Is this enzyme associated with an increased risk of COVID-related death?

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A University of Arizona study showed that an enzyme with a crucial involvement in severe inflammation may be a critical mechanism in COVID-19 severity and could present a novel target for drug development.

The researchers analysed blood samples from two COVID-19 patients in collaboration with Stony Brook University and Wake Forest School of Medicine and determined that the circulation of the sPLA2-11A enzyme may be a significant way in determining which patients would die from COVID-19.

The enzyme has the ability to “shred” the membranes of essential organs in excessive concentrations.

“It’s a bell-shaped curve of disease resistance versus host tolerance,” said Floyd (ski) Chilton, senior author on the paper and director of the UArizona Precision Nutrition and Wellness Initiative at the university. “In other words, this enzyme is trying to kill the virus, but at a certain point it is released in such high amounts that things head in a really bad direction, destroying the patient’s cell membranes and thereby contributing to multiple organ failure and death.”

“The idea to identify a potential prognostic factor in COVID-19 patients originated from Dr. Chilton,” said Maurizio Del Poeta, a co-author of the study. “He first contacted us last fall with the idea to analyze lipids and metabolites in blood samples of COVID-19 patients.”

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The research team analyzed thousands of patient data points. The team focused on traditional risk factors like age, body mass index and preexisting conditions, but they also focused on biochemical enzymes and patients’ levels of lipid metabolites.

 COVID-19 cell (credit: BAR ILAN UNIVERSITY)

COVID-19 cell (credit: BAR ILAN UNIVERSITY)

“In this study, we were able to identify patterns of metabolites that were present in individuals who succumbed to the disease,” said Justin Snider, an assistant research professor at the University of Arizona and lead study author. “The metabolites that surfaced revealed cell energy dysfunction and high levels of the sPLA2-11A enzyme. The former was expected but not the latter.”

The analysis showed that most healthy people have approximately half a nanogram of the enzyme per milliliter, 63% of people who had severe COVID-19 and died had more than 10 nanograms per milliliter.

“Some of the patients who died from COVID-19 had some of the highest levels of this enzyme that have ever been reported,” said Chilton.

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Previous research into the enzyme shows that it has similar genetic ancestry to a key enzyme contained in snake venom.

“Like venom coursing through the body, [the enzyme] has the capacity to bind to receptors at neuromuscular junctions and potentially disable the function of these muscles,” said Chilton.

“Roughly a third of people develop long COVID, and many of them were active individuals who now cannot walk 100 yards,” he added. “The question we are investigating now is: if this enzyme is still relatively high and active, could it be responsible for part of the long COVID outcomes that we’re seeing?”

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