected something was

seriously wrong with his virus hypothesis. If evidence for the invisible

virus could not be found anywhere but in unpurified brain tissue, if it did

not elicit any defensive reactions by the body, and if it could not be

transmitted in pure form to animals, then probably no virus existed at all.

The homogenized brain tissue of dead kuru patients - full of every

imaginable protein and other compounds-should in itself be toxic when

inoculated into monkeys' brains.

Nevertheless, the sick monkeys convinced Gajdusek and his colleagues he had

found a virus. Since he could not isolate it apart from the brain tissue, he

decided to study the virus and its structure with a standard experiment.

He would define which chemical and physical treatments would destroy the

microbe, thereby gathering clues about its nature. But to his astonishment,

almost nothing seemed to harm the mystery germ. Powerful chemicals, acids

and bases, boiling temperatures, ultraviolet and ionizing radiation,

ultrasound - no matter how he treated the brain tissue, it still caused

" kuru " in his lab monkeys. Further tests also proved that no foreign genetic

material, which all viruses require for their existence, could be found

anywhere in kuru-affected brains.

Employing the strongest virus-destroying treatments, Gajdusek had failed to

render the kuru brain tissue harmless in his experiments. His results lent

themselves to one obvious interpretation: No virus existed in the first

place, so it could not possibly be destroyed.

But Gajdusek clung to his virus hypothesis. Despite his disappointing

experiments, he turned the results upside down and argued that the " kuru

virus " was actually a new type of super-microbe or, as he put it, an

" unconventional virus. " This new virus also needed to act as a slow virus,

since long periods of time elapsed between an act of cannibalism and the

onset of kuru; he liberally suggested latent periods extending into years or

even decades.

At an earlier time, and in another context, Gajdusek probably would have

been ignored by orthodox scientists. But he offered this hypothesis to a

generation of scientists dominated and impressed by virus hunters.

The year was 1965, polio had largely disappeared, and the burgeoning ranks

of NIH-funded virologists welcomed any new research direction on which to

use their skills. Thus, they embraced Gajdusek's slow virus hypothesis

enthusiastically.

They listened uncritically when he claimed a similar unconventional virus

caused Creutzfeld-Jakob disease, a rare brain disorder that seems to strike

mostly Westerners having undergone previous brain surgery (obviously such

medical operations might well be suspected as the real cause).

Gajdusek proposed slow or even unconventional viruses as the causes of a

huge laundry list of nerve and brain disorders, ranging from scrapie in

sheep to multiple sclerosis and Alzheimer's disease in humans, and he was

taken seriously even though he offered no proof. Entranced, his peers

awarded him the 1976 Nobel Prize for medicine, specifically for the kuru and

Creutzfeld-Jakob viruses he has yet to find. And the NIH promoted him to

head its Laboratory of Central Nervous System Studies.

In the meantime another crucial, if embarrassing, bit of information has

emerged as a challenge to Gajdusek's virus-kuru hypothesis. The published

transcript of his Nobel acceptance speech, in a 1977 issue of Science

magazine, included a photo ostensibly showing New Guinea natives eating

their cannibalistic meal. The photo is not very clear.

When colleagues asked Gajdusek if the photo truly showed cannibalism, he

admitted the meal was merely roast pork. According to Science, " He never

publishes actual pictures of cannibalism, he says, because they are 'too

offensive.' " Unconvinced, anthropologist Lyle Steadman of Arizona State

University has investigated and directly challenged Gajdusek, claiming

" there is no evidence of cannibalism in New Guinea. "

Steadman, who spent two years doing fieldwork in New Guinea, noted that he

often heard tales of cannibalism but when he probed, " the evidence

evaporated. "

Gajdusek, angered by the hint of malfeasance, has insisted that " he has

actual photographs of cannibalism, but he would never publish them because

they 'so offend the relatives of the people who used to do it.' " This

statement contradicts his earlier claims that the tribesman proudly ate

their dead relatives out of respect, quitting the practice only in deference

to outside pressure from government authorities.

For evidence of cannibalism, Gajdusek also cited Australian arrests of

tribesmen for the alleged crime - which, as it turned out, were based on

hearsay accusations. So perhaps New Guinea natives stand falsely accused of

ritual cannibalism.

In addition, few people outside of Gajdusek's original research team have

ever personally witnessed kuru victims. This means we also depend on his own

descriptions and statistics for our knowledge of the disease itself,

particularly since he claims cannibalism and kuru both ceased to exist

within a few years after his 1957 trip. Phantom viruses, transmitted through

phantom cannibalism, cause phantom disease.

