Watts Up With That by Rud Istvan 4/8/2020
This post updates global WUWT readers with new facts and maybe new ‘knowledge’, some for sure now as controversial as climate change stuff. Incorporates all past facts, plus some important stuff buried in previous comments to other’s related posts. There are a number of separate fact categories itemized below.
Post 1 explained my ‘qualifications’, explained virion shed via a lot of basic virology 101, and concluded a US pandemic was unlikely thanks to effective quarantine, unlike flu—WRONG.
Post 2 explained why #1 was wrong—conclusive proof of pre-symptomatic/asymptomatic ‘spreaders’, completely unlike SARS 2003 where there was NO asymptomatic spread and the peak virion shed was 4 days after symptoms appeared. Unlike SARS, there is no way for a CoViD-19 symptom (fever>100.4) test at borders to contain infection. Very Bad News.
Post 3 analyzed the two most hopeful therapeutics, including my Remdeisvir adenosine drug analog RNA nucleic alphabet ‘A’ brain cramp—each of those ‘alphabets’ is only 4 letters. -----
Attack rateWe previously derived a projected Korean viral attack rate (AR) of about 2.6% and a related projected case fatality rate (CFR) of about 2.0% with extreme contact tracing, massive testing, and a capable (un-overwhelmed) medical system. Now stable tested Korean attack rate is still 2.6%. and the resulting CFR is now 1.9%, and projecting forward will settle finally at ~1.7%. -----
Viral LoadWe know generally that infectivity depends on the viral load ingested. We do not know what that load is per unit time to symptoms.
When a person becomes originally infected, it could be from a single virion per day or from (say) a titer of 1000 per day. If the one virion infects a cell and eventually creates 10 viables (previous comment post RNA transcription error example) then it takes 1E3 replication times (whatever those are) to equal the other initial infection viral titer. -----
SeasonalityDr. Fauci now says probably. I still say probably not, for reasons explained previously in guest posts and comments to others. Facts/logic before assumptions follow.
Fact: Common colds are still common in summer (albeit less common than in winter thanks to winter contact proximity); summer flu is almost non-existent.
Reason is simply explained by differential route of infection (See previous posts and comments, not worth explaining in detail yet again). In short, flu aerosols dry in dry winter indoor air, so remain circulating longer, so the main route of transmission is infected aspirate inhalation. In humid summers they remain wet, so heavy, so sink, so are not inhaled. Fu becomes winter seasonal. Colds are different, (including all three types: rhino, corona, adeno), because their main transmission route is contact (hands/face), so much less seasonal. Seasonal flu/cold data is incontrovertible.
More:
https://wattsupwiththat.com/2020/04/08/coronavirus-wuhan-coronavirus-guest-post-four/
