The
River: A Journey to the Source of HIV and AIDS
by Edward Hooper
Chapter 1
the river in cross section: frozen
moments of flow We shall not cease from exploration And the end of all
our exploring Will be to arrive where we started And know the place for
the first time.
—T. S. Eliot, Little
Gidding
frozen in time: 1959
Let us take a moment in time. Let us freeze
it. Let us watch as the crystals form, as it becomes translucent. Let us
mount it on a slide and lift it carefully to the microscope stand. Using
strong light and mirrors, adjusting the focus, let us see what can be
seen.
Truth, like beauty, resides in the eye in
the beholder. Whatever the material on that glass slide —be it a moment
in history or a cluster of cells —it is inevitable that what you see and
what I see will be different. I may see colors, a myriad of dots, a divine
impressionistic sweep of light and shade. You, the historian, may see a
pattern, a grand design, the beginning of a chain of cause and effect. Now
let us change the eyepiece, increase the magnification. This time I may
see a meaningless smudge with specks of darkness within, while you, the
biologist, may see a nucleus and mitochondria, the beauty of simplicity,
the pulsating potential of a cell ready to divide.
How will we describe our truths, you and I,
for the blind man, for the child without a microscope? And whose
description will be more accurate? While I pack away the lenses, and you
put the glass rectangle into its slot in the velvet-upholstered case,
remember this. Empirically, the image that you see and that which I see
are the same. What differs is our relative clarity of vision, level of
understanding, power of analysis —and the language we choose to describe
what lies beneath the lens.
It is the February of 1959. It is a
particular moment in the history of the world. The old order is breaking
up; the barriers of time and space are tumbling. The first jet planes are
taking off, heading for destinations —Hong Kong, Nairobi, Sydney —that
once were days away, but are now just hours. There is a new type of global
language too, as people talk of atom bombs, the cold war, of international
power blocs, and the arms race.
It is also a particular time in the history
of Africa. The wind of change is blowing hard: in the last two years Ghana
and Guinea have attained independence, and across the continent the clamor
is rising. The old colonial powers —the British, the French, the
Belgians —are, each in their own time, recognizing the inevitability of
the process, acknowledging that these are the final days of the Raj; only
the Portuguese are still defiantly opposed. Here, in the Belgian Congo,
amidst the wide, gracious, tree-lined avenues of the capital,
Leopoldville, the first round of riots has just ended, with more than
fifteen hundred Africans arrested. The Belgians are bewildered. People
returning to Brussels tell the man from the London Times that
"something untoward is brewing at Stanleyville," the town a
thousand miles upstream at the great bend in the river.
Meanwhile two doctors, one American and one
Belgian, are traveling around the capital immersed in their own world,
which is one of scientific inquiry. The American, funded by grants from
the U.S. Public Health Service and the Rockefeller Foundation, arrived in
Leopoldville just after the end of the unrest, and neither saw evidence of
its impact nor, one suspects, would have had much appreciation of its
significance had he done so. The Belgian, for his part, has just been
appointed chair of microbiology at the newly built university of Lovanium,
eight miles from the city center on the banks of the Congo River —but
for all that, he is happy for the chance to collaborate with such a rising
star in the firmament of human genetics. These are impassioned men
operating in an era that reveres their activities, in an era when science
is the new religion, and the men in white coats its prophets and priests.
Over the next few weeks the American, Arno
Motulsky, and the Belgian, Jean Vandepitte, with the help of other local
doctors, start collecting blood samples from medical staff, hospital
patients, and police recruits in Leopoldville, and from a large group of
villagers living to the south, near the Angolan border. Motulsky is keen
to investigate the relative incidence of two genetic traits in different
ethnic groups in sub-Saharan Africa, and their possible relationship to
malaria. Later, he visits several other regions of the Belgian Congo and
the neighboring territory of Ruanda-Urundi, administered by the Belgians
as a trusteeship since Germany was dispossessed of its African colonies
after the First World War. At the end of three months, he and his Belgian
colleagues have collected nearly eighteen hundred blood samples from eight
different population groups, including pygmies from the Ituri Forest,
hospital patients from Stanleyville, and schoolchildren from the two
principal ethnic groups in Ruanda-Urundi, the Tutsi and the Hutu. Most of
these samples are finger-prick specimens mounted on glass slides and
examined in local laboratories the same day, but more than seven hundred
are samples of whole blood, which are then refrigerated and flown back to
Motulsky's department at the University of Washington in Seattle.
