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I
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.1
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,2 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.3
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.4 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."5
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."6 Unfortunately, of all the twelve groups tested by
Motulsky,7 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.8 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.9
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.10 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.11
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,12 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.14
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,15 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.16
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.17
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.18 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.19 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.20
He repeated a claim that he had first made three months earlier, in an
article in the British Medical Journal,21 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.22
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,23 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 2000.24 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.25
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.26 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.27 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.28
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,29 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.30 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.31 "Salk, Sabin,
Koprowski, Cox —I would have loved to see them tag-team wrestling,"
said another, referring to the four great polio vaccine-makers.32
"They were fighting like dogs over a bone —about who would make the
vaccine of choice," said a third.33
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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