The Biotech Death of Jesse Gelsinger
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New York Times, Sunday Magazine, 28 Nov 99
The Biotech Death of Jesse Gelsinger
Ever since it became a reality nine years ago, gene therapy has been the
bright promise of medicine. Then an experiment went very wrong.
By SHERYL GAY STOLBERG
The jagged peak of Mount Wrightson towers 9,450 feet above Tucson,
overlooking a deep gorge where the prickly pear cactus that dots the
desert floor gives way to a lush forest of ponderosa pine. It is said
that this is as close to heaven as you can get in southern Arizona. Jesse
Gelsinger loved this place. So it was here, on a clear Sunday afternoon
in early November, that Paul Gelsinger laid his 18-year-old son to rest,
seven weeks after a gene-therapy experiment cost him his life.
The ceremony was simple and impromptu. Two dozen mourners -- Jesse's
father; his mother, Pattie; his stepmother, Mickie; and two sisters, a
brother, three doctors and a smattering of friends -- trudged five miles
along a steep trail to reach the rocky outcropping at the top. There,
Paul Gelsinger shared stories of his son, who loved motorcycles and
professional wrestling and was, to his father's irritation, distinctly
lacking in ambition. Jesse was the kind of kid who kept $10.10 in his
bank account -- You need $10 to keep it open," Gelsinger explained
-- but those assembled on the mountaintop agreed that he had a sharp wit
and a sensitive heart.
At Gelsinger's request, the hikers had carried Jesse's medicine bottles
filled with his ashes, and now they were gathered at the edge of the
peak. Steve Raper, the surgeon who gave Jesse what turned out to be a
lethal injection of new genes, pulled a small blue book of poetry from
his pocket. "Here rests his head upon the lap of Earth," Raper
read, reciting a passage from an elegy by Thomas Gray, "a youth to
Fortune and Fame unknown./Fair Science frowned not on his humble
birth." Then the surgeon, the grieving father and the rest scattered
Jesse's ashes into the canyon, where they rose on a gust of wind and fell
again in a powerful cloud of fine gray dust. "I will look to you
here often, Jess," Paul Gelsinger said sadly.
Jesse Gelsinger was not sick before died. He suffered from ornithine
transcarbamylase (OTC) deficiency, a rare metabolic disorder, but it was
controlled with a low-protein diet and drugs, 32 pills a day. He knew
when he signed up for the experiment at the University of Pennsylvania
that he would not benefit; the study was to test the safety of a
treatment for babies with a fatal form of his disorder. Still, it offered
hope, the promise that someday Jesse might be rid of the cumbersome
medications and diet so restrictive that half a hot dog was a treat.
"What's the worst that can happen to me?" he told a friend
shortly before he left for the Penn hospital, in Philadelphia. "I
die, and it's for the babies." As far as government officials know,
Jesse's death on Sept. 17 was the first directly related to gene therapy.
The official cause, as listed on the death certificate filed by Raper,
was adult respiratory distress syndrome: his lungs shut down. The truth
is more complicated. Jesse's therapy consisted of an infusion of
corrective genes, encased in a dose of weakened cold virus, adenovirus,
which functioned as what scientists call a vector. Vectors are like
taxicabs that drive healthy DNA into cells; viruses, whose sole purpose
is to get inside cells and infect them, make useful vectors. The Penn
researchers had tested their vector, at the same dose Jesse got, in mice,
monkeys, baboons and one human patient, and had seen expected, flulike
side effects, along with some mild liver inflammation, which disappeared
on its own. When Jesse got the vector, he suffered a chain reaction that
the testing had not predicted -- jaundice, a blood-clotting disorder,
kidney failure, lung failure and brain death: in Raper's words,
"multiple-organ-system failure." The doctors are still
investigating; their current hypothesis is that the adenovirus triggered
an overwhelming inflammatory reaction -- in essence, an immune-system
revolt. What they do not understand yet is why.
Every realm of medicine has its defining moment, often with a human face
attached. Polio had Jonas Salk. In vitro fertilization had Louise Brown,
the world's first test-tube baby. Transplant surgery had Barney Clark,
the Seattle dentist with the artificial heart. AIDS had Magic Johnson.
Now gene therapy has Jesse Gelsinger.
Until Jesse died, gene therapy was a promising idea that had so far
failed to deliver. As scientists map the human genome, they are literally
tripping over mutations that cause rare genetic disorders, including OTC
deficiency, Jesse's disease. The initial goal was simple: to cure, or
prevent, these illnesses by replacing defective genes with healthy ones.
