Jesse Gelsinger (18 June 1981 17 September 1999) was the first person publicly identified as having died in a clinical trial for gene therapy. Gelsinger suffered from ornithine transcarbamylase deficiency, an X-linked genetic disease of the liver, the symptoms of which include an inability to metabolize ammonia a byproduct of protein breakdown. The disease is usually fatal at birth, but Gelsinger had not inherited the disease; in his case it was apparently the result of a spontaneous genetic mutation after conception and as such was not as severe some of his cells were normal, enabling him to survive on a restricted diet and special medications. <\/p>\n
Gelsinger joined a clinical trial run by the University of Pennsylvania that aimed at developing a treatment for infants born with severe disease. On 13 September 1999, Gelsinger was injected with an adenoviral vector carrying a corrected gene to test the safety of the procedure. He died four days later at the age of 18, on 17 September at 2:30 pm, apparently having suffered a massive immune response triggered by the use of the viral vector used to transport the gene into his cells, leading to multiple organ failure and brain death. <\/p>\n
A Food and Drug Administration (FDA) investigation concluded that the scientists involved in the trial, including the co-investigator Dr. James M. Wilson (Director of the Institute for Human Gene Therapy), broke several rules of conduct: <\/p>\n
The University of Pennsylvania later issued a rebuttal,[1] but paid the parents an undisclosed amount in settlement. Both Wilson and the University are reported to have had financial stakes in the research.[2][3] The Gelsinger case was a severe setback for scientists working in the field.[4] <\/p>\n
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Jesse Gelsinger - Wikipedia<\/a><\/p>\n","protected":false},"excerpt":{"rendered":" Jesse Gelsinger (18 June 1981 17 September 1999) was the first person publicly identified as having died in a clinical trial for gene therapy. Gelsinger suffered from ornithine transcarbamylase deficiency, an X-linked genetic disease of the liver, the symptoms of which include an inability to metabolize ammonia a byproduct of protein breakdown. Continue reading