As Jean Vandepitte bids farewell to Arno
Motulsky at the airport, neither man has any inkling of the additional
significance which one of these 5-milliliter blood samples will assume
just over a quarter of a century later.
Independence arrives, and the countries
where Motulsky obtained his specimens subsequently become known as the
Republic of the Congo, Rwanda, and Burundi. Over the next few years, all
three experience tragic events, as ethnic tensions and the meddling of
foreign powers combine to promote upheavals, violence, and bloodshed.
Meanwhile, back at the University of Washington, various tests are
conducted on the blood samples, and a series of papers published in
journals of genetics.
Several years later, Moses Schanfield, a
professor from Emory University, contacts Motulsky to ask if he can
undertake further genetic studies on the Congo cohort, and the remaining
672 frozen plasmas are flown to Atlanta. Finally, in 1985, they change
hands once more, and are given to another Emory professor, André Nahmias,
who has an entirely different interest. He wants to test them for the
presence of antibodies to a virus that has suddenly entered the medical
limelight —the virus that causes AIDS. He examines not only the Motulsky
samples, but a further 500 plasmas originating from South Africa,
Mozambique, and Congo-Brazzaville, and collected at various times between
1959 and 1982.
Over the next few months, the specimens are
examined exhaustively, first at Emory and then at Harvard; the results are
then confirmed at two other laboratories, by a total of four different
testing procedures. Of all the plasma samples, just one comes out strongly
positive on all the tests. Its code number is L70, and it comes from a
group of ninety-nine specimens taken in 1959, somewhere in or around
Leopoldville.
In the mid-eighties, scientists are just
awakening to the possibility that HIV (as it will soon become known) may
have been present in sub-Saharan Africa for some years before the
recognized start of the AIDS epidemic in North America and Europe in 1981,
and the Nahmias investigation provides the first really dramatic evidence
in support of this hypothesis. No further details appear to be available,
however, about the source of the L70 sample. In the 1986 letter to The
Lancet in which he reports the results of his investigations, Nahmias
comments simply: "The identity of the donor is no longer known."
Nearly four decades have passed since his
trip to Africa, but Arno Motulsky, now professor emeritus, still lives in
Seattle and is still a man of spiky brilliance. And his papers do reveal a
little more about the identity of the L70 donor. They record that the
blood was taken from a Bantu male, one of seventy-eight men in the group
of ninety-nine designated as "Leo." Unfortunately, of all the
twelve groups tested by Motulsky, there is less documentation about the
"Leo" series than any of the others. Motulsky says that most of
them were normal members of the population, and that around 20 percent
were hospital patients. The identity of the hospital is not recorded,
although Jean Vandepitte, now professor emeritus at the University of
Leuven and the Institute of Tropical Medicine in Antwerp, believes that it
was probably that at Lovanium, the great campus the Belgians constructed
on the outskirts of Leopoldville, and which many consider to have been
their parting gift to the country they ruled for seventy-five years.
Whatever, it appears that this tiny amount
of blood, taken in 1959 from an unknown man living in the city now known
as Kinshasa, the bustling capital of the Congo, represents the oldest
specimen of the human immunodeficiency virus in existence. We shall return
to it later in the story.
As with the early course of a river, where
water may seep unnoticed through sphagnum bogs, or plunge underground
through limestone, so with the early course of a new disease. It is, of
course, entirely possible that the first traces of an unusual and hitherto
unseen condition (especially a disease syndrome with a diverse range of
presentations and a long latency period, like AIDS) will pass by
unremarked. There again, perhaps because of serendipity, or an especially
conscientious team of doctors, it can also happen that the crucial clues
are noticed and recorded for posterity.
On January 31, 1959, just as Arno Motulsky
was leaving for Africa, a twenty-five-year-old man from Reddish, a
working-class suburb adjoining Manchester, was getting engaged. At the
same time (though he could not have known it) he was becoming involved in
a chain of events that would end up with his becoming public property,
part of global folklore. For this man, David Carr, was about to become
inextricably entwined with the early history of the AIDS epidemic.