Biotech companies have poured millions into research -- not for rare
hereditary disorders but for big-profit illnesses like cancer, heart
disease and AIDS. As of August, the government had reviewed 331
gene-therapy protocols involving more than 4,000 patients. Just 41 were
for the "monogeneic," or single-gene, defect diseases whose
patients so desperately hoped gene therapy would be their salvation.
At the same time, the science has progressed slowly; researchers have had
trouble devising vectors that can carry genes to the right cells and get
them to work once they are there. Four years ago, Dr. Harold Varmus, the
director of the National Institutes of Health, commissioned a highly
critical report about gene therapy, chiding investigators for creating
"the mistaken and widespread perception of success." Since
then, there have been some accomplishments: a team at Tufts University
has used gene therapy to grow new blood vessels for heart disease
patients, for instance. But so far, gene therapy has not cured anyone. As
Ruth Macklin, a bioethicist and member of the Recombinant DNA Advisory
Committee, the National Institutes of Health panel that oversees
gene-therapy research, says, bluntly, "Gene therapy is not yet
On Dec. 8, the "RAC," as the committee is called, will begin a
public inquiry into Jesse's death, as well as the safety of adenovirus,
which has been used in roughly one-quarter of all gene-therapy clinical
trials. The Penn scientists will report on their preliminary results, and
investigators, who at the RAC's request have submitted thousands of pages
of patient safety data to the committee, will discuss the side effects of
adenovirus. Among them will be researchers from the Schering-Plough
Corporation, which was running two experiments in advanced liver cancer
patients that used methods similar to Penn's. Enrollment in those trials
was suspended by the Food and Drug Administration after Jesse's death.
The company, under pressure from the RAC, has since released information
showing that some patients experienced serious side effects, including
changes in liver function and blood-cell counts, mental confusion and
nausea; two experienced minor strokes, although one had a history of
them. Once all the data on adenovirus are analyzed at the Dec. 8 meeting,
the RAC may recommend restrictions on its use, which will almost
certainly slow down some aspects of gene-therapy research.
The meeting will be important for another reason: it will mark an
unprecedented public airing of information about the safety of gene
therapy -- precisely the kind of sharing the RAC has unsuccessfully
sought in the past. Officials say gene therapy has claimed no lives
besides Jesse's. But since his death, there have been news reports that
other patients died during the course of experiments -- from their
diseases, as opposed to the therapy -- and that the scientists involved
did not report those deaths to the RAC, as is required. This has created
a growing cloud of suspicion over gene therapy, raising questions about
whether other scientists may have withheld information that could have
prevented Jesse's death. That question cannot be answered until all the
data are analyzed. But one thing is certain: four years after the field
was rocked by Varmus's highly critical evaluation, it is now being rocked
again, this time over an issue more fundamental than efficacy -- safety.
"I think it's a perilous time for gene therapy," says LeRoy
Walters, a bioethicist at Georgetown University and former chairman of
the RAC. "Until now, we have been able to say, 'Well, it hasn't
helped many people, but at least it hasn't hurt people.' That has
No one, perhaps, is more acutely aware of gene therapy's broken promise
than Mark Batshaw, the pediatrician who proposed the experiment that cost
Jesse Gelsinger his life.
At 54, Batshaw, who left the University of Pennsylvania last year for
Children's National Medical Center, in Washington, is tall and gangly
with slightly stooped shoulders and a shy smile that gives him the air of
an awkward schoolboy, which he once was. As a child, Batshaw struggled
with hyperactivity: he didn't read until the third grade; in the fourth,
his teacher grew so irritated at his constant chatter that she stuck his
chair out in the hall. The experience has left him with a soft spot for
developmentally disabled children, which is how he has become one of the
world's foremost experts in urea-cycle disorders, among them OTC
The urea cycle is a series of five liver enzymes that help rid the body
of ammonia, a toxic breakdown product of protein. When these enzymes are
missing or deficient, ammonia -- the same ammonia that you scrub your
floors with," Batshaw explains -- accumulates in the blood and
travels to the brain, causing coma, brain damage and death. OTC
deficiency is the most common urea-cycle disorder, occurring in one out
of every 40,000 births. Its genetic mutation occurs on the X chromosome,
so women are typically carriers, while their sons suffer the disease.
