VOC's & elevated levels of endotoxinsAs far as i am aware, the "Sepsis-like" reaction experienced by seriously ill Covid patients, does not depend on the particular Covid variant.
So far 800,000 americans have lost their lives to Covid (and another 30,000 Cdns)... many of them (as some new evidence suggests*) could have perished as a result of endotoxins being released into the bloodstream leading to an increase in proinflammatory cytokines, followed by multiple organ failure, follwed by death.
The latest variants of concern are riling the markets (Dow down 1000 pts). Will there be a new, more deadly wave? Will existing vaccines be as effective?
Hopefully if there is another deadly round, doctors will be able ot add a new weapon in the war against Covid -19? One thing for sure is that the war is far from being over.
https://www.science.org/doi/10.1126/science.abc6261#body-ref-R29-1
*Severe COVID-19 infection is associated with the systemic release of bacterial products
The increased levels of proinflammatory mediators in the plasma—including IL-6, TNF, TNFSF14, EN-RAGE, and OSM —coupled with suppressed innate immune responses in blood monocytes and DCs and fig. S5) suggested a sepsis-like clinical condition In this context, it has been previously suggested that proinflammatory cytokines and bacterial products in the plasma may play pathogenic roles in sepsis, and the combination of these factors could be important in determining patient survival. Therefore, to determine whether a similar mechanism could be at play in patients with severe COVID-19, we measured bacterial DNA and lipopolysaccharide (LPS) in the plasma. Notably, the plasma of severe and ICU patients had significantly higher levels of bacterial DNA, as measured by PCR quantitation of bacterial 16S ribosomal RNA (rRNA) gene product, and of LPS, as measured by a TLR4-based reporter assay Furthermore, there was a significant correlation between bacterial DNA or LPS and the plasma levels of the inflammatory mediators IL-6, TNF, MCP-3, EN-RAGE, TNFSF14, and OSM and fig. S19). These results suggest that the enhanced cytokine release may in part be caused by increased bacterial products in the lung or in other tissues.