I think we have made a mountain of a molehill
by ignoring secondary infections.

And depending on antivirals - some of which like ritonavir/lopinavir have no reason to work https://twitter.com/sanchak74/status/1242148451552382976
3/n
There is clear immune suppression (note 1/4th of the RNA is from Prevotella, so its in huge amounts)

This is what elongation factor Tu does...
https://www.researchgate.net/publication/277456852_Elongation_Factor_Tu_Tuf_is_a_new_virulence_factor_of_Streptococcus_pneumoniae_that_binds_human_complement_factors_aids_in_immune_evasion_and_host_tissue_invasion
4/
Even in SARS-Cov1 2003, severity/death was 100% correlated with secondary infection.

Correlation was also high in Spanish flu 2018
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5481322/
"with S. pneumoniae, Haemophilus influenzae, and S. aureus reported as the most common causes." https://twitter.com/sanchak74/status/1237047795380391936
5/
See data from San Diego country - the same pathogens are lurking.

They may not take over - as in most patients who get better - but they are in immunocomprised people, where the % fatality is very high.

And then Interleukin 6 (IL-6) goes high. https://twitter.com/sanchak74/status/1241747243582910464
6/
But that's a late stage, where IL-6 blockers are working - but you dont want to be there.

And note what increases IL-6, bacteria - and in diabetic patients.
https://sanchakblog.wordpress.com/2020/03/22/prevotella-link-to-increased-plasmsa-il-6-type-2-diabetes-azithromycin-etc https://twitter.com/sanchak74/status/1241638371174125568
7/
Tells you why there are false negatives - very low viral low (and much more bacterial load) https://twitter.com/sanchak74/status/1243860855965364225
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