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“The death is the latest in a series of setbacks for a promising approach that has so far failed to deliver its first cure and that has been criticized as moving too quickly from the laboratory bench to the bedside,” the Washington Post reported, in the first of many articles about Jesse’s death and the ensuing crisis it set off.
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News coverage portrayed the trial researchers as overeager and undercautious, taking shortcuts and disregarding rules meant to protect the people in their care. The news that an experimental treatment had killed a basically healthy volunteer rocked the field of gene therapy and the broader world of biological research. The team of doctors and nurses caring for him were stunned by his rapid decline and death. Four days after receiving the shot Jesse was declared brain dead and taken off life support. He had an intense inflammatory response and developed a dangerous blood-clotting disorder, followed by kidney, liver, and lung failure. Within a day he became disoriented and showed signs of jaundice. Previous patients in the trial had experienced flu-like symptoms, but he had a much worse reaction. Jesse was the 18th person to receive the modified virus. But Jesse was eager to help, and he flew to Philadelphia in September 1999 to take part. The trial Jesse would join was a safety study, aimed at moving toward a treatment for babies with OTCD, and was not intended to improve the participants’ health. But the researchers’ experimental treatment had lengthened the lives of lab mice bred to be deficient in OTC enzymes, and the scientists were hopeful the gene-repair method they were testing could eventually be used to treat many liver diseases. The field of gene therapy had so far helped just a few people with genetic diseases. The virus, altered to be harmless, would infect the patients’ liver cells and integrate the added gene into their chromosomal DNA. Patients would be injected with working copies of the gene that had been attached to an adenovirus, a type of cold virus. Researchers at the University of Pennsylvania in Philadelphia were developing a fix for the OTC gene, which produces an enzyme that prevents ammonia buildup. So when a doctor told Jesse that a clinical trial for a potential OTCD treatment was in the works, he was very interested.
He had to be intubated and kept in an induced coma until his ammonia levels were brought under control. One day his father came home to find him curled up on the couch, vomiting uncontrollably. When he was 17, he stopped taking the drugs regularly. Jesse’s milder version of the deficiency was diagnosed when he was two years old, and he managed the condition with a low-protein diet and a regimen of nearly 50 pills a day. Babies born with OTCD usually fall into comas soon after birth and suffer brain damage. Jesse had a rare metabolic disorder called ornithine transcarbamylase deficiency syndrome, or OTCD, in which ammonia builds up to lethal levels in the blood. As he got older, he became more independent and, like many teens, a touch rebellious in his case that led to life-threatening health problems. In 1999 he was living in Tucson, Arizona, with his parents and siblings, attending high school, and working part-time as a supermarket clerk.
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By all accounts Jesse Gelsinger was a sweet, sharp-witted, if not particularly ambitious kid who loved motorcycles and professional wrestling.