It was only yesterday I wrote the following in reply to @DjAnomaly 's thread on antivenom and his question on whether antivenom could help to combat Covid....
"PPS: I am not aware of any Covid drugs being developed. But there are teams on it. The PLA2 enzymes in snake venom can kill the Covid virus."
I just found out that, it was only two days ago an article has been published on the JCI (The Journal of Clinical Investigation) under the headline of
"There is an urgent need to identify cellular/molecular mechanisms responsible for severe COVID-19 progressing to mortality. We initially performed untargeted/targeted lipidomics and focused biochemistry on 127 plasma samples and found elevated metabolites associated with secreted phospholipase A2 (sPLA2) activity and mitochondrial dysfunction in severe COVID-19 patients. Deceased COVID-19 patients had higher levels of circulating, catalytically active sPLA2 Group IIA (sPLA2-IIA), with a median value 9.6-fold higher than mild patients and 5.0-fold higher than severe COVID-19 survivors. Elevated sPLA2-IIA levels paralleled several indices of COVID-19 disease severity (e.g., kidney dysfunction, hypoxia, multiple organ dysfunction). A decision tree generated by machine learning identified sPLA2-IIA levels as a central node in stratifying patients that succumbed to COVID-19. Random forest analysis and LASSO-based regression analysis additionally identified sPLA2-IIA and blood urea nitrogen (BUN) as the key variables among 80 clinical indices in predicting COVID-19 mortality. The combined PLA-BUN index performed significantly better than either alone. An independent cohort (n=154) confirmed higher plasma sPLA2-IIA levels in deceased patients vs. severe or mild COVID19, with the PLA-BUN index-based decision tree satisfactorily stratifying mild, severe, and deceased COVID-19 patients. With clinically tested inhibitors available, this study supports sPLA2-IIA as a therapeutic target to reduce COVID-19 mortality."
PS: The following is the short description of it.
PLA2 is the abbreviation for Phospholipase A2 enzyme. Scientists from the University of Arizona, have reported findings that the enzyme phospholipase A2 group IIA, referred to as sPLA2-IIA, may be the most important factor in predicting which patients with severe COVID-19 eventually succumb to the virus.
The sPLA2-IIA enzyme is similar to one contained in rattlesnake neurotoxin as it can destroy cell membranes and is usually found in low concentrations in healthy individuals since it is a key defense against bacterial infection.
An average healthy person usually has about half a nanogram per milliliter (mL) of blood of sPLA2-IIA enzyme levels, but findings of the study showed that COVID-19 infection was lethal in 63% of patients who had severe COVID-19 and levels of sPLA2-IIA equal to or greater than 10 nanograms per mL of blood.
The sPLA2-IIA is associated with high Covid mortality and the scientists now suspect that this enzyme could be the reason for long Covid as well. This is a new finding and note that this study is only a starting point for further investigation with the possibility of controlling sPLA2-IIA enzyme levels in Covid patients.
"PPS: I am not aware of any Covid drugs being developed. But there are teams on it. The PLA2 enzymes in snake venom can kill the Covid virus."
I just found out that, it was only two days ago an article has been published on the JCI (The Journal of Clinical Investigation) under the headline of
"Group IIA secreted phospholipase A2 is associated with the pathobiology leading to COVID-19 mortality"
"There is an urgent need to identify cellular/molecular mechanisms responsible for severe COVID-19 progressing to mortality. We initially performed untargeted/targeted lipidomics and focused biochemistry on 127 plasma samples and found elevated metabolites associated with secreted phospholipase A2 (sPLA2) activity and mitochondrial dysfunction in severe COVID-19 patients. Deceased COVID-19 patients had higher levels of circulating, catalytically active sPLA2 Group IIA (sPLA2-IIA), with a median value 9.6-fold higher than mild patients and 5.0-fold higher than severe COVID-19 survivors. Elevated sPLA2-IIA levels paralleled several indices of COVID-19 disease severity (e.g., kidney dysfunction, hypoxia, multiple organ dysfunction). A decision tree generated by machine learning identified sPLA2-IIA levels as a central node in stratifying patients that succumbed to COVID-19. Random forest analysis and LASSO-based regression analysis additionally identified sPLA2-IIA and blood urea nitrogen (BUN) as the key variables among 80 clinical indices in predicting COVID-19 mortality. The combined PLA-BUN index performed significantly better than either alone. An independent cohort (n=154) confirmed higher plasma sPLA2-IIA levels in deceased patients vs. severe or mild COVID19, with the PLA-BUN index-based decision tree satisfactorily stratifying mild, severe, and deceased COVID-19 patients. With clinically tested inhibitors available, this study supports sPLA2-IIA as a therapeutic target to reduce COVID-19 mortality."
PS: The following is the short description of it.
PLA2 is the abbreviation for Phospholipase A2 enzyme. Scientists from the University of Arizona, have reported findings that the enzyme phospholipase A2 group IIA, referred to as sPLA2-IIA, may be the most important factor in predicting which patients with severe COVID-19 eventually succumb to the virus.
The sPLA2-IIA enzyme is similar to one contained in rattlesnake neurotoxin as it can destroy cell membranes and is usually found in low concentrations in healthy individuals since it is a key defense against bacterial infection.
An average healthy person usually has about half a nanogram per milliliter (mL) of blood of sPLA2-IIA enzyme levels, but findings of the study showed that COVID-19 infection was lethal in 63% of patients who had severe COVID-19 and levels of sPLA2-IIA equal to or greater than 10 nanograms per mL of blood.
The sPLA2-IIA is associated with high Covid mortality and the scientists now suspect that this enzyme could be the reason for long Covid as well. This is a new finding and note that this study is only a starting point for further investigation with the possibility of controlling sPLA2-IIA enzyme levels in Covid patients.
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