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to subsequent clarification to this article.
This article is part of a
collection of material on
Polio vaccines and the origin of AIDS
which in turn is part of the website on suppression of dissent.
University of California San Francisco, Mission Center, 1855
Folsom Street, Suite 566, San Francisco California 94143-0286, USA.
*California Pacific Medical Center, California Campus, 3700
California Street, PO Box 7999, San Francisco, California 94120, USA
(Correspondence to RBS).
Date received 21 September 1992
Date accepted 5 January 1993
The development of vaccines against infectious diseases has been a
boon to mankind. For example, the global eradication of smallpox was
announced by the World Health Assembly in May 1980. This long-dreaded
disease was defeated with a vaccination program that extended
throughout the poorest countries and reached the most inaccessible
areas of the world (1). There are now vaccines
that are effective in preventing such viral infections as rabies,
yellow fever, poliovirus and hepatitis B. Eventually, vaccines will
probably prevent malaria, some forms of heart disease and cancer.
Even venereal diseases may someday be a target of vaccination
programs.
Modern vaccine technology originated with the work of Pasteur in the
late 19th century. Pasteur created his successful vaccine against
rabies by weakening the virulence of the rabies virus, repeatedly
passing virus-laden saliva from the mouths of rabid dogs through the
brains of rabbits. The rabbit brains were then allowed to age in
glass bottles. Graded doses of emulsions made from the infected
rabbit brains were given in a series of injections to people bitten
by rabid animals. The injections gave these individuals immunity to
the virus before disease symptoms had a chance to appear (1).
Pasteur's technique was the first step in the giant strides of
vaccine technology that would lead to health improvements for the
future. However along with the benefits of vaccines would come some
serious new risks. Some of these risks were tragically unforeseen. In
1902, 19 Punjabi villagers given an experimental plague vaccine died
of a tetanus contaminant (2); and in 1906 an
American scientist in the Philippines inoculated 24 prisoners with an
experimental cholera vaccine that inadvertently had been contaminated
with plague. 13 of the men died (3).
The Pasteur technique was used in 1936 by Dr Max Theiler of the
Rockefeller Institute to create a vaccine against yellow fever. To
produce the new vaccine, virus strains obtained from infected
individuals were passed through the tissues of mice instead of
rabbits. Fertilized chicken eggs were then seeded with these weakened
yellow fever viruses. After a week of incubation, the chick-embryos
were removed from the eggs and finely minced. Human blood serum was
then added to stabilize the viruses. In 1938 more than one million
Brazilians were inoculated with the vaccine before it was discovered
that it had been contaminated with hepatitis B virus (1).
Despite this disaster, human blood serum continued to be used as a
stabilizer in yellow fever vaccines until 1942, when approximately
330 000 people came down with hepatitis B virus infection linked to
vaccine lots given to approximately 50 000 US Army personnel. There
were at least 84 deaths from the 1942 hepatitis outbreak (4).
However, the largest vaccine contamination in medical history
occurred from 1954 through early 1963, when millions of people around
the world received polio vaccines that had been contaminated with a
monkey virus.
The road to the successful Salk and Sabin polio vaccines was a
difficult one. The first attempt at a killed polio vaccine ended in
complete failure. In 1935, a young researcher at the New York
University School of Medicine isolated a poliovirus strain and
injected it into monkeys. He then ground up the spinal cords of the
infected monkeys and put the tissues into formaldehyde, which was
supposed to kill the virus. The researcher then inoculated monkeys,
as well as hundreds of children, with the 'killed' virus. When some
of the vaccinated monkeys were challenged with live poliovirus,
however, they promptly died of the disease. Investigation then
revealed that at least 1 child had died and 3 others had become
paralyzed after receiving the 'killed' vaccine (5).
It was thought for some time that, since laboratory signs of
poliovirus infection were found in the nervous system, the virus
could only be grown in nerve tissue. After the 1935 disaster,
scientists were afraid to use monkey nervous tissue to make a killed
vaccine. Then it was discovered that the poliovirus could grow in
monkey kidneys. This finding allowed Dr Jonas Salk to begin producing
polio vaccines with factory-like efficiency in 1952. Eventually, the
laboratories making these vaccines would consume 200 000 monkeys a
year (6).
