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Covid Re-Infection Questions to Akiko Iwasaki & Her VuMedi Video of 11-13-20

Dear Readers and Fans, I have been working on a new book, a very short one, about Covid-19, ‘How Covid-19 Attacks Our Body (Pandemic Pointers and Guidelines)’  During these past months I have been doing a lot of research, reading a lot of Medscape and other medical journals/articles plus watching videos especially on the Vu Medi website. Here is a letter/comment I posted today:

Re the Akiko Iwasaki VuMedi Nov 13, 2020 Video Concerning: Covid Re-Infection:

https://www.vumedi.com/video/can-you-get-covid-19-twice-will-the-severity-of-illness-be-milder/

Dear Dr. Iwasaki,

Thank you for the presentation. On the question of the re-infections that you mentioned, only 4. Of course, there are others in the world. Were your four patients re-infected by the same strain? I believe the D614 was the first strain in the USA of Covid-19 coronavirus. Then along came D614G as the taking-over summer strain that was responsible for about 70% of the new cases, mostly in the USA in the southwest. A Florida PhD from FAU stated that that new strain was more infectious, but less deadly.  I just read a Medscape article a few minutes ago, that said that Covid-19 right now is 30% less deadly, though the authors reasoned it was because of better medical care, and more knowledge about the offending coronavirus – they made NO mention of it being possibly another strain, whether D614G or another strain with totally different lettering/numbering.

I am very interested to know about someone who has been exposed to Covid, gotten slightly sick or maybe had no symptoms and perhaps tested positive either via nasal test or antibody – or never was tested – and then is re-exposed to a new viral load. What happens with that new viral load, that say would be sufficient inoculum (no, we do not know what the inoculum dose is for Covid-19 SARSCoV2) to cause disease? Can the body’s immune system martial the troops, the T and B Cells and the macrophages and the antibody platoon and prevent sufficient bodycell takeover to prevent significant reproduction & transmission of that new viral load to other humans? Can our immune system do that? as you seem to have intimated in the beginning of this talk? Kimberly Prather PhD out of Scripps in San Diego who has been working with aerosols for ?20 years now claims that the reason asymptomatic people can transmit Covid is because the virus gets into the nose or respiratory tree circumventing the immune system while it sneakily multiplies, without necessarily sickening the exposed individual, yet multiplying in that respiratory tree to such numbers as to be a significant reservoir for the virus to be talked or breathed or coughed or sneezed out to infect other individuals and nobody knowing it is happening or happened. She also thinks it could take only one viral particle to cause Covid syndrome, and that aerosols on a deserted beach necessitate wearing a facemask. [All very questionable.]

Wikipedia does say in its section on Norovirus that the inoculum for this cruise ship virus is less than 20 viral particles, and possibly as low as 5. Any comments on this?

Also, a report in mid-July fyi stated on the Medium platform, and elsewhere – that there had been 353,000 mutations of the coronavirus already. Many/most had no effect in terms of functionality/infectiousness/etc.  Some produced ‘variants’ that withered out into oblivion; others eventuated in ‘strains’ most of these less infectious or virulent than the predominant D614, and then the D614G.  Any comment on that?

I am writing a very short book on Covid, how we get attacked via the ACE2 receptors in our body from the roof of our nasal cavity to endothelial cells all over our body; plus Pandemic Pointers & Guidelines. Thank you for your work, Conrad Miller MD

deeperinthetube@yahoo.com

Gainesville Georgia

11-18-20