https://www.sciencedaily.com/releases/2021/08/210824135358.htm
"Researchers from the University of Arizona, in collaboration with Stony Brook University and Wake Forest University School of Medicine, analyzed blood samples from two COVID-19 patient cohorts and found that circulation of the enzyme -- secreted phospholipase A2 group IIA, or sPLA2-IIA -- may be the most important factor in predicting which patients with severe COVID-19 eventually succumb to the virus.
sPLA2-IIA, which has similarities to an active enzyme in rattlesnake venom, is found in low concentrations in healthy individuals and has long been known to play a critical role in defense against bacterial infections, destroying microbial cell membranes.
When the activated enzyme circulates at high levels, it has the capacity to "shred" the membranes of vital organs,"
That damage to cell membranes sounds like it could account for ME symptoms too. Maybe we are producing too much of this enzyme in response to even mild inflammatory events. Exert a bit, which activates immune cells, which then increases production of this enzyme, which in turn damages cells. My ME responds to different types of fatty acids, which are used to build/repair membranes.
A quick Google didn't show any links for 'sPLA2-IIA me/cfs', so the amount in circulation is something that researchers should check in their patients.
"Researchers from the University of Arizona, in collaboration with Stony Brook University and Wake Forest University School of Medicine, analyzed blood samples from two COVID-19 patient cohorts and found that circulation of the enzyme -- secreted phospholipase A2 group IIA, or sPLA2-IIA -- may be the most important factor in predicting which patients with severe COVID-19 eventually succumb to the virus.
sPLA2-IIA, which has similarities to an active enzyme in rattlesnake venom, is found in low concentrations in healthy individuals and has long been known to play a critical role in defense against bacterial infections, destroying microbial cell membranes.
When the activated enzyme circulates at high levels, it has the capacity to "shred" the membranes of vital organs,"
That damage to cell membranes sounds like it could account for ME symptoms too. Maybe we are producing too much of this enzyme in response to even mild inflammatory events. Exert a bit, which activates immune cells, which then increases production of this enzyme, which in turn damages cells. My ME responds to different types of fatty acids, which are used to build/repair membranes.
A quick Google didn't show any links for 'sPLA2-IIA me/cfs', so the amount in circulation is something that researchers should check in their patients.