By that year, Reddish was a place in
decline. Cotton manufacturing was moving overseas to new nations where
wages were lower, and the town's huge mill finally closed its doors at the
end of 1958. Many were reemployed at the breweries and railway repair
yards, but the soul of Reddish seemed to have departed, together with much
of its disposable income. There was only a light scattering of TV aerials
on the long terraced roofs around the mill. For the fortunate few in the
black-and-white flicker below, Harold Macmillan was meeting with General
Eisenhower, issuing joint communiqués from Chequers, reminding Britons
that —with a nuclear deterrent of their own —they were one of
"The Big Three," telling them they had never had it so good. Not
all believed him.
The country that had, until recently,
viewed itself as lying at the fulcrum of global activity was now in
reality a leviathan, grown loose-eyed and sleepy, still touched by
memories of wartime sacrifice and ration books. Its grandiose dreams were
fading, as one by one the countries of Africa and Asia were granted
freedom; the sun was setting on an empire over which, it was once boasted,
the sun never set.
Dave Carr was a former seaman, a local
Reddish lad with crinkly eyes and wavy brown hair. "Elsie," his
fiancé, was from northern Manchester; she had a strikingly trim figure
and bright red hair, worn in a perm. They worked within yards of each
other in the city center —he as a printer on the Manchester Evening
Chronicle; she as a mantle machinist, making ladies' gowns and raincoats.
Each had a good sense of humor, but whereas Dave was easygoing, Elsie was
strong-willed and known for speaking her mind. Their friends thought them
a perfect match. To save money, they had bought the engagement ring from a
pawnbrokers' shop —a pledge made but broken, never redeemed.
Whether or not Dave and Elsie were planning
an early wedding is a moot point, for since the end of the previous year,
Dave's health had suddenly collapsed. Throughout 1958 he had suffered from
small but persistent ailments —chronic gingivitis, and a funny
measles-like rash on his back and shoulders, for which he attended a local
skin clinic on a monthly basis, receiving steroid creams and two courses
of radiotherapy. In November, he had to have part of his lower gum removed
in a gingivectomy, but for some reason, the wounds never healed properly.
Then, toward Christmas, he developed a nagging cough and began having
serious problems with his breathing. He had only to walk a few hundred
yards or climb a flight of steps to end up gasping, panting, propped up
against wall or lamppost. He was losing weight as well —a lot of it.
In the weeks that followed the engagement,
Dave Carr got substantially worse. In February the hemorrhoids and
pruritis ani from which he had suffered intermittently for years suddenly
became more inflamed, and he developed a painful sore around the anus. The
weight loss, night sweats, and fevers also became more pronounced, and now
his chronic cough began bringing up mucus which was flecked with blood. He
began to take more and more time off work at the Chronicle, and after
work, over a pint, his mates would talk in undertones about leukemia, or
about his picking up some strange bug while swimming in the local canal or
during his National Service in the navy.
In March, Dave began seeing a private
consultant, Dr. Charles Don. On the morning of his second appointment, in
early April, a telegram was delivered, requesting a postponement, but
Dave's parents told him to turn up anyway. It was as well that he did. Dr.
Don took one look at his patient's anal fissure, now three inches long,
and arranged for him to be admitted to the Manchester Royal Infirmary.
Ward M4 (male) at the MRI was to become Dave's home for the next five
months.
The physicians in charge of the ward,
notably the senior registrar, John Leonard, and the senior house officer,
Trevor Stretton, were baffled by David Carr's various maladies —the
weight loss, persistent cough, breathing difficulties, the sore on his
bottom, and the small "blind boil" that had appeared at the tip
of his left nostril. All they knew was that here was a man just a few
years younger than themselves, who until recently had appeared quite
healthy, and who was now wasting away before their eyes, strafed by a
series of apparently untreatable infections.
Their first response was to suspect miliary
TB, an unusual form of tuberculosis, but when Dave failed to respond to
the appropriate drugs, they wondered about sarcoidosis, and the collagen
diseases (nowadays known as autoimmune disorders). They had already
checked all the known cancers and lymphomas, but now they began to wonder
about the possibility of an unknown malignancy.
Of course, they asked him questions about
his past, about his time in the navy —and noted that he did not recall
having any tropical diseases. They tested for syphilis and found him
negative, but they did not question him about his sexuality, for such
matters were less frequently and openly discussed in 1959 and, in any
case, did not seem relevant to the case. They tried further radiotherapy,
together with chemotherapy, steroids, and an even wider range of drugs.
Once or twice he picked up briefly, for a week or two, but the remission
never lasted.
