The autopsy showed…
Man with transplanted pig heart died from swine virus
The cause of death of the first ever patient to whom a genetically modified pig heart was transplanted was infection with porcine cytomegalovirus — Suid betaherpesvirus 2, reports MIT Technology Review.
At the University of Maryland Clinic on January 11 of this year, 57-year-old David Bennett, who suffered from severe arrhythmia, received a donor pig heart. Bennett became a participant in the experiment because he was close to death from heart failure and did not receive the right to a human heart transplant due to the fact that he had neglected medical advice in the past. The animal that became a donor was genetically modified in a special way to reduce the risk of organ rejection by the human body. The operation was successful, the donor heart was working, the biopsy taken on the 34th day showed no signs of a dangerous immune attack. But forty days later, the patient's condition worsened, and on March 8 he died. A statement released by the University of Maryland in March said that "no apparent cause had been identified at the time of his death."
Now, transplant surgeon Bartley Griffith, who performed the operation, during the webinar of the American Society of Transplantologists, named the cause of death — porcine cytomegalovirus introduced into the body along with the transplant. Revivicor, a biotech company that raised and modified pigs, declined to comment and has not yet made public statements about the virus.
According to Griffith, in order to monitor the health of the transplanted heart, scientists constantly checked the patient's blood for the presence of pig DNA fragments. An increase in their number would be a sign that the heart cells are dying. Another new test tested Bennett's blood for traces of hundreds of bacteria and viruses. It was this test that found that pig cytomegalovirus was present in the blood taken from Bennett 20 days after surgery. But the level was very low, and scientists considered that the result could be erroneous. Since the test takes ten days, doctors missed the moment when the virus began to multiply massively in the cells of the transplanted heart. The reproduction of the virus caused a violent reaction of the immune system — a cytokine storm. On the 43rd day after the operation, Bennett's temperature rose and he had difficulty breathing.
Treatment of the viral infection was complicated by the fact that Bennett, like all patients after organ transplantation, underwent a course of therapy that suppressed the immune response. Doctors used cyclovir, a drug sometimes used to treat AIDS patients. Since the patient's immune system was very weak, he was also injected intravenously with donor immunoglobulin. A day later, there was an improvement, but a week later Bennett's condition deteriorated significantly and the transplanted heart began to fail.
Griffith suggests that Bennett could have the same syndrome that was previously observed by German scientists in baboons who received donated pig hearts. In the case of cytomegalovirus in the heart tissues, a broad inflammatory reaction began, accompanied by edema and other effects. In these experiments, the transplanted heart worked for no more than two weeks, whereas in the absence of the virus, it remained viable for at least six months. According to Griffith, a biopsy of Bennett's transplanted heart showed no obvious signs that it had been rejected by the immune system, although this was what doctors feared most. Instead, the damage pattern turned out to be similar to that observed in German baboons.
During his presentation, Griffith painted a picture of how a viral syndrome could cause heart failure, escalating into a larger infection and triggering a destructive cascade of inflammation. "I suspect he developed capillary permeability in response to inflammation, and that caused the swelling of the heart, the swelling turned into fibrous tissue, and he developed severe and irreversible diastolic heart failure," Griffith said.
Scientists believe that the experiment was justified due to the "invaluable information" that was obtained. Bennett's son expressed similar feelings. A March statement from the University of Maryland quoted him as saying about his father: "We hope that what we learned from his surgery will benefit future patients and hopefully one day put an end to the organ shortage that claims so many lives every year."
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