Guest post by Rud Istvan,
I have been following this closely for a number of previously explained reasons, while mostly self-isolating with my significant other in South Florida (groceries once a week0. 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. RNA ACTU, DNA ACTG. Adenosine is “A” in both. Not the exactly 20 amino acids that build all proteins in all of life based on their four alphabet coding. Each RNA/DNA ‘ three letter word’ codes for a single ‘amino acid’ to build onto the eventual protein —the complexity comes with newly discovered non ‘coding’ DNA epigenetics (regulating gene expression frequency). See my illustrated musings on MesoAmerican dried beans over at Judith Curry’s Climate Etc some years ago if you want to ‘view’ the current roughly understood state of epigenetic ‘knowledge’.
Comments to other’s previous posts are also redeveloped here, using two continually revised related math models of fatalities, making them easier to find. The issues that new data shed insight on are: infectivity attack rate (seasonality?), asymptomatic infectives, mild/hospitalizations, S/C hospital ratio, number of C dying, and intervention efficacy. We deal with each changing factor in turn.
We 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%. The final viral attack rate CFR in US is unknown, except that it must still be much worse than Korea now. Lets compare that to known common flu in US at about 0.1% CFR after variably effective seasonal vaccines. >10x Not Good.
This AR depends on R0. Which we do not know, because depends on how we societally ‘bend the curve’. Initial US valid estimates were 2.6-3.0. Very bad. Now, much less for sure but by how much we dunno because of ‘bend the curve’ measures that for sure temporarily also kill the economy.
But lets assemble and project some simple ‘math’ outcome models, previously derived only in comments. We know from their extensive Korea testing data (then about 39600k then to find about 9.6K then positives as of last weekend) that the Korean AR is about 2.6%. We also know now from Korea that the asymptomatic/total is about 20% AFTER 14 day positive test quarantine. Those are potential “Typhoid Mary’s”, which make the pandemic difficult to control absent an effective vaccine, still probably at least 18 months away. Two potential vaccines in US have now started initial human phase one trials.
And from NYC/NOLA last week we know that hospitalized ((serious~=oxygen/critical=~ICU and probably a ventilator) is about 0.12, while the hospitalized/critical ratio is about 0.3. The most recent figures this past Friday as opposed to last Friday, 0.14 and 0.26 — giving about the same end fatality result via more hospitalizations for supplemental oxygen but a bit less deaths in the ICU. And per a NOLA critical care pulmonologist, about 50% of ventilated ICU criticals eventually die. It was anecdotaly higher (~80%) in Wuhan. So the end fully diagnosed (by testing) US math plus Korean CFR will land somewhere between 1.7% and 1.9% based on current data.
That is real bad, as the US Surgeon General said earlier this week (4/5/20). Attack rate >2.6% * about 327.2 million legal US citizens (dunno illegals) * optimistic 1.7% CFR implies 145,000 deaths in next few months. The president is not exaggerating, as some conservative blogs have implied.
There is a second way to derive this death estimate without CFR. Asymptomatics 0.8. Hospitailzation of symptomatics 0.14 (this past Friday). Criticals of hospitalized 0.26 (this past Friday). Deaths among criticals 0.5 (could be higher). Then:
327000*0.026*0.8*0.14*0.26*0.5= 124 thousand deaths next few months.
Now overload the ICU (>0.26 spike), and/or increase the viral attack rate because US is NOT Korea with strict contact tracing and testing, and Dr. Fauci’s recent horrible projected worst case 240K deaths is plausible.
We 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. Immune system has 1000x more time to respond to a minimal infection titer than to a high initial titer. That compounds if exposure happens equally each day, like in a hospital. Fully explains observational clinical asymptomatics, plus a mean incubation of 5.1 days and a 97.5% symptom display of 11.5 days.
If the initial viral load is E+3 in ‘one’ dose (an un-self-distanced cough), then in the same dimensionless time example the immune system has to respond in a E-3 time frame but cannot. Voila, fast symptomatic infection.
Dr. 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.
Fauci thinks Wuhan virus may be seasonal– flu aerosol spread assumptions– based on ‘new’ science observations. I think not based on historic facts. An artificially high virus titer from his nebulizer experiment by NIH ALSO found a virus half life (not like nuclear, just remaining RNA independent of possible infectivity) of Wuhan (just remaining RNA found, not infective envelope found) of about 1.5 hours in air, 3.5 hours on cardboard, 5.5 hours on steel, and about 6.8 hours on plastic. Now, since the infective minimum viral titer is not yet known, this is all speculative. But strongly suggests low aerosol spread and much more close contact viral transmissivity, implying without much seasonality. Translation, social distancing and frequent hand washing works, DIY masks don’t.