By June, Dave's fevers were becoming more
frequent, and his breathing steadily worse. The spot in his nostril became
an ulcer, which started eating away at his nasal cartilage and upper lip;
shaving became impossible, so he grew a mustache, but it did little to
hide the spreading open wound from view. The anal lesion also grew, until
it became an excavated sore the size of a small football, covering most of
his buttocks. A cradle was placed over him to keep the weight of the
blankets from his body. But most dramatic of all was the emaciation. One
year before, David Carr had been a strapping lad of 185 pounds,
broad-shouldered and somewhat overweight for his five foot seven inch
frame. Now, however, his face was drawn and his bones clearly visible
through the skin. Elsie and his parents called at the hospital every day,
but Dave began to discourage visits from friends.
Just a few days before Dave and Elsie's
engagement, an unusual death occurred in Canada, at Toronto General
Hospital. The deceased was a thirty-six-year-old Japanese-Canadian man,
who had been admitted six weeks earlier with severe breathing
difficulties. Eventually he suffocated to death. At autopsy, Dr. John
Barrie, a British émigré pathologist, found a honeycomb of cyst-like
cavities throughout the man's lungs, which he ascribed to Pneumocystis
carinii, a rare pathogen that takes advantage of a state of lowered
resistance in the human host.
However, in the case of this patient,
George Y., there were no clear indications as to what might have caused
his resistance to be diminished, and for this reason Dr. Barrie wrote a
paper about the case, which was published the following year.13 "We
are not aware of any reports of deaths in adults which have been caused
primarily by infection with Pneumocystis," wrote Barrie, in the
introduction. He reported that the patient had been well until March 1958,
when he had experienced a five-day fever with chills, headache, and
nonproductive cough, an episode that was repeated several times in the
following months. In late October, he began to experience sharp pains in
his chest, drenching night sweats, and pronounced weight loss. By December
1958, when he was admitted to hospital, he was losing weight dramatically,
had chest pains, and would become breathless after the slightest exertion.
The physicians administered a range of drugs in a bid to save his life
—culminating in 100 milligrams (a very heavy dose) of a steroid,
prednisone, every day for the final fortnight. At the autopsy, the only
contributory factor noted was a mild cirrhosis of the liver, presumably
from drinking.
In 1991, I located Dr. Barrie, by then in
his late eighties, and he managed to procure a copy of his original
autopsy report. This revealed that George had worked as a sawmill operator
during the forties and then, for ten years from 1948, as a carpenter in
Edmonton, Alberta. In 1958, however, he abandoned his steady job and
migrated north to work in the Northwest Territories. It was when he
arrived there in March that he suffered his first illness, followed by
another in May, when "he developed . . . a virus infection common in
the camp in which he was working at that time." Something, it seems,
had caused George Y. to become immunocompromised at some point during the
final year or so of his life, leading to his demise from PCP in January
1959.
A few months later, in June of that year,
Pneumocystis carinii pneumonia was responsible for another most unusual
adult death at the Kings County Hospital in Brooklyn, New York. The
patient, Ardouin A., had been born in Jamaica of Jamaican parents, but the
family had moved to Haiti when he was seven, and he emigrated from there
to the United States ten years later, marrying a Haitian émigré soon
afterward. Ardouin was an attractive man, with slicked-back hair, a thin
mustache, and sharp dress sense —and he apparently had several
girlfriends on the side. He also had several jobs, but after the Second
World War began working as a shipping clerk for a dress manufacturer on
Seventh Avenue in Manhattan —a post he was to keep for the rest of his
life.
Ardouin had never been seriously ill in his
forty-nine years, but in March 1959 his smoker's cough became more severe
and productive of large amounts of sputum, and he began losing weight. By
June, his chest pains and wheezing had gotten so serious that he was
admitted to hospital, where he was quickly placed on a respirator and
treated with steroids. His doctors asked many questions and wanted to know
whether he had ever been to Nevada, which suggests they thought he might
have been present at an atom bomb test; he had not. They also tested his
blood, bone marrow, and urine (including a check for beryllium content,
since he had apparently broken a fluorescent lamp some while earlier), but
found nothing untoward. Ardouin, meanwhile, became weaker, and told his
family that he wanted to be buried in his blue suit. His prognosis was
correct, for on June 28 he had to have a hole cut in his windpipe to
assist his breathing, and he died later the same day.