As in 1935, formaldehyde was used by Salk to kill the polioviruses
that he had isolated. Initial tests of his vaccine showed efficacy in
preventing disease upon challenge of inoculated laboratory animals
with live virus. The largest testing of a medical product in the
history of man was then organized by the March of Dimes organization
(5). But just before the mass public inoculations
began in 1954. a worrying incident occurred. Monkeys at the National
Institutes of Health (NIH) collapsed and died after receiving an
injection of the Salk vaccine. Scientists, however, were relieved to
discover upon postmortem examination that the monkeys had not died of
polio but of some other disease frequently found in monkeys (5).
The Salk vaccine trials were interrupted again when it was discovered
that vaccine lots produced by the Cutter Company had caused some
monkeys and a total of 250 children and their contacts to develop
complete or partial paralysis. 11 of the victims died. The Cutter
product was hurriedly withdrawn, and the vaccine trial continued. It
was later determined that bottles of tissue culture fluid containing
the virus had been stored at Cutter before going through the
formaldehyde-inactivation process. Bits of monkey kidney tissue
debris had then settled to the bottom of the containers and covered
virus particles, protecting them from the formaldehyde (5).
Like Salk with his killed vaccine, Dr Albert Sabin had to isolate
viable virus from polio victims in order to develop his live oral
polio vaccine. The virus strains had to be potent enough to cause
immunity when ingested, but not so strong as to return to virulence
after undergoing Pasteur's method of repeatedly infecting laboratory
animals and harvesting the weakened viruses. Sabin grew his viruses
in monkey kidney tissues, as Salk had done. But unlike Salk, he did
not treat the viruses with formaldehyde (5).
Beginning in 1956, Sabin's live polio vaccine was tested in the
Soviet Union and Eastern Europe by the administration of sweet syrup
and sugar cubes to over 77 000 000 people. The live oral vaccine was
then adopted in 1962 as the polio vaccine of choice for the United
States and most of the world (5).
Euphoria at the triumph over the crippling disease of polio came
to an abrupt end among some members of the scientific community when
it was discovered in 1960 that both the Salk and Sabin vaccines had
been contaminated. As a result, 10 to 30 million Americans and
hundreds of millions of other people world-wide had been exposed to a
simian virus called SV40 (7). This virus was found
to produce a latent infection in monkey kidneys and had a
cancer-causing potential, as indicated by its ability to produce
tumors in laboratory animals. Tumors caused by SV40 in these animals
were often sarcomas occurring at the site of inoculation, but were
also found in kidneys and lungs. 3-week-old hamsters infected with
SV40 produced a wide variety of tumors, most of which were lymphomas
and bone cancers. SV40 was also discovered to transform human cells
in vitro, and the transformed cells could then produce localized
tumors when injected back into the human donors (7).
Initially, there was no definite evidence that SV40 was active in
humans. Even as late as 1975, the journal Science wrote:
Who could have argued against the benefits of polio vaccine in the
1950s -- yet the vaccine received by millions of people in the United
States and abroad is now known to have been contaminated with SV40, a
monkey virus which causes tumors in hamsters, though not, as luck
would seem to have it, in man. (8)
However, by then SV40 had been isolated from the brains of 2 patients
with progressive multifocal leukoencephalopathy (PML) (9)
and from an advanced melanoma (10). Moreover, an
Australian study demonstrated a correlation between polio
immunization and the development of cancers in children over 1 year
of age (11). In other reports, footprints of SV40
were found in adult and pediatric brain tumors (12),
(13), and an increased occurrence of intracranial
tumors was noted among persons who had received the contaminated
vaccines (14). SV40 was also implicated in the
development of bladder, oromaxillofacial, and parotid gland tumors
(15), (16), (17).
More recently, it has been discovered that endothelial cells
transformed by SV40 cause Kaposi sarcoma-like tumors in
immunodeficient mice (18), and that latent SV40
infection can be reactivated by simian immunodeficiency virus (SIV)
to cause kidney cancers and PML in monkeys (19).
Yet despite these findings, no major studies of the possible
consequences of the massive population exposure to SV40 have been
conducted to date.
However, in 1988, a study conducted between 1959 and 1965 in 58 807
pregnant women was reviewed (20). Data from this
Collaborative Perinatal Project demonstrated that the risk of brain
tumors among offspring of mothers who had received the Salk vaccine
was 13 times the risk among offspring of mothers who had not. The
stored serum samples of the mothers of offspring with cancers were
tested for antibodies to SV40. Despite the association between the
vaccine and the occurrence of brain tumors in vaccinee offspring,
none of the mothers' sera were positive (20). The
conclusion of the reviewers was intriguing: the cancers were probably
caused by a still-unidentified infection originating in the polio
vaccine. which (according to the reviewers) was known to have been
contaminated with numerous simian viruses (21).