Yet Gajdusek has reshaped the thinking of an entire generation of

biologists, his seductive message of slow viruses having landed on eager

ears. He and the virus hunters inspired by him have built careers chasing

viruses and attributing them to latent periods in order to connect them to

noninfectious diseases.

SMON, the nerve-destroying disease that struck Japan during the 1960s,

became one unfortunate example. Japanese virologists, greatly impressed with

Gajdusek's accomplishments, spent years searching for slow viruses they

presumed would cause the disease and thereby delayed finding the true

cause - a prescribed medication.

Another example of a pointless virus hunt involved diabetes. Beginning in

the early 1960s, some scientists tried to blame this noncontagious syndrome

on the virus that also causes mumps. The evidence has been pathetically

sparse, forcing virologists to point to occasional children who become

diabetic after they have also suffered mumps or, if they really stretch

their case, to argue that both mumps and diabetes become most common during

the same annual season in one county of New York.

Having become soldiers without a war, veteran polio virologists invaded the

diabetes field as well, proposing since the early 1970s that sackie

viruses may cause the disease. Antibodies against several strains of these

harmless viruses, first discovered as by-products of polio research, have

been found in a few diabetic children.

But between 20 percent and 70 percent of young diabetics have never been

infected, and the remainder have already neutralized the virus with their

immune systems long before the onset of diabetes. Apparently, an equal

percentage of non-diabetic children have also been infected with these

sackie viruses. Needless to say, none of the above viruses meets Koch's

postulates for causing diabetes.

Koprowski, like Gajdusek, typifies the modern virus hunter. Although

Koprowski's virology career began earlier, Gajdusek's work helped rescue

Koprowski from the obsolescence that threatened polio researchers after the

war on polio. Like so many of his colleagues, he found his newest calling in

the war on AIDS.

Koprowski's work on viruses started at the Rockefeller Institute in New

York. By the late 1940s he moved across town to the Lederle pharmaceutical

company, where he worked feverishly to develop a polio vaccine. By 1954 he

had invented one, but Jonas Salk was announcing the field trials for another

vaccine, and Koprowski's already-tested product was shunted aside by Salk's

public acclaim.

Koprowski left Lederle in I957 to take a position as director of the

privately endowed Wistar Institute of Pennsylvania, where he began tests on

humans and stepped up the campaign to get approval for his vaccine. By now

Albert Sabin had tested his own polio immunization on millions of people in

foreign countries, completely overshadowing Koprowski's equally successful

but less-promoted vaccine. Nevertheless, Koprowski's day did arrive. His

vaccine became the standard used by the World Health Organization in America

during the late 1950s and 1960s.

In the meantime he spent several years studying the rabies virus and

creating a vaccine against that virus, which attacks the brain and nervous

system. But because rabies is relatively rare, Koprowski's vaccine never

achieved the stardom of other immunizations. More important, however, his

rabies research placed him squarely in the field of neurological diseases

just in time to meet up with Gajdusek's kuru work.

The news of slow viruses enticed Koprowski with visions of groundbreaking

science. He quickly realized that the notion of slow viruses could become a

useful tool, allowing him to source slow, noninfectious diseases to viruses,

so long believed to be fast-acting agents. He participated as a " program

advisor " in Gajdusek's first major conference on slow and unconventional

viruses held in 1964 at the NIH headquarters in Bethesda, land. From

that point forward, Koprowski joined the new virus-hunting trend from

which he would never turn back.

His first big opportunity to take a crack at slow viruses came at the end of

the 1960s. Subacute sclerosing panencephalitis (SSPE), a mouthful of a name

for such a rare condition, attacks a small number of schoolchildren and

teenagers each year, causing dementia, learning disabilities, and finally

death.

Doctors first recognized SSPE in the 1930s, and by the 1960s the virus

hunters were searching for an SSPE germ. At that time, the most fashionable

viruses for research belonged to the myxovirus family, which included the

viruses that caused influenza, measles, and mumps. Animal virologists

therefore started by probing for signs of myxoviruses.

Excitement mounted after trace quantities of measles virus were detected in

the brains of SSPE patients, and in 1967 most of the victims were found to

have antibodies against measles. The facts that SSPE affected only one of

every million measles--infected people and that this rare condition appeared

from one to ten years after infection by measles were no longer a problem:

Researchers simply hypothesized a one- to ten-year latency period. Little

wonder they could also easily rationalize that one virus could cause two

totally different diseases.