Severe OTC deficiency is, Batshaw says, "a devastating
disease." Typically, newborns slip into a coma within 72 hours of
birth. Most suffer severe brain damage. Half die in the first month, and
half of the survivors die by age 5. Batshaw was a young postdoctoral
fellow when he met his first urea-cycle-disorder patient in 1973,
correctly diagnosing the disease at a time when most other doctors had
never heard of it. Within two years, he and his colleagues had devised
the first treatment, a low-protein formula called keto-acid. Later, they
came up with what remains standard therapy to this day: sodium benzoate,
a preservative, and another type of sodium, which bind to ammonia and
help eliminate it from the body.
But the therapy cannot prevent the coma that is often the first sign of
OTC and ravages the affected infant. By the time Batshaw joined the
faculty at Penn in 1988, he was dreaming of a cure -- gene therapy.
Patients were dreaming, too, says Tish Simon, former co-president of the
National Urea Cycle Disorders Foundation, whose son died of OTC
deficiency three years ago. "All of us saw gene therapy as the hope
for the future," Simon says. "And certainly, if anybody was
going to do it, it had to be Mark Batshaw."
Gene therapy became a reality on Sept. 14, 1990, in a hospital room at
the National Institutes of Health, in Bethesda, Md., when a 4-year-old
girl with a severe immune-system deficiency received a 30-minute infusion
of white blood cells that had been engineered to contain copies of the
gene she lacked. Rarely in modern medicine has an experiment been filled
with so much hope; news of the treatment ricocheted off front pages
around the world. The scientist who conducted it, Dr. W. French Anderson,
quickly became known as the father of gene therapy. "We had got
ourselves all hyped up," Anderson now admits, "thinking there
would be rapid, quick, easy, early cures."
Among those keeping a close eye on Anderson's debut was Jim Wilson, a
square-jawed, sandy-haired Midwesterner who decided to follow his
father's footsteps in medicine when he realized he wasn't going to make
it in football. As a graduate student in biological chemistry, Wilson had
taken a keen interest in rare genetic diseases. "All I did," he
says, "was dream about gene therapy."
Today, as director of the Institute for Human Gene Therapy at the
University of Pennsylvania, Wilson is in an excellent position to make
that dream a reality. Headquartered in a century-old building amid the
leafy maple trees and brick sidewalks of the picturesque Penn campus, the
six-year-old institute, with 250 employees, state-of-the-art laboratories
and a $25 million annual budget, is the largest academic gene-therapy
program in the nation. In a field rife with big egos, Wilson is regarded
as first-rate. "Present company excluded," Anderson says,
"he's the best person in the field."
Batshaw was banging on Wilson's door even before Wilson arrived at Penn
in March 1993, and within a month they were collaborating on studies of
OTC-deficient mice. Their first task was to develop a vector. Adenovirus
seemed a logical choice.
There had been some early problems with safety -- a 1993 cystic fibrosis
experiment was shut down when a patient was hospitalized with inflamed
lungs -- but Wilson and Batshaw say they figured out how to make a safer
vector by deleting extra viral genes. Adenovirus was the right size: when
its viral genes were excised, the OTC gene fit right in. It had a
"ZIP code," on it, Batshaw says, that would carry it straight
to the liver. And while its effects did not last, it worked quickly,
which meant that it might be able to reverse a coma, sparing babies from
brain damage. "It wasn't going to be a cure soon," Batshaw
says, "but it might be a treatment soon."
The mouse experiments were encouraging. Mice that had the therapy
survived for two to three months even while fed a high-protein diet.
Those that lacked the treatment died. "It wasn't subtle,"
Wilson says. "We felt pretty compelled by that." But when the
team contemplated testing in people, they ran smack into an ethical
quandary: who should be their subjects?
To Wilson, the answer seemed obvious: sick babies. Arthur Caplan, the
university's resident bioethics expert, thought otherwise. Caplan says
parents of dying infants are incapable of giving informed consent:
"They are coerced by the disease of their child." He advised
Wilson to test only stable adults, either female carriers or men like
Jesse, with partial enzyme deficiencies. The National Urea Cycle
Disorders Foundation agreed. When Batshaw turned up at their 1994 annual
meeting asking for volunteers, so many mothers offered to be screened for
the OTC gene that it took him four hours to draw all the blood.