And previous media reports on this same experiment of 3 days max viability on plastic did NOT cite the viral half life factors above bearing on minimum infectious titer, so overstate the unknown contact residual viral titer infection scare (heck, me too) (hand washing and face touching at 6 hours half life still says real important). All good for social distancing and frequent hand washing to ‘bend the curve’.
Second cited evidence, the WA massive spreader church choir event. Except, my late Dad was in a much smaller such church choir. They greeted each other weekly with hugs and handshakes. Aerosols not needed. Just usual church choir enthusiasm. Discounted ‘science’.
Basic observational Fauci seasonality
The common cold is caused by about ~100 naked rhinovirus serotypes (abut 75% of common colds), exactly four enveloped humanized coronaviruses (about 20%) and about 20 of about 60 enveloped DNA adenoviruses, of which about 20 (~5% infectivity because of immunity against DNA mutation) cause common cold symptoms. The other ~40 adeno serotypes are much worse (e.g. various forms of conjunctivitis).
There is no evidence that the common cold (4 coronas included) is seasonal. It is more common in winter simply because people are in more confined spaces so there is more contact transmission. Summer colds are common. Summer flu is rare.
So Dr. Fauci speculates a case based on flu analog aerosols, when his own epidemiological mask message says the opposite, as does the data on common cold coronas. He is publicizing a dubious message based mostly on tenuous non-observational science. We have seen that before in climate ‘science’.
This corona virus is unlikely to be seasonal, because its main route of transmission is not aspirate aerosols, just like other corona common colds.
There is much present internet nonsense about face masks. Lets clarify. IF Wuhan coronavirus is spread by breath aerosols and therefore seasonal (defined as less than 5 micron droplets) (doubtful biologically, see above), then N95 will by definition intercept 95% (their definition is <=0.3 micron 95% stopped), and likely drop the viral load below infectivity. All else will not.
So IF Covid-19 is actually seasonal, then everything else except N95 masks is USELESS. So then why the new public home made cloth mask recommendations? Like climate change renewable deals, makes you feel good while being practically useless.
Now IF the route is cough sneeze, not aspirate aerosol, then nose/mouth coverings make sense—for the infected only. And the advice already is, if you have symptoms, stay home and self isolate. So either way the public face mask recommendations are mostly ‘feel good’ rather than effective
There is much new data.
First is the viral attack rate. This number is not a constant. It depends on many other societal measures like contact tracing, testing, and social distancing: ‘bend the curve’ stuff. Korea is down to 2.6%. US must be worse despite current efforts.
The second and third factors are what happens to those identified as infected/hospitalized/criticals. There, we have real time updated data. To a first approximation last week based on NY and NOLA, we had the following: (.12*0.3*0.5)
This week we had on the same data basis 14% of cases would become serious/critical (s/c, serious defined as needing supplemental hospital oxygen, times 0.26 critical defined as ICU (ventilator)). Half of those in ICU die. Run the alternative last week /this week math math per 10000 infected, is 0.12*0.3*0.5 or 180 deaths per 10000 symptomatic. Or, 0.14*0.26*0.5 = 182 deaths per 1000. Close into the zone of Korea actuals noted above–Rough closure is a good enough approximation.
On the HCQ/Z pac/Zinc ‘Trump cocktail,’ the Orthodox Jewish doctor’s successful NY treatment of his 699 patients has now explained his thinking and gives an alternative therapeutic pathway. X-pak antibiotic is only for opportunistic bacterial infections. His supplemental zinc enhances a possible secondary HCQ mechanism of action. I previously posted that the first was via the same liposomal enhanced pH mechanism as it’s use in RA, deforming the ACE2 receptor.
There may be a second. HCQ is a zinc ionophore—extra zinc into the intracellular metabolism inhibits RNA viral reproduction. Dunno for sure, but a cursory review of the medical literature says his idea is very plausible.
HCQ is also zinc ionophore for sure. Extra zinc transported into a cell’s interior is a known RNA Polymerase inhibitor (common colds). So, the azithromax antibiotic in the “Trump cocktail’ may be a secondary bacterial against Wuhan, and the doctor’s extra zinc loading is a primary agent. Maybe.
Now, why this is important is that there are two other known non prescription zinc ionophores, EGC in green tea extract, and the flavonoid quercetin in gingko biloba extract (both are in varying degrees in both, and in many other greens plus apples). Both are proven cellular zinc ionophores. So there may be OTC treatments cheaper than generic hydroxychloroquine for treating WuFlu.
Dunno. Do know green tea is good no matter what. Salud.