What happened when SV40 was discovered in the vaccines? The Director
of the Division of Biologics Standards of the NIH issued a memorandum
to manufacturers of the live oral polio vaccine on June 30, 1961,
ordering them to exclude SV40-contaminated lots from all vaccines
used in the United States (7). Since the Asian
monkeys used in vaccine production were up to l00% infected with
SV40, the manufacturers began to import large quantities of African
green monkeys which did not naturally harbor the virus or show
antibodies to it upon capture in the wild (22).
Thus vaccine production switched from predominantly Asian monkeys to
African green monkeys in 1961.
Acquired immunodeficiency syndrome (AIDS) is a pandemic disease of
high mortality afflicting all countries of the world. The majority of
cases reported to date have been in North America, Western Europe,
Equatorial African and Brazil. The pandemic is also rapidly spreading
among other Third World countries such as Thailand and India, and has
reached such high levels in parts of Africa that some countries are
now threatened with negative population growth.
AIDS first came to the attention of medical researchers in early 1981
when the Centers for Disease Control in Atlanta, Georgia, reported
some unusual infections and cancers occurring among homosexual men in
New York, Los Angeles and San Francisco. Epidemiologists then began
looking for more cases in other cities around the United States. What
they discovered was that the first cases of the disease in the
homosexual community had probably occurred in New York City in 1978
(23).
Also occurring in New York City's homosexual community that same year
was the first large scale clinical trial of a new vaccine against
hepatitis B virus. This vaccine was derived from the blood of healthy
human carriers of the virus. The New York City Blood Center trials
were placebo-controlled, double-blind randomized tests conducted in
1083 male homosexual volunteers (1). Had this
medical experiment anything to do with the outbreak of AIDS in the
homosexual community? Since the 1000 medical workers in other parts
of the country were also given the experimental vaccine and had not
come down with AIDS, the timing was thought to be only
coincidental.
By the fall of 1981, AIDS had apparently spread beyond the homosexual
communities. The Montefiore Hospital in the Bronx began treating
cases in heterosexual intravenous drug users, and the New York and
New Jersey state health departments reported that some prison inmates
had the tell-tale opportunistic infections. The Jackson Memorial
Hospital in Miami then reported that Haitians were coming down with
the disease. Soon hemophiliacs and recipients of blood transfusions
were also dying of it (23).
In October 1983, French physicians reported that a deadly disease
almost identical to AIDS was raging in Equatorial Africa. It was
readily apparent that a contagion was causing the deaths. A
breakthrough in the mystery came when Drs F. Barre-Sinoussi and Luc
Montagnier of the Pasteur Institute in Paris discovered an unusual
new retrovirus in the blood of two victims. A year later. US
researchers led by Dr Robert C. Gallo confirmed the French finding of
the retrovirus implicated in AIDS. The new retrovirus was called
human immunodeficiency virus (HIV) (23).
The notion that AIDS was a new disease in the Western hemisphere was
supported by the fact that no hemophiliac in the United States had
died from the disease before 1980, even though blood from Haiti was
often used to produce the coagulant factor that the patients' lives
depended on (23). That the disease was also a
recent occurrence in the rest of the world was shown by the fact that
the earliest detection of HIV in the tissues of a European was in a
British sailor who died in Manchester, England in 1959 (24).
The earliest known serum sample containing antibodies against HIV
also dates from that same year (25). The serum
was collected from an unknown patient visiting a clinic in
Leopoldville, the Belgian Congo (now Kinshasa, Zaire). There is no
laboratory evidence of HIV infecting humans before 1959 (26).
In February 1983, veterinary scientists made a startling
discovery. Monkeys at the University of California Primate Research
Center and at Harvard's New England Primate Center were suffering
waves of illnesses strikingly similar to those seen in AIDS patients.
These monkey epidemics actually had begun in 1969, but were not
thought of as significant (monkeys often died in captivity) until the
recognition of AIDS in 1981 (23).
A retrovirus which was 40% identical to HIV was soon isolated from an
ailing macaque monkey. It was called simian immunodeficiency virus
(SIV). The monkey had probably been infected with SIV while in
captivity, since it was discovered that the natural hosts of SIV were
African green monkeys, just as Asian macaque monkeys had been found
in 1960 to be the natural hosts for SV40 (27).
