PHOENIX (ABC4) – COVID-19, a virus, and rattlesnakes, slithering venomous reptiles, may not seem very similar. New research out of Arizona says they may just have one thing in common.
Researchers with the University of Arizona analyzed blood samples from two COVID-19 patient cohorts to determine if doctors can predict the severity of a patient’s virus infection.
While analyzing the blood samples, researchers say they found an enzyme – secreted phospholipase A2 group IIA, or sPLA2-IIA – that could be a key mechanism driving COVID-19 severity and may provide a new therapeutic target to reduce mortality. The report, published in the Journal of Clinical Investigation, says the enzyme may be the most important factor in predicting which patients with severe COVID-19 eventually succumb to the virus.
According to the University of Arizona, the enzyme has similarities to an active enzyme in rattlesnake venom. It is found in low concentrations in healthy individuals and has long been known to play a role in defending against bacterial infections by destroying microbial cell membranes. When circulating in high volumes, researchers say the enzyme has the ability to ‘shred’ the membranes of vital organs.
“It’s a bell-shaped curve of disease resistance versus host tolerance,” says Floyd Chilton, a member of the University of Arizona’s BIO5 Institute. “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.”
In their study, researchers collected stored plasma samples and analyzed medical charts for over 280 patients. They reviewed traditional risk factors like age, body mass index, and pre-existing conditions, the team also analyzed biochemical enzymes in patients.
Researchers say most healthy individuals have circulating levels of the sPLA2-IIA enzyme hovering around half a nanogram per milliliter. They found COVID-19 was deadly in 63% of patients with severe cases and levels of the enzyme equal to or greater than 10 nanograms per milliliter – 20 times that of healthy individuals.
“Many patients who died from COVID-19 had some of the highest levels of this enzyme that have ever been reported,” says Chilton, who has been studying the enzyme for over three decades. According to the University of Arizona, previous research has shown the sPLA2-IIA enzyme has been recorded in severe inflammation events like bacterial sepsis and hemorrhagic and cardiac shock.
The protein “shares a high sequence homology to the active enzyme in rattlesnake venom and, like venom coursing through the body, it has the capacity to bind to receptors at neuromuscular junctions and potentially disable the function of these muscles,” Chilton says.
“Roughly a third of people develop long COVID, and many of them were active individuals who now can’t walk 100 yards,” Chilton adds. “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?”
To view the full study, click here.