Slow Viruses

[Guest guest]

OFF TOPIC BUT A GOOD READ...THANKS MERMIE FOR SENDIG TO ME:)

Subject: SLOW VIRUSES

Date: Sun, 27 May 2001 10:23:14 -0700

Slow Viruses: The Original Sin Against the Laws of Virology - This

excerpt from 'Inventing the AIDS Virus' by Duesberg and

Ellison explores the recently coined term " latent period " ,

maintaining that it is a fabrication established to support the false

theories of diseases such as HIV/AIDS and Hepatitis C

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, how-ever, 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 head-quarters 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, more-over 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 I980s 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 ofthese

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.