His widow was terrified, fearing that
voodoo was involved —while the pathologist, Gordon Hennigar, was
mystified as to why he could find no underlying disease that might explain
why the Pneumocystis infection had taken hold and proved so remorseless.
The case was sufficiently unusual to be written up in two medical
journals, and although one of the papers pointed out that the white blood
cell count had sometimes been high (which might suggest a leukemoid
reaction), its conclusion was that Ardouin represented "the first
reported instance of unassociated [Pneumocystis carinii] disease in an
adult." Dr. Hennigar, meanwhile, decided to pickle Ardouin's lungs
for posterity.
While Gordon Hennigar filled his bell jar
with formalin, back in the Manchester Royal Infirmary, David Carr's
symptoms were progressing inexorably. By July, the latest theory of his
doctors was that he was suffering from Wegener's granulomatosis, a fatal
disorder of the connective tissue that often involves the respiratory
tract. Altogether, just fifty-six cases of Wegener's had been recorded in
the medical literature.
Dave kept cheerful to the end, but by
August he and Elsie and his parents all knew that he was dying. At this
stage, pustular ulcers were appearing on his stomach, inner thighs, and
fingers, over both his lips, and inside his mouth. He developed spiking
fevers and found it more and more difficult to breathe. He had what
appeared to be an untreatable pneumonia, and sometimes he became cyanotic,
with his extremities turning blue from lack of oxygen and his fingers
swelling at the tips. In the final week of his life, he was put in a
separate room and treated with Euphoricus, a sedative cocktail of
morphine, cocaine, and gin. At three o'clock on the afternoon of August
31, as he was being lifted on to the commode, he died.
It was only when the tissues taken at
autopsy were examined microscopically by pathologist George Williams that
two unexpected conditions were identified. One was disseminated "cytomegalic
inclusion disease," a condition caused by a virus that, the following
year, would be renamed cytomegalovirus, or CMV. The other was Pneumocystis
carinii pneumonia, PCP.
Thus, in the first eight months of 1959,
three apparently healthy men from different parts of the world died
primarily as a result of PCP, a disease previously unrecognized in healthy
adults. During the next twenty-five years, the doctors who had been
involved with these three patients, either alive or dead, continued to be
intrigued by their illnesses, and by the continuing mystery of underlying
cause. At times they would review their papers, and wonder about this
possibility or that —exposure to some toxic agent, an undiagnosed cancer
or leukemia, a congenital immunodeficiency that they had failed to spot.
But none of these tentative explanations was entirely convincing. It was
only in the eighties, after the recognition of the AIDS epidemic, that a
solution to the mystery seemed to have emerged —for between 1983 and
1987, several researchers proposed that these three deaths might represent
pre-epidemic cases of AIDS.
Were they right? Was David Carr in Reddish
an antecedent of the coming epidemic? Were George in Toronto and Ardouin
in New York? Were these men the harbingers of a new disease beginning its
global spread, the earliest, unfortunate infectees with some new pathogen
that was already —in 1959 —becoming widely dispersed, albeit extremely
thinly? This is one of the hypotheses that we will be investigating in
some detail in the course of this book. As the condition of David in
Manchester deteriorated ever faster, and as Ardouin in Brooklyn entered
the final week of his life, a very different event was taking place in
Washington, D.C. Whereas the savage disease processes affecting these two
men were graphic reminders of how, even in the best-equipped medical
systems in the world, nature could still get the better of doctors, this
latter event was essentially a celebration of the triumph of modern
medicine over disease.
Poliomyelitis, until then the most dreaded
of illnesses, the one that caused authorities to close down schools and
swimming pools, and that persuaded people across America to donate their
small change to the March of Dimes, was about to be vanquished, and the
world's pre-eminent virologists and physicians had gathered in the
national capital to witness the coup de grace.
The event was called the First
International Conference on Live Poliovirus Vaccines, and among the
seventy attendees from the ranks of the great and the good were two
doctors —Albert Sabin and Hilary Koprowski —who had probably done more
than any others to bring about this hugely popular scientific achievement,
this metaphorical lunar landing of the fifties. Both of them had developed
their own sets of oral polio vaccines (OPVs), and all the indications were
that the United States was about to adopt either Sabin's or Koprowski's
strains. In fact the stakes were even higher, for it was apparent that
whichever vaccine set was approved in America would —in all probability
—be adopted by the rest of the world also.