By the time Mark Batshaw and Jim Wilson submitted their experiment to the
Recombinant DNA Advisory Committee for approval, the panel was in danger
of being disbanded. Varmus, the N.I.H. director, who won the Nobel Prize
for his discovery of a family of cancer-causing genes, had made no secret
of his distaste for the conduct of gene-therapy researchers. He thought
the science was too shoddy to push forward with human testing, and it
bothered him that so few experiments were focusing on genetic diseases.
It irked him to have to sign off on protocols the RAC approved, and it
irked him even more to see biotech companies touting those approvals,
like some kind of N.I.H. imprimatur, in the business pages of the papers.
"Some days," says Dr. Nelson Wivel, the committee's former
executive director, who now works for Wilson at Penn, "it felt as
though the RAC was helping the biotech industry raise money. Dr. Varmus
At the same time, the pharmaceutical industry and AIDS activists were
complaining that the RAC was redundant: the F.D.A. already reviewed
gene-therapy proposals. So in mid-1995, after seeking the advice of an
expert panel, Varmus reorganized the RAC, slashing its membership from 25
to 15 and stripping it of its approval authority -- a decision that, some
say, has enabled gene-therapy researchers to ignore the panel and keep
information about safety to themselves. "The RAC," complains
Dr. Robert Erickson, a University of Arizona medical geneticist who
served on the panel, "became a debating society."
The Batshaw-Wilson protocol was among the last the committee would ever
approve. The plan was for 18 adults (19 eventually signed up, including
Tish Simon, but the last patient was never treated, because of Jesse's
death) to receive an infusion of the OTC gene, tucked inside an
adenovirus vector, through a catheter in the hepatic artery, which leads
to the liver. The goal was to find what Wilson calls "the maximum
tolerated dose," one high enough to get the gene to work, but low
enough to spare patients serious side effects. Subjects would be split
into six groups of three, with each group receiving a slightly higher
dose than the last. This is standard fare in safety testing. "You go
up in small-enough increments," Wilson explains, "that you can
pull the plug on the thing before people get hurt."
The experiment stood in stark contrast to others that had earned Varmus's
scorn. It was paid for by N.I.H., which meant it had withstood the rigors
of scientific peer review. It was aimed at a rare genetic disease, not
cancer or AIDS. It was supported by plenty of animal research: Wilson and
his team had performed more than 20 mouse experiments to test efficacy
and a dozen safety studies on mice, rhesus monkeys and baboons. Still, it
made Erickson, one of two scientists assigned by the RAC to review the
He was troubled by data showing that three monkeys had died of a
blood-clotting disorder and severe liver inflammation when they received
an earlier, stronger version of the adenovirus vector at a dose 20 times
the highest dose planned for the study. No one had injected adenovirus
directly into the bloodstream before, either via the liver or otherwise,
and the scientists admitted that it was difficult to tell precisely how
people would respond. They planned to confine the infusion to the right
lobe of the liver, so that if damage occurred it would be contained
there, sparing the left lobe. And they outlined the major risks:
bleeding, from either the gene-therapy site or a subsequent liver biopsy,
which would require surgery; or serious liver inflammation, which could
require an organ transplant and might lead to death.
Both Erickson and the other scientific reviewer thought the experiment
was too risky to test on asymptomatic volunteers and recommended
rejection. But in the end, Batshaw and Wilson prevailed. They offered up
Caplan's argument that testing on babies was inappropriate. And they
agreed to inject the vector into the bloodstream, as opposed to putting
it directly into the liver. That decision, however, was later reversed by
the F.D.A., which insisted that because the adenovirus would travel
through the blood and wind up in the liver anyway, the original plan was
The RAC, in such disarray from Varmus's reorganization that it did not
meet again for another year, was never informed of the change.
Jesse Gelsinger was 17 when his pediatric geneticist, Dr. Randy
Heidenreich, first told him about the Penn proposal. He wanted to sign up
right away. But he had to wait until he was 18.
Paul Gelsinger was also enthusiastic. A trim 47-year-old with intense
blue eyes, Gelsinger, who makes his living as a handyman, gained custody
of his four children nine years ago, when he divorced their mother, who
suffers from manic depression. He had been having some difficulty with
Jesse then; the boy was in the midst of an adolescent rebellion and was
refusing to take his medicine. "I said: 'Wow, Jess, they're working
on your disorder. Maybe they'll come up with a cure.'"
