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Anthony J Leonardi, PhD, MS Profile picture
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22 Jun, 6 tweets, 3 min read
Cov2 is NOT comparable to flu

Don't ever listen to those comparing Cov2 to influenza.

In *terminal* cases of Influenza, there were no T cells in the brain.

In Cov2, *all* but 1 patient in this paper had T cells in the brain. ImageImageImageImage
From this paper. nature.com/articles/s4158…
Why did people wait for harm to emerge instead of looking at the mechanisms?
Only ignorant charlatans had been looking at the short-term effects of the virus without considering the long-term damage that would unfold, given the mechanisms of the virus. Especially re: vaccinating kids.
Here's another person comparing it to a flu. Unfortunately this guy is an accomplished pathologist that should have known better. He blocked me for this response.

Fluthers do not employ rigorous independent analysis (not in a textbook).
Clear warnings. Why didn't they listen? Image

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Anthony J Leonardi, PhD, MS Profile picture
17 Jun
If you leave critical decisions up to charlatans and people that overextend their expertise you end up with repeat waves and reinfections like in India when challenged with new variants.

Infected should have a boost with mrna for variant protection.
studies come out all the time showing this. Only herd immunity apologists who called it wrong and the recklessly ignorant will maintain infection confers better protection.
In regard to the cleveland clinic preprint: Charlatans that cannot contextualize a study with its environment by grasping temporal shifts in context (aka a delta, P1, or b1351 driven encroaching wave) should not be allowed near policy.
Read 4 tweets
Anthony J Leonardi, PhD, MS Profile picture
16 Jun
This is concerning.

When controlling for age, body habitus, and other variables, people who had covid had sizes of key brain structures 4 standard deviations below average.

The hippocampal gyrus is responsible for memory, in part.
medrxiv.org/content/10.110… ImageImage
These changes were not found to be different whether one was hospitalized or not.

The one metric where size increased post covid- ventricle volume- is a good marker for loss of brain matter. This usually increases with age. ImageImage
And before people tell you this was unexpected- no. This was predictable. Furin cleavage sites confer neurotropism and this was my primary concern with the virus. With the knowledge it had a Sag, the situation appeared more dire. Downplayers are culpable. Image
Read 5 tweets
Anthony J Leonardi, PhD, MS Profile picture
23 May
Kids need to be vaccinated. Why?

Because things can go horribly wrong with infection, and infection is a process with proof of continuation.

Let's look at a few coronavirus examples and how they relate to cov2 🧵
Feline Infectious Peritonitis has a Furin Cleavage Site *EQUIVALENT* to Cov2

Fip in cats is notably a fatal, incurable, chronic illness, which interestingly requires a form/precursor of remdesivir to cure.

This must be given for 100 days.
So the cats bodies mount a response to the virus, but it is able to hide out and mutate in some, and cause vasculitis and neuroinflammation.

Sound familiar? vet.cornell.edu/departments-ce…
Read 9 tweets
Anthony J Leonardi, PhD, MS Profile picture
23 May
People seem to equate lockdowns with a 0 covid tolerance approach

I recall lockdowns are used in a "herd immunity" approach just before hospitals are overwhelmed.

In fact, "herd immunity" pursuant countries have arguably spent the most time in lockdown
The pursuit of herd immunity is probably why schools are used by some countries for a populational "natural" immunity

Infected children are less frequently hospitalized (1%). However, they are also less likely to seroconvert

Children do, however, infect young parents
In fact, you can see this pattern of children infecting parents from schools.

This could be why there are right-wing lobby groups for no masking.

They want to achieve an infection-based immunity period all the more quickly.
Read 9 tweets
Anthony J Leonardi, PhD, MS Profile picture
11 May
This is important:

B.1.617 has mutations that may *enhance* pathogenesis

A mutation at P681R in combination with L452R and E484Q significantly increases syncitia formation

This is when the cells fuse together, and it's linked to fatal disease.
2/ The Gupta lab found the mutations L452R/E484Q/P681R together significantly increase Syncitia formation.

This is a function of the polybasic cleavage site. Syncitia formation is linked to fatal diseasehttps://www.biorxiv.org/content/10.1101/2021.05.08.443253v1
3/ Syncitia are a way the virus kills T cells

This paper in Cell Death and Differentiation discusses how Syncitia internalize T cells in order to kill them

nature.com/articles/s4141…
Read 7 tweets
Anthony J Leonardi, PhD, MS Profile picture
18 Apr
This thread is in regard to the concerning things about Cov2.
I owe the idea to @LgSOS

To start, we have the neuroinvasion seen by @ericsongg @VirusesImmunity et al. rupress.org/jem/article/21…
2/ There is also a predominant symptom of anosmia (loss of sense of smell).

This anosmia is seen as unlikely to be from mucosal/nasal swelling ncbi.nlm.nih.gov/pmc/articles/P…
3/ Interestingly, a few case reports have emerged of Parkinson's following infection.
thelancet.com/journals/laneu…
A worrisome correlate may exist as seen by this preprint: monkeys had precursors of Parkinson's after infection, called Lewy Bodies biorxiv.org/content/10.110…
Read 7 tweets

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