Koprowski's foray into SSPE research began in the early 1970s. He began

isolating the measles virus from dying SSPE victims, a nearly impossible

task because their immune systems had long before completely neutralized the

virus (some SSPE cases, moreover had never had measles, merely the measles

vaccine). His characteristic patience nonetheless paid off, yielding a tiny

handful of virus particles from some patients that could be coaxed to begin

growing again, if only in laboratory cell culture.

In other patients only defective viruses that were unable to grow had

remained so many years after the original measles infection.

Rather than concluding the measles virus had nothing to do with SSPE, he

employed the new logic of virus hunting to argue that a defective measles

virus caused SSPE!

Koprowski continued this line of SSPE research for several more years. But

in 1985 Gajdusek himself entered the SSPE fray, publishing a paper with

leading AIDS researcher Gallo in which they proposed that HIV, the

supposed AIDS virus, caused SSPE while remaining latent. With hardly a

blink, several leading virologists jettisoned the old measles-SSPE

hypothesis in favor of a newly popular, but equally innocent, virus.

Multiple sclerosis (MS), the notorious disease that also attacks the nervous

system and ultimately kills, has provided yet another opportunity for the

virus hunters.

First, they blamed the measles virus starting in the 1960s, since many MS

patients had antibodies against the virus. Ten years later others suggested

the mumps virus, which is similar to measles. The early I980's brought the

coronavirus hypothesis of MS, the category of virus better known for causing

some colds. In 1985, with Gajdusek stealing his thunder for SSPE, Koprowski

also published a scientific paper that year in Nature with Gallo, in

this case arguing that some virus similar to HIV now caused MS.

Unfortunately for Koprowski, even this hypothesis was abandoned within just

a few years.

Phantom Viruses and Big Bucks

Most virus hunters prefer chasing real, if arguably harmless, viruses as

their deadly enemies. But Gajdusek's " unconventional " viruses - the ones

neither he nor anyone else have ever found - have been making a comeback in

recent years. Given the abundance of research dollars being poured into

biomedical science by the NIH and other agencies, opportunistic virus

hunters have been finding creative ways to cash in. One increasingly

successful method utilizes modern biotechnology to isolate viruses that may

not even exist.

Hepatitis, or liver disease, has yielded profitable virus-hunting

opportunities in recent years. Hepatitis can be a truly painful affliction,

starting like a flu but progressing to more severe symptoms, including high

fevers and yellow skin. At least three varieties seem to exist.

Hepatitis A is infectious, spread through unsanitary conditions, and is

caused by a conventional virus.

Hepatitis B also results from a virus (discovered in the 1960s) and is

transmitted mostly between heroin addicts sharing needles, among sexually

active and promiscuous people, or in the Third World from mothers to their

children around the time of birth.

A third type of hepatitis was found in the 1970s, again restricted to heroin

addicts, alcoholics, and patients who have received blood transfusions.

Most scientists assumed these cases were either hepatitis A or B, until

widespread testing revealed neither virus in the victims. Roughly

thirty-five thousand Americans die each year of any type of the disease, a

fraction of those from this " non-A, non-B hepatitis, " as it was known for

years.

Today it is called hepatitis C. This form of hepatitis does not behave as an

infectious disease, for it rigidly confines itself to people in well-defined

risk groups rather than spreading to larger populations or even to the

doctors treating hepatitis patients. Yet virologists have been eyeing the

disease from the beginning, hoping one day to find a virus causing it.

That day arrived in 1987. The laboratory for the job was no less than the

research facility of the Chiron Corporation, a biotechnology company located

directly across the bay from San Francisco. Equipped with the most advanced

techniques, a research team started its search in 1982 by injecting blood

from patients into chimpanzees. None of monkeys contracted hepatitis,

although subtle signs vaguely resembling infection or reddening did appear.

For the next step, the scientists probed liver tissue for a virus. None

could be found. Growing desperate, the team fished even for the smallest

print of a virus, finally coming across and greatly amplifying a small piece

of genetic information, encoded in a molecule known as ribonucleic acid

(RNA), that did not seem to belong in the host's genetic code.

This fragment of presumably foreign RNA, the researchers assumed, must be

the genetic information of some undetected virus. Whatever it was, liver

tissue contains it only in barely detectable amounts. Only about half of all

hepatitis C patients contain the rare foreign RNA. And in those who contain

it, there is only one RNA molecule for every ten liver cells - hardly a

plausible cause for disease.

The Chiron team used newly available technology to reconstruct pieces of the

mystery virus. Now they could test patients for antibodies against this

hypothetical virus and soon discovered that only a slight majority of

hepatitis C patients had any evidence of these antibodies in their blood.