Jesse's was not a typical case of OTC deficiency: his mutation appears to
have occurred spontaneously in the womb. His disease having been
diagnosed when he was 2, Jesse was what scientists call a mosaic -- a
small portion of his cells produced the missing enzyme. When he watched
what he ate and took his medicine, he was fine. But one day last
December, Paul Gelsinger arrived home to find his son curled up on the
couch. He had been vomiting uncontrollably, a sign, Paul knew, that
Jesse's ammonia was rising. Jesse landed in the hospital, comatose and on
life support. When he recovered, he never missed another pill.
On June 18, the day Jesse turned 18, the Gelsingers -- Paul, Mickie and
the children -- flew to Philadelphia to see Paul's family. They played
tourists, visiting the Liberty Bell and the Rocky statue, where Jesse was
photographed, fists raised, a picture that would circulate in the
newspapers after his death. On the 22nd, they went to the University of
Pennsylvania, where they met Raper, the surgeon, who explained the
experiment and did blood and liver-function tests to see if Jesse was
eligible. He was, and his treatment was scheduled for the fall. Jesse
would be the youngest patient enrolled.
On Sept. 9, Jesse returned to Philadelphia, this time alone. He took one
duffel bag full of clothes and another full of wrestling videos. Paul
Gelsinger planned to fly in a week later for the liver biopsy, which he
considered the trial's most serious risk.
The treatment began on Monday, Sept. 13. Jesse would receive the highest
dose. Seventeen patients had already been treated, including one woman
who had been given the same dose that Jesse would get, albeit from a
different lot, and had done "quite well," Raper says. That
morning, Jesse was taken to the interventional-radiology suite, where he
was sedated and strapped to a table while a team of radiologists threaded
two catheters into his groin. At 10:30 a.m., Raper drew 30 milliliters of
the vector and injected it slowly. At half past noon, he was done.
That night, Jesse was sick to his stomach and spiked a fever, 104.5
degrees. Raper was not particularly surprised: other patients had
experienced the same reaction. Paul Gelsinger called; he and Jesse talked
briefly, exchanging I love yous. Those were the last words they ever
Early Tuesday morning a nurse called Raper at home; Jesse seemed
disoriented. When Raper got to the hospital, about 6:15 a.m., he noticed
that the whites of Jesse's eyes were yellow. That meant jaundice, not a
good sign. "It was not something we had seen before," Raper
says. A test confirmed that Jesse's bilirubin, a breakdown product of red
blood cells, was four times the normal level. Raper called Gelsinger, and
Batshaw in Washington, who said he would get on a train and be there in
Both doctors knew that the high bilirubin meant one of two things: either
Jesse's liver was failing or he was suffering a clotting disorder in
which his red blood cells were breaking down faster than the liver could
metabolize them. This was the same disorder the scientists had seen in
the monkeys that had been given the stronger vector. The condition is
life-threatening for anyone, but particularly dangerous for someone with
Jesse's disease, because red blood cells liberate protein when they break
By midafternoon Tuesday, a little more than 24 hours after the injection,
the clotting disorder had pushed Jesse into a coma. By 11:30 p.m., his
ammonia level was 393 micromoles per liter of blood. Normal is 35. The
doctors began dialysis.
Paul Gelsinger had booked a red-eye flight. When he arrived in the
surgical intensive care unit at 8 Wednesday morning, Raper and Batshaw
told him that dialysis had brought Jesse's ammonia level down to 72 but
that other complications were developing. He was hyperventilating, which
would increase the level of ammonia in his brain. They wanted to paralyze
his muscles and induce a deeper coma, so that a ventilator could breathe
for him. Gelsinger gave consent. Then he put on scrubs, gloves and a mask
and went in to see his son.
By Wednesday afternoon, Jesse seemed to be stabilizing. Batshaw went back
to Washington. Paul felt comfortable enough to meet his brother for
dinner. But later that night Jesse worsened again. His lungs grew stiff;
the doctors were giving him 100 percent oxygen, but not enough of it was
getting to his bloodstream. They consulted a liver-transplant team and
learned that Jesse was not a good candidate. Raper was beside himself. He
consulted with Batshaw and Wilson, and they decided to take an
extraordinary step, a procedure known as ECMO, for extracorporeal
membrane oxygenation, essentially an external lung that filters the
blood, removing carbon dioxide and adding oxygen. It had been tried on
only 1,000 people before, Raper says. Only half had survived.
"If we could just buy his lungs a day or two," Raper said
later, they thought "maybe he would go ahead and heal up."
