According to research from a new study, catching covid-19 can be just as bad as being bitten by a venomous rattlesnake.
The Paper published in the Journal of Clinical Investigation pinpoints how neurotoxins that flood the body after an excruciating rattlesnake bite damage our cells in the same way as an enzyme in coronavirus that causes severe inflammation.
The scientists behind the paper hope that this new discovery could help us treat serious Covid cases by targeting the specific enzyme.
The paper’s co-author Dr Maurizio Del Poeta, from Stony Brook University’s school of medicine in New York, said: “The study supports a new therapeutic target to reduce or even prevent Covid-19 mortality because inhibitors of sPLA2-IIA 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.”
The Covid enzyme sPLA2-IIA is remarkably similar to one found in rattlesnake venom, which is also seen naturally at low levels in humans. However high levels of this enzyme “shred” the membranes of vital organs according to the paper.
Dr Floyd Chilton, from the University of Arizona and another author of the study, explained: “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.”
There were 281 blood samples taken from different US hospitals were analysed throughout 2020 as part of the study. The research spread across Wake Forest University in North Carolina, Stony Brook University in New York and the University of Arizona.
Researcher Jeehyun Karen You said: “Our study is especially timely given how the Delta variant is contributing to rising COVID-19 incidence and hospitalisation rates both in the US and worldwide.”
Although this research has the potential to aid Covid treatment, it also throws up other questions. Researchers fear that the enzyme’s biting characteristics may be linked to so-called ‘long Covid’, with symptoms affecting patients for longer than the normal version of the illness.
Dr Chilton said: “Roughly a third of people develop long Covid, and many of them were active individuals who now can’t walk 100 yards.
“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?”“