Koch's first postulate, of course, demands that a truly harmful virus be

found in huge quantities in every single patient. His second postulate

requires that the virus particles be isolated and grown, although this

supposed hepatitis virus has never been found intact. And the third

postulate insists that newly infected animals, such as chimpanzees, should

get the disease when injected with the virus.

This hypothetical microbe fails all three tests. But Koch's standards were

the furthest thing from the minds of the Chiron scientists when they

announced in 1987 that they had finally found the " hepatitis C " virus.

Now more paradoxes are confronting the viral hypothesis. Huge numbers of

people testing positive for the hypothetical hepatitis C virus never develop

any symptoms of the disease, even though the " virus " is no less active in

their bodies than in hepatitis patients.

And according to a recent large-scale study of people watched for eighteen

years, those with signs of " infection " live just as long as those without.

Despite these facts, scientists defend their still-elusive virus by giving

it an undefined latent period extending into decades.

Paradoxes like these no longer faze the virus-hunting research

establishment. Indeed, rewards are generally showered upon any new virus

hypothesis, no matter how bizarre. Chiron did not spend five years creating

its own virus for nothing. Having patented the test for the virus, the

company put it into production and began a publicity campaign to win

powerful allies.

The first step was a paper published in Science, the world's most

prestigious science magazine, edited by Dan Koshland, Jr., professor of

molecular and cell biology at the University of California at Berkeley.

Penhoet, chief executive officer for Chiron, also holds a position as

professor of molecular and cell biology at the University of California at

Berkeley. The NIH-supported virology establishment soon lent the full weight

of its credibility to the hepatitis C virus camp. As Chiron's CEO boasted,

" We have a blockbuster product. "

A regulatory order from the Food and Drug Administration (FDA) to test the

blood supply would reap enormous sales for Chiron.

Their big chance presented itself in late 1988 as a special request from

Japanese Emperor Hirohito's doctors. The monarch was dying and constantly

needed blood transfusions; could Chiron provide a test to make sure he

received no blood tainted with hepatitis C? The biotech company jumped at

the opportunity, making for itself such a name in Japan that the Tokyo

government gave the product its approval within one year.

The emperor died in the meantime, but excitement over Chiron's test was

fueled when the Japanese government placed hepatitis C high on its medical

priority list. Chiron's test kit now earns some $60 million annually in that

country alone.

By the middle of 1990, the United States followed suit.

The FDA not only approved the test, but even recommended the universal

testing of donated blood.

The American Association of Blood Banks followed suit by mandating the $5

test for all 12 million blood donations made each year in this country -

raking in another $60 million annually for Chiron while raising the nation's

medical costs that much more.

And all this testing is being done for a virus that has never been isolated.

Profits from the test kit have generated another all-too-common part of

virus hunting. With Chiron's new income from the hepatitis C test, Penhoet's

company bought out Cetus, another biotech company, founded by Glaser,

who, like Penhoet, also holds a position as professor of molecular and cell

biology at the University of California at Berkeley. And Chiron made an

unrestricted donation of about 12 million to the Department of Molecular and

Cell Biology at the University of California at Berkeley that generates

$100,000 in interest each year.

Unfortunately for Duesberg, who belongs to the same department, his

supervisor is yet another professor who consults for Chiron Corporation -

and displays little sympathy for Duesberg for challenging modern virus

hunting by restricting his academic duties to undergraduate student teaching

and by not appointing him to decision-making committees.

Such conflicts of interest have become standard fixtures in university

biology departments.

The modern biomedical research establishment differs radically from any

previous scientific program in history. Driven by vast infusions of federal

and commercial money, it has grown into an enormous and powerful bureaucracy

that greatly amplifies its successes, all the while stifling dissent.

Such a process can no longer be called science, which by definition depends

on self-correction by internal challenge and debate.

Despite their popularity among scientists and their companies, " latent, "

" slow, " and " defective " viruses have achieved only little prominence as

hypothetical causes of degenerative diseases before the AIDS era. Their

hypothetical role in degenerative diseases, which result from the loss of

large numbers of cells, remained confined to rare, exclusive illnesses like

kuru and hepatitis C.

However, because latent, slow, and defective viruses cannot kill cells, such

" viruses " eventually achieved prominence as hypothetical causes of cancer

and thus entered the courts of health care and medical research. The next

chapter describes the terms under which these viruses were promoted as

causes of cancer and how some of these terms were eventually used to promote

latent, slow, and defective viruses as causes of degenerative diseases

including, above all, AIDS.

Reprinted from Health, Education, AIDS Liaison (HEAL), Toronto

http://www.harmsen.net/heal/