Top Section (Left to Right)
1a/ comparison of common colds HCoVs, SARS, SARS-2, MERS, Flu pathogen characteristics, SARS-2 has blend characteristics of SARS, NL63, and MERS (uncommon)
1b/ SARS-2 receptor ACE2 similar to that for SARS and NL63 with varying outcomes determined by ACE2 down-regulation differentials, facilitatory receptor Sialic Acid to enhance attachment to ACE2 similar to that found for DPP4 in MERS
1c/ multibasic site protease Furin similar to MERS (found as well in HKU1 and OC43), Furin drives infectivity in FLU, C19 is one of the most transmissible pathogen, C19 will “swallow” seasonal FLU cases and most likely its mortality numbers
Middle Section (Left to Right)
2a/ pre-existing cross-reactive C19 T- & B-cell immunity from previous HCoVs exposure
2b/ most probably, C19 follows a seasonal infection pattern similar to that of FLU driven by humidity and temperature effects
2c/ ACE2 down-regulation from C19 infection knocks down RAS on “disease” side, if you have chronic disease(s), your RAS is already knocked down, C19 on top of chronic disease(s) equate to double knock-down leading to severe outcomes
2d/ unchecked ACE2 down-regulation leads to well-established downward spiral of pathologies and for C19 “long-hauler” survivors, accelerated chronic disease(s)
Bottom Section
3a/ viral infection, disease progression, and mechanisms of working drugs are known, definitely better to go in early and clear the virus, once ACE2 down-regulation gets too deep, more at risk for severe outcomes!
3b/ BOTTOMLINE: with pre-existing T- & B-cell immunity and working arsenal of drugs, we can live with C19 and resume normalcy