The discovery of a virus related to HIV occurring naturally in the
monkey species that was preferred for vaccine production
caused the World Health Organization (WHO) to convene two 'informal'
meetings of experts in 1985. At the time, the conclusions issued by
WHO seemed reassuring: first, live polio vaccines prepared in African
green monkey kidney cultures during the 1970s had been tested for
retroviruses using reverse transcriptase assays and electron
microscopy, and (given the nature of the tests) none had been found;
second, WHO had tested vaccine seed stocks as well as 20 batches of
vaccine for retroviruses, and again (given the tests used) none had
been found. In addition, WHO had checked 250 vaccine recipients for
HIV antibodies, and none were positive. 30 of these recipients were
also tested for SIV antibodies, and all were negative. Finally, WHO
said that long-term follow-up of vaccine recipients had shown no sign
of adverse effects potentially associated with a retrovirus (28).
Apprehensions were revived, however, when it was discovered that some
West Africans were infected with a virus that resembled SIV (29).
The virus identified in their blood was called HIV-2. Like HIV-1, it
was soon implicated in the development of AIDS. Researchers from the
Japan Poliomyelitis Research Institute then undertook their own
investigation of vaccine contamination. They found that approximately
26% of the African green monkeys used in vaccine production in Japan
had antibodies against SIV. They killed 2 of these monkeys and looked
for the virus, but couldn't isolate it in the monkey kidneys --
though they readily found it in blood, bone marrow, spleen, tonsils
and lymph nodes. Vaccine stocks were then tested, and again (given
the tests used) no SIV was found. In addition, no antibodies to the
virus were detected in 190 vaccine recipients. However, the
conclusion of the Japanese researchers was that more caution should
be exercised. They recommended that monkeys infected with SIV should
not be used in the preparation of vaccines (30).
And sure enough, in May 1991, it was reported that researchers using
more sensitive tests for SIV had found virus DNA in virtually all of
the tissues and organ systems of infected monkeys, including the
kidneys (31). Furthermore, a SIV not previously
known to infect humans was recovered from the cancer cells of an AIDS
patient (32) and SIV infection has now been
discovered in laboratory workers, agricultural workers and urban
dwellers (33), (34).
To some researchers. there appeared little doubt that human AIDS had
its origins in the recent cross-species transfer of African monkey
viruses to man (35), and to others that this
transfer took place via contaminated vaccines (36),
(37), (38), (39),
(40). Since SIV was quite different from HIV-1,
however, it was unclear exactly how this cross-species transfer could
occur through vaccines. In 1990, 2 wild chimpanzees in Africa were
discovered to be infected with a strain of SIV that was 75-84%
identical to HIV-1 (41), leading some researchers
to call it 'the missing link' to the origins of HIV-1 in man
(42). It was thought that the chimpanzees may
have been infected through contact with an unknown monkey species
(23). This finding gave no comfort to those who
disputed the vaccination theory, since chimpanzees had been used to
attenuate and test viruses for potential use in vaccines and were
often kept in captivity by vaccine laboratories (43),
(44). Chimpanzees, therefore, could be a source
of vaccine contamination and infection of other captive monkeys. It
is now known that HIV can infect at least 1 species of macaque monkey
(45), and HIV antibodies have been detected in
captive African green monkeys (46).
Because of the size of the current epidemic in Africa and because of
HIV-positive serum showing up there as early as 1959, it is now
generally agreed that AIDS originated in Africa (23).
But if contaminated polio vaccines were responsible for the
introduction of HIV to man, why was its early occurrence so
geographically localized and not more widely distributed? Certainly
vaccination programs such as the Salk vaccine trial in the United
States and the Sabin trials in the Soviet Union and Eastern Europe
were affecting millions of people around the world. If the vaccines
were linked to the origin of AIDS, why were Africans the first to
come down with the disease? Perhaps the answer is that Africans were
not immune to polio vaccine trials.
In the 1950s there were other researchers besides Salk and Sabin
who were racing to win the polio vaccine honors. One of them was an
American who worked for one of the largest pharmaceutical
manufacturers in the world. Before attempting to develop an oral
polio vaccine, this researcher had done studies on yellow fever virus
in Brazil (47). Like Salk and Sabin, he had to
perform successful isolation of poliovirus strains, weaken the
viruses by infecting humans and laboratory animals with them, test
them for virulence, and then make the viruses proliferate in culture.
