A new study has been released that compares COVID-19 to rattlesnake bites, of all things.
The similarity is not in the delivery mechanism (a painful bite from a reptile), but in an enzyme within the virus that is actually quite similar to the rattlesnake’s neurotoxic venom.
This enzyme, sPLA2-II reportedly causes severe inflammation, and is naturally present in humans, albeit in very low concentrations. When those concentrations spike to very high levels through some malfunction or an antagonizing agent (such as certain viruses and venoms), it can “shred” the membrane lining of vital organs, according to Floyd Chilton of the University of Arizona, a senior author of the medical research paper.
This has potentially very significant medical implications for the treatment of COVID-19, and its latest delta variant surge. As co-author, Dr. Maurizio Del Poeta of Stony Brook’s Renaissance School of Medicine explained, “Because inhibitors of sPLA2-IIA (the enzyme in rattlesnake venom) already exist, our study supports the use of these inhibitors in patients with elevated levels of sPLA2-IIA to reduce, or even prevent, COVID-19 mortality.”
Simply put, the means and medical technology already exist to target and reduce sPLA2-IIA, which can theoretically be used to target and reduce sPLA2-II in COVID-19, potentially dramatically reducing the severity and impact of the virus on an already infected patient. The two enzymes are similar enough that a treatment for one could very well yield good results in treating the other. This is not to say rattlesnake anti-venom can treat COVID-19, rather that similar properties can be used to synthesize a sPLA2-II inhibitor treatment specific to COVID-19.
In healthy adults, the sPLA2-IIA enzyme is crucial in the defense of the body, particularly against bacterial infections. The enzyme destroys microbial cell membranes, which is important in defeating and neutralizing contaminated cells. Dr. Chilton explained how this healthy immune system response can actually hurt the host (your body) when levels of the enzyme get too high, however:
“It’s a bell-shaped curve of disease resistance versus host tolerance. 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 study was based on 127 medical charts from hospitalized patients at Stony Brook University Hospital between January and July of 2020. A second study was undertaken using 154 blood samples from hospitalized COVID-19 patients. The authors included researchers from Stony Brook University, Wake Forest University, and the University of Arizona.
If the research team’s theory is correct, it could potentially be an important turning point against COVID-19, which has surged with the new “Delta variant.”
The treatment being researched by the team appears to be after the fact, only useful to those already seriously ill from COVID-19. The best form of preventative care is still vaccination although, so far, no one treatment appears to be absolutely infallible.
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