FYI, "Most people who die of COVID-19, seasonal flu, or a bacterial infection technically die of sepsis – their organs shut down under the weight of the body's own runaway inflammatory response.. In-hospital sepsis mortality [in the US] rose 37.5% among patients 65 and older, and 44% among adults 18–64, between 2019 and 2021. The steepest relative jump in sepsis mortality was among younger adults.. An estimated 36,000 sepsis deaths occurred in 2020 alone, beyond what pre-pandemic trends would have predicted.. Post-sepsis syndrome – lasting cognitive and physical effects seen in up to half of survivors – extends the true cost of pandemic-driven sepsis well beyond the initial hospitalisation, in much the same way long COVID has.. sepsis was formally coded in only about 9% of COVID deaths, while clinical and autopsy studies find sepsis present in 52–93% of those same deaths. The official numbers understate the true toll – by the data's own admission." Long COVID is similar to long sepsis. 'The hidden pandemic within the pandemic: How COVID-19 impacted sepsis – and what comes next' pharmaphorum.com/rd/hidden-p…

"the SARS-CoV-2 accessory protein ORF3a binds to the endoplasmic reticulum (ER) chloride channel CLCC1, thereby impairing ER ion homeostasis, activating the unfolded protein response, and inducing endomembrane remodeling.. during early infection, ORF3a accumulates in the ER, co-assembles with CLCC1 into puncta, and disrupts ER homeostasis; at the later stage, ORF3a overload enables its escape from CLCC1-mediated ER retention and subsequent translocation to lysosomes, facilitating viral egress. This ER-centric function is conserved across diverse beta-coronaviruses, including SARS-CoV-1 and bat- or pangolin-derived strains, revealing a unified pathogenic strategy. Furthermore, in mouse brains, the ORF3a-CLCC1 axis recapitulates key neuropathological features, including ER stress, autophagic dysfunction, neuronal death, and neuroinflammation, providing a mechanistic link to COVID-19-associated neurological symptoms." So, what's our strategy? 'The accessory protein ORF3a hijacks the CLCC1 chloride channel to disrupt ER homeostasis in betacoronavirus pathogenesis' nature.com/articles/s41421-0…