The principle of vaccination is that a tiny
amount of a virus (either a weakened live virus, or else a virus that has
been killed by chemicals like formalin) is introduced to the vaccinee,
whose immune system responds by producing the appropriate antibodies. The
subject will then be protected against exposure to the "wild"
form of the virus found in nature, which might otherwise cause serious
disease. In the case of poliomyelitis, the first vaccine to be adopted for
general use in America —in 1955 —was the killed vaccine developed by
Jonas Salk. Referred to by scientists as an inactivated polio vaccine, or
IPV, this preparation had already, by 1959, been given to millions of
children around the world. It was, however, gradually falling out of favor
by the end of the decade —and not just because sugar lumps are more
popular with kids than shots in the arm. More crucially, there were
demonstrable problems with its safety and effectiveness. In one infamous
episode, the "Cutter incident," hundreds of vaccinees and their
close contacts contracted polio because a batch of vaccine had been
improperly inactivated. Furthermore, by the end of the decade, an
increasing number of vaccinees were becoming paralyzed even after
receiving the full course of three shots, showing that not all batches of
the vaccine were protective.
By 1959, many virologists were persuaded
that the more easily administered oral vaccines of Sabin and Koprowski
were also capable of giving longer-lasting protection. On the question of
safety, opinions were more divided. The live poliovirus in OPVs has first
been weakened, or attenuated, by a series of passages* through animals
(such as rodents and monkeys) or through tissue cultures (layers of cells
—typically from chicken embryos or the kidneys of monkeys —that are
kept alive under laboratory conditions). However, the theoretical side of
attenuation (relating to what causes the poliovirus to become innocuous
for humans, and what keeps it that way) was still shrouded in mystery. For
this reason there was considerable interest when, in a discussion session
on the fourth day of the conference, Professor Albert Sabin made a
dramatic accusation.
He repeated a claim that he had first made
three months earlier, in an article in the British Medical Journal, that
at least one batch of his rival Koprowski's CHAT vaccine, which had been
fed to hundreds of thousands of vaccinees in the Belgian Congo, had been
contaminated with an unidentified simian virus, one that had nothing to do
with polio —but which, like polio, was cytopathic (it killed cells when
introduced into monkey kidney tissue culture). The unspoken inference was
clear —that such a virus might also do damage when introduced into human
beings.
A renowned Swedish virologist, Dr. Sven
Gard, who had been on several months' sabbatical at Koprowski's research
center, the Wistar Institute, spoke up in his defense. Gard said that he
had tested the same lot of vaccine for the presence of extraneous virus,
both in Sweden and the United States, and had found nothing.
And there, apparently, the matter rested.
Certainly there is no further reference to the affair in the published
record of the conference. But by voicing his concern, Albert Sabin had
invoked a specter that was hovering over the proceedings —the fear that
OPVs, even while they were bringing the most feared viral disease of the
era under control, might also be introducing new and perhaps more sinister
viral agents into mankind, ones that proliferated during the process of
vaccine manufacture.
This was a fear that was to become very
much more substantial over the years that followed, as virologists began
to learn a lot more about tissue cultures, especially monkey kidney tissue
cultures, and the many ways in which they could become contaminated.
Naturally, new procedures were introduced to ensure the safety of
vaccines. But many of these men, when they looked back years later with
the benefit of hindsight, would shiver at the risks which they had
inadvertently taken in those days of blissful ignorance, those days of
hope and courage, in the fifties.
Put the slide back in the case. Pick
another. Here, try this one, from the nineties. Let us see whether it
provides a different perspective —one that benefits from the
accumulation of scientific wisdom. Perhaps try another lens, too. Some, of
course, may have the corrective properties of hindsight.
It is March of 1993. The intervening years
have seen further great victories for vaccination programs and the public
health system, with the conquest of smallpox, and the suppression of
malaria, measles, and cholera. But they have also witnessed significant
reverses, such as the emergence of AIDS and the re-emergence of
tuberculosis.
And now, almost thirty-four years after
that first international conference on live poliovirus vaccines, Albert
Bruce Sabin has died peacefully at his home in Washington, D.C., at the
age of eighty-six. Despite his many achievements during more than six
decades of scientific toil, he was always best known for his development
of the OPVs, which would later be adopted in almost every country in the
world. Now, in 1993, the World Health Organization is promoting a campaign
of global poliomyelitis eradication by the year 2000. Even if this may be
optimistic, polio is likely to become only the second viral disease to be
conquered by human intervention, a state of affairs that owes much to the
success of Albert Sabin's slightly dirty-looking sugar lumps.
