Reaction Remedy: UA prof exploring promising new COVID treatment — to slow body’s over-response to bug

CDC on Unsplash

University of Arizona professor Dr. Floyd Chilton is on the precipice of finding a new treatment for patients suffering from severe COVID-19 symptoms that commonly lead to death.

Chilton is the senior author of a recently published study correlating the sPLA2-IIA enzyme to COVID severity and death.

sPLA2-IIA is a protective enzyme that typically protects our bodies from pathogens by identifying bacteria membranes and ripping them apart. However,
according to the study, higher levels of the enzyme are associated with severe COVID symptoms such as organ failure.

“We know this enzyme will begin to recognize the organ or the tissue as being foreign and begin to wipe it out,” said Chilton. In short, too much of a good thing (sPLA2-IIA) leads to a bad outcome.

Chilton’s study compared blood samples from patients with mild symptoms and severe symptoms as well as patients who died from COVID.

The initial sample size of the study is small, so Chilton cautioned “to get to causality as opposed to a bystander effect, we need more sophisticated samples.” Chilton’s study had one cohort of 127 samples and a second with 154 samples. After the initial results, Chilton’s acquired another cohort of around 300 samples. Chilton said they are now in contact with global organizations that have access to larger sample sizes.

These global organizations have an interest in Chilton’s study because combating the sPLA2-IIA enzyme in COVID patients could be a viable treatment for preventing COVID deaths.

Inhibitors for the sPLA2-IIA enzyme were in light clinical trials in the early 2000s, according to Chilton. Inhibitors of the enzyme are also being tested to counteract rattlesnake venom. Chilton expressed excitement for the possibility of repurposing these inhibitors to treat severe COVID patients.

“We’re not talking about years to come up with an inhibitor to block this enzyme. We just need a large multicenter clinical trial to test the efficacy of these utilizing a precision medicine approach that was outlined in the paper,” Chilton said.

To strengthen Chilton’s findings, the team used machine learning programs at UA to create an unbiased prediction of what perpetuated the most severe symptoms in COVID patients. On three separate machine learning algorithms, Chilton could test his hypothesis without human biases. 

“We fed these levels of this enzyme, along with all other clinical parameters that we could get our hands on, into artificial intelligence, machine-learning algorithms, and those machine learning models kept saying that this enzyme was the primary cause of mortality,” Chilton said.

Chilton’s samples were taken before the release of the COVID vaccines and the rise of the Delta variant. Chilton believes inhibitors would work regardless of which variant the patient had contracted. 

“I think it’s incredibly important that we move to the other end of the research, which focuses on specific therapies that are likely not to care what variant it is because these are probably the common death mechanisms that lead to late-stage organ failure,” Chilton said.

As a medical treatment for severe COVID symptoms, inhibitors would be a useful tool for doctors or nurses who may be treating vaccine-hesitant patients. Chilton said we need to begin focusing on treatments that will help all patients survive a COVID infection as more vaccine-hesitant patients are hospitalized for COVID.

Chief Clinical Officer at Banner Health Dr. Marjorie Bessel said this past week that 90% of all COVID patients at Banner hospitals were unvaccinated.

“This is many, many times more important than anything I’ve ever done. To say I’m excited would be an understatement,” Chilton said. “I’m honored and humbled that I might have a chance to somehow help in the treatment of this  disease.” 

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