His supervisor at the pharmaceutical company preferred using fertile
chicken eggs instead of monkey kidney cultures (he was afraid of the
unseen dangers), but kidney cultures were more effective in growing
polioviruses, and so the researcher began to use them in conjunction
with chick embryo cultures (48).
The problem that the researcher faced was in testing his live polio
vaccines. His first attempt to inoculate humans came to light in
March 1951, when he announced at a medical conference that he had
given his vaccine in chocolate milk to a group of mentally defective
children in an institution in New York State (49).
When the Salk vaccine trials began, the researcher had to find a
population in another country in order to test his product. He chose
Belfast, Northern Ireland. But his vaccine trial in Belfast was
stopped when his weakened viruses appeared to return to virulence. He
then left the pharmaceutical company and went to head a research
institute, announcing, however, that he would continue to develop a
live polio vaccine (5).
In 1955, the researcher attended a rabies course organized by the
World Health Organization in Kenya. There he met the director of a
medical laboratory in Stanleyville, Belgian Congo. He proposed to the
laboratory director a program of experiments administering a new
polio vaccine to chimpanzees. The director agreed, and a colony of
chimpanzees was created in Lindi Camp, Belgian Congo, for the
American researcher's use. The animal keepers were inoculated with
the new vaccine, supposedly 'to protect them' from the experiments
with the chimps. The successful inoculation of the animal keepers was
the excuse then used to propose a mass public inoculation program
(30).
From 1957 to 1959, the American researcher's vaccine was given to
hundreds of thousands of inhabitants of the Belgian Congo, including
the area which now comprises Kinshasa and eastern Zaire as well as
the countries of Rwanda and Burundi. Over 320 000 of the vaccine
recipients were infants and children (49). In a
preliminary report in the British Medical Journal of July 26,
1958, the American researcher and his colleagues printed a detailed
map of the areas in which residents had been inoculated with the
Congo vaccine (49). This map correlates with
another map provided by authors of a report 30 years later
identifying areas of high levels of HIV infection in Equatorial
Africa (51). Another study in 1985 concluded that
HIV infection among adult residents of this area had probably
occurred in childhood (52).
In 1958, another polio vaccine researcher studied the particular
strain of attenuated poliovirus used in the Congo vaccine. He
discovered that the strain was contaminated with an 'unidentified
non-poliomyelitis virus' (53). In response, the
American researcher wrote that all vaccines made in monkey
tissues were probably contaminated with unknown simian viruses
(54), (55). In addition,
because of an embargo in India that affected the monkey trade
beginning in 1955, some of the kidneys used in producing the vaccine
may have been obtained from African green monkeys or other simian
species (6). Thus the origin of contaminating
virus, as well as the exact nature of the manufacture of the vaccine,
is uncertain (56), (57),
(58).
Because of independence and resulting tribal chaos and civil war
breaking out in the Belgian Congo in 1960, there was no long-term
follow-up of this mass inoculation. The American researcher claimed
that he had the permission of the World Health Organization to
conduct the trial, but WHO later denied it (5).
Since the Congo vaccine was never approved for human use, it was
never used after 1960. (Sabin won the live vaccine honors.) When WHO
tested seed stocks of poliovirus for HIV and SIV in 1985, had it also
tested seed stocks of this researcher's viruses? And when WHO tested
actual polio vaccines in 1985, had his 1957 Congo product been one of
them?
It is now known that HIV can readily be transmitted through mucosal
tissues (59). The 1957-1959 inoculations in the
Congo were performed by squirting live polio vaccines from syringes
into the mouths of the vaccinees (60). This
procedure would have aerosolized some of the liquid and been a very
efficient mode of HIV transmission. Assuming that the average time
between infection with HIV and development of AIDS symptoms is 8-10
years (as is currently believed), the first outbreaks of disease
occurring in Africa and related to this vaccine would have taken
place in the period from 1965 to 1971. Is it only a coincidence that
this is exactly the same period when scientists now believe that AIDS
began occurring in Equatorial Africa (61)?
It is difficult to believe that the outbreak of HIV infection in
Africa at the same time and location as this mass polio vaccine trial
is a coincidence. But medical scientists also assumed that it was a
coincidence when the first cases of AIDS in the homosexual community
in New York followed the first hepatitis B vaccine trial in that
community, just as NIH scientists believed in 1954 that some monkeys
falling down and dying of a monkey disease after receiving the
Salk-vaccine was a coincidence.