The next day, Thursday, Sept. 16, Hurricane Floyd slammed into the East
Coast. Mickie Gelsinger flew in from Tucson just before the airport
closed. (Pattie Gelsinger, Jesse's mother, was being treated in a
psychiatric facility and was unable to leave.) Batshaw spent the day
trapped outside Baltimore on an Amtrak train. He ran down his cell phone
calling Raper; when it went dead, he persuaded another passenger to lend
him his. The ECMO, Raper reported, appeared to be working. But then
another problem cropped up: Jesse's kidneys stopped making urine.
"He was sliding into multiple-organ-system failure," Raper
That night, at his hotel, Paul Gelsinger couldn't sleep. He left his wife
a note and walked the half mile to the Penn medical center to see Jesse.
The boy was bloated beyond recognition; even his ears were swollen shut.
Gelsinger noticed blood in Jesse's urine, an indication, he knew, that
the kidneys were shutting down. How can anybody, he thought, survive
On the morning of Friday the 17th, a test showed that Jesse was brain
dead. Paul Gelsinger didn't need to be told: "I knew it
already." He called for a chaplain to hold a bedside service, with
prayers for the removal of life support.
The room was crowded with equipment and people: 7 of Paul's 15 siblings
came in, plus an array of doctors and nurses. Raper and Batshaw,
shellshocked and exhausted, stood in the back. The chaplain anointed
Jesse's forehead with oil, then read the Lord's Prayer. The doctors
fought back tears. When the intensive-care specialist flipped two toggle
switches, one to turn off the ventilator and the other to turn off the
ECMO machine, Raper stepped forward. He checked the heart-rate monitor,
watched the line go flat and noted the time: 2:30 p.m. He put his
stethoscope to Jesse's chest, more out of habit than necessity, and
pronounced the death official. "Goodbye, Jesse," he said.
"We'll figure this out."
Wilson reported the death immediately, drawing praise from government
officials but criticism from Arthur Caplan, who says they should have
made the news public, in a news conference. In the weeks since, the Penn
team has put every detail of Jesse's treatment under a microscope. It has
rechecked the vector to make certain it was not tainted, tested the same
lot on monkeys, re-examined lab and autopsy findings. Wilson's biggest
fear was that Jesse died as a result of human error, but so far there has
been no evidence of that. "That's what's so frightening,"
French Anderson says. "If they made a mistake, you would feel a
The death has rattled the three doctors in various ways. Wilson has asked
himself over and over again whether he should have done anything
differently. "At this point, I say no, but I'm continuing to
re-evaluate constantly." He has been besieged by worry, about the
morale of his staff, about whether his institute's financial sponsors
would pull out, about whether patients would continue to volunteer, about
whether he would lose his bravado -- the death knell for a scientist on
the cutting edge. "My concern," he confessed, over dinner one
night in Philadelphia, "is, I'm going to get timid, that I'll get
Raper has thrown himself into his work, trying to live up to his promise
to "figure this out." There are a number of possible
explanations, he says: the vector may have reacted badly with Jesse's
medication; Jesse's status as a mosaic may have played a role; or perhaps
the early testing in monkeys, which showed that the stronger vector had
deleterious side effects, was more of a harbinger of danger than the
doctors realized. An answer may take months, but he is determined to find
one; only by understanding what happened to Jesse, and how to prevent it
in others, can the research continue. "That," Raper says,
"would be the best tribute to Jesse."
Of the three, Batshaw seems to have taken it the hardest. He is not a
particularly religious man, but a few days after Jesse died he went to
synagogue to say Kaddish, the Jewish mourner's prayer. He struggles with
the idea of personal responsibility. He has cradled many a dying child in
his career, but never before, he says, has a patient been made worse by
his care. "What is the Hippocratic oath?" Batshaw asks
rhetorically, looking into the distance as his fingers drum the tabletop.
He pauses, as if to steel himself, and says, "I did harm."
Paul Gelsinger does not hold the doctors responsible, although he is
acutely interested in knowing what other scientists knew about adenovirus
before Jesse died. He has experienced a deep spiritual awakening since
losing his son; in dying, he says, Jesse taught him how to live. He
speaks frequently of God, and of "purity of intent," which is
his way of saying that Jesse demonstrated an altruism the rest of us
might do well to emulate. "I hope," he said on the mountaintop
that Sunday afternoon, "that I can die as well as my son has
November 28, 1999
Copyright 1999 The New York Times Company