One of Sabin's many other achievements was
to identify a herpes virus of monkeys (B virus, or herpes B), which is
harmless to its natural host but almost invariably fatal when transferred
into humans, as evidenced by the deaths of some two-dozen monkey handlers
and laboratory workers since the thirties. Sabin's discovery of herpes B
virus identified what then seemed the most formidable danger inherent in
handling monkeys and their organs, and facilitated the adoption of minced
monkey kidneys as a tissue culture for in vitro research and for the
cultivation of viruses. This in turn paved the way for the golden age of
virology in the fifties, and the production of polio vaccines on a
commercial scale.
During his final years, Albert Sabin became
increasingly concerned by the problem of AIDS, and wrote articles and
letters about the problems inherent in developing an effective vaccine
against the syndrome. The last of these was published in Nature a
fortnight after his death. Like its predecessors, it predicted that
attempts to vaccinate against HIV would prove unsuccessful, and ended with
the words "In my judgment, it would be disastrous to continue the
current inadequate methods of study of HIV and SIV* vaccines, and to carry
out large scale tests in humans of vaccines without adequate evidence that
such vaccines can protect against natural infection." From such an
eminence grise, these were powerful final words of warning.
Five weeks after Sabin's death, an obituary
was published in Nature. It opened with a reference to "the heroic
age of poliomyelitis research" and an acknowledgment that Sabin had
been "one of the heroes," before moving on to review Sabin's
life and works. By this stage of the obituary, the observant reader might
have begun to suspect that writer and subject had not always been in
agreement.
This was frankly admitted in the final
paragraph, which read: At one time, Sabin and I became adversaries over
the selection of polio virus strains to be used as oral vaccines. This did
not affect our long-lasting friendship and mutual respect. In a letter to
me written just a year ago, reviewing a paper speculating that AIDS
started with polio vaccination in the Belgian Congo, Sabin expressed his
opinion that this was "a most irresponsible and uncritical
communication." Courageous and wise. This is how I see him. I will
miss him sorely.
The obituary was signed Hilary Koprowski,
from the Wistar Institute in Philadelphia.
Several of the scientists who knew the two
men from the time of their great rivalry in the fifties and early sixties
were intrigued by the obituary. They too had vivid recollections of the
period, though their memories were rather different from Koprowski's. They
spoke of two Jewish émigrés from Eastern Europe, both possessed of keen
intellects and quick tempers —coupled, however, with great powers of
persuasion (and, in Koprowski's case, of charm). They spoke of two men
cast from the same mold, men who shared many of the same tendencies and
personality traits —but who had somehow evolved into polar opposites.
Few of them recalled any tangible
friendship (let alone one that was long-lasting) between Sabin and
Koprowski, or remembered demonstrations of mutual respect. Instead, they
spoke of a bitter enmity that had been barely —if at all —concealed in
their respective articles in the medical literature and papers delivered
at the great virology conferences of the day. They remembered the
occasions when the great men had posed together, smiling, for the
photographers, and then each had swiftly turned on his heel the moment the
cameras were packed away. This rivalry, some of them hinted, had perhaps
stemmed from the fact that Koprowski had been the first to feed an oral
polio vaccine to humans in 1950, fully three years before Sabin had
entered the field —and yet it was Sabin's vaccines that had been
licensed, Sabin who had won the lasting acclaim. "Koprowski and Sabin
hated each other," one contemporary told me. "Salk, Sabin,
Koprowski, Cox —I would have loved to see them tag-team wrestling,"
said another, referring to the four great polio vaccine-makers. "They
were fighting like dogs over a bone —about who would make the vaccine of
choice," said a third.
Given this history, many scientists were
dubious about Koprowski's motivation for praising Sabin's wisdom
—particularly as, in the same breath, he noted Sabin's rejection of a
theory that suggested that one of his (Koprowski's) vaccines had given
birth to AIDS. Perhaps in 1993 few scientists would have recalled that,
back in 1959, it was Sabin who had introduced the first slither of doubt
about the safety of this very vaccine.
All in all, there was much that the
obituary left unsaid, some of which has great relevance for the story that
follows. We shall return to the tale of the obituary writer, and his
uneasy relationship with his subject —a relationship that helped define
the characters of both men —later in this book.
© 1999 by Edward Hooper
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