Whether the 1957-59 polio vaccine inoculations in the Belgian
Congo were the cause of the cross-species transfer of HIV to man
remains to be proven. What we do know is that the Congo vaccine was
passaged in monkey tissue, that it was contaminated with at least one
unidentified non-poliomyelitis virus, and that it was given to
hundreds of thousands of people (including infants and children) in
an area that is now endemic for HIV disease. But instead of
acknowledging the possible role of medical science in the origin of
the AIDS pandemic, some researchers have been throwing stones at the
first victims. Among theories expounded to explain the African
genesis of AIDS are: Africans eating monkeys; Africans keeping
monkeys as pets; and Africans engaging in rituals in which monkey
blood is used as a magic potion (51), (62),
(63). But Africans have engaged in these
practices for thousand of years, while AIDS is an entirely new
disease. Is it only a coincidence that HIV infection manifested
itself at the same time as the introduction of vaccines that are now
known to have been contaminated with simian viruses? Whatever the
case, as one scientist has written: 'The story of AIDS teaches us
that animal tissues should not be injected into humans, because the
risk of introducing a new virus is too great' (63).
The authors wish to acknowledge Peggy Tahir and Kathy Kimber for
research assistance, and Ann Giudici Fettner and Tom Curtis for
helpful discussion. We also thank Steven Koontz for expert technical
assistance.
After we independently developed our hypothesis and original
manuscript in September, 1991, we discovered that Louis Pascal had
already proposed a similar hypothesis about the Congo vaccine
(64). We wish to acknowledge Mr Pascal's
pioneering work (65).
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Science and Technology Analysis Working Paper No 9, Department of
Science and Technology Studies, University of Wollongong, Australia,
December 1991.
Dear Sir
Our article on polio vaccines and the origin of AIDS (Medical
Hypotheses 1994; 42: 347-354) has provoked extensive discussion
of issues related to the origin and spread of human immunodeficiency
virus (HIV). We wish to address two of these issues.
Our article failed to mention the fact that the Congo poliovirus
vaccine trials began as early as February, 1957 (1). The Manchester
sailor who presumably died of AIDS in 1959 purportedly did not return
to England until the 'first half of 1957' (2). Therefore, the
possibility exists that the sailor could have been exposed to the
HIV-like contaminant that we hypothesize may have been transmitted in
the Congo vaccine. The sailor's rapid disease progression and death
from P. carinii pneumonia may have been due to the fact that
he was unwittingly treated with massive doses of corticosteroids by
his physicians (3).
Further research has also identified the fact that sexually active
homosexuals in the United States did not initially receive the same
hepatitis B virus (HBV) vaccine that was given to US medical workers.
Homosexual men were recruited not only for participation in the HBV
vaccine trials but also for serum donation of the HBV subtype antigen
adw that was given to the homosexual volunteers (4). In the
trials involving medical workers, however, an entirely different HBV
antigen subtype obtained from dialysis patients (ayw) was used
(5). Formaldehyde was employed for inactivation of HBV in the vaccine
given to homosexual men (6). The same inactivation method was used by
Salk for his 'killed' poliovirus recipients (7). Thus, the control
and sterilization methods used in the HBV vaccine trials are open to
question.
Finally, we wish to point out two typographical errors among the
references in our article. On page 351, second column, second
paragraph, the reference cited as number 30 should be number 50.
Likewise, the preliminary report in the British Medical
Journal of July 26, 1958, cited in the next paragraph should also
be reference number 50.
B. ELSWOOD MA
*R. B. STRICKER MD
North American Biomedical Technologies, Inc.
Mt Pleasant
UT 84647
*HemaCare Corporation
San Francisco
CA 94108, USA
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PA, 1992.
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disease and Pneumocystis carinii infection in an adult. Lancet
1960; ii: 951-955.
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the USA: baseline data and protocols. J Med Virol 1979; 4:
327-340.
5. Szmuness W, Stevens C E, Harley E J et al. Hepatitis B vaccine in
medical staff of hemodialysis units. New Engl J Med 1982; 307:
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risk population in the United States. N Engl J Med 1980; 303:
833-841.
7. Shah K, Nathanson N. Human exposure to SV40. Am J Epidemiol 1976;
103: 1-12.
Date received 21 September 1994
Date accepted 25 October 1994