@noyes @BE

You guys are a bit beyond me in understanding.

I’ve only attempted scientific literacy for four years now, self-taught.

Let me ask you this…

Does “Dr” Jha tweeting to dispute immune damage from SARS2 mean that more people are getting the info?

I mean, he didn’t tweet it before, why now?

The few of us paddling this nightmare didn’t all of a sudden get on his radar, did we?

Tell me there’s some light making its way through.

@BigBadDog
1)Because he told people it was no big deal. He should be charged with Crimes Against Humanity.

He also told us that Covid was never going away to hide the fact that a new virus had been released as the Wuhan Lineage reached an evolutionary conclusion. Omicron BA.1, with a surface so orderly that it barely registered as non-self, arrived on the scene. That orderliness isn't happening in anything other than graduated Complement sera (C3, C5, Factors B, D, H et al)

@BigBadDog
2)In case it's not abundantly clear, I said that there was no way in hell that Omicron BA.1 evolved from the Wuhan lineage in a jawed vertebrate of any kind.

@noyes

I recall him blithely sneering “have you ever gotten a cold?” as stood calmly underneath germicidal lighting, and his kids enjoyed ventilation upgrades in their schools mine might never.

I’ve lost faith, sleepwalking through this nightmare sold by the likes of him, bought by those far more educated than I am, our kids in the same class, while only mine masks.

I want to think he’s responding today because some of the lemmings are changing course, enough to stem the dive.

Shall I hope?

@BigBadDog
He's trying to save his reputation.

@noyes

But not people’s lives.

Great, he was better at school than I was.

But, he’s not very bright.

A newly suspicious reader, hearing the rumblings of “immune damage”, would have to spend some time navigating Twitter to find the info they seek.

Now, it’s all compiled in one tidy place, below his nonsense.

He tidied up the search, and enlisted many credentialed people to cite all the harms it does indeed do, all in one concise place.

Kind of dumb.

@BigBadDog
I can only assume that he has an agent of Malice.

@noyes

I’m adjusting to veil of naïveté being lifted.

There’s more of them than I thought.

@noyes @BigBadDog “released”?

@TransitBiker @BigBadDog

1)Yeah. Released. The immunogenicity of BA.1/BA.2 was notably poor. Many took two infections to seroconvert. That could only happen if the signaling that guides phagocytosis and therefore antigen presentation doesn't occur. It takes a special kind of surface to make that happen, a 'self' surface with abundant Complement regulatory proteins like CD55 or CD59, or unnaturally efficient mimic thereof. The surface of BA.1/2 lacks the former so it must be the latter.

@TransitBiker @BigBadDog

2)It started to break from this unnaturally glycosylated state at BA.3. By the BA.4/BA.5 wave it had broken from it entirely. Lineages don't necessarily select for traits that make them more evasive, they select for traits that make them more productive. Non-ACE2 bearing tissue residents have since been revealed as an important reservoir, particularly in terms of long term persistence. It makes sense that it would acquire traits that draw residents towards it yet no

@TransitBiker @BigBadDog
3)sense that it would abandon them.

3)I should probably explicitly state what has me in such a tizzy about BA.1/BA.2.

The lack of sufficient IgG3 seroconversion implies that the Germinal Center follicles were never seeded with IgM. This implies that IgM producing B-cells were never presented with Complement opsonized viral antigen. This implies that C3 convertases never formed on the surface of the viral envelope even though they obviously do on all other variants

@TransitBiker @BigBadDog
4)before BA.1 and after BA.3. This implies that the envelope of BA.1/BA.2 resists Activating Surfaces, or at least resists it long enough for most virions to avoid capture during transit of the ECF.

4)There is a class of bone fide non-converters that produce higher than average titers of C1-INH (and probably Factor H, too but the study failed to capture that value). They shed for weeks without ever displaying symptoms, but they're very rare. Fun stuff.

@TransitBiker @BigBadDog

5)It's probably not clear what I mean by 'activating surfaces' so here's a paper that does an excellent job of explaining them. Activator Surfaces are the foundation of extracellular immune response. They take time to build. One of the principle functions of an antibody is to shorten that time. The sort of condense the information in the opsonins on the presented antigen to make capture by phagocyte faster and more efficient.

https://febs.onlinelibrary.wiley.com/doi/full/10.1002/1873-3468.12284

@noyes @TransitBiker

Flattered, teach. You have much confidence in me.

I told myself it was tough to comprehend as I was sleepy.

I told myself I’ll see what coffee does to help, in the morning.

I’ll have to apprise myself of many sub-concepts.

The one thing that struck me…

It appears as though transplant organs need to have aligned offenses to thwart the recipients defenses, in order to successfully take.

@BigBadDog
The majority of Complement proteins are produced in the liver with the remainder being produced in tissues local to wherever the liver-produced proteins end up being consumed. This allows for fine resolution control of the immune response. Sort of like an analog radio with two separate dials for tuning in station.

Tp'd organs last longer in patients that also have the donor liver transplanted. Even more so when the liver goes in first.

https://www.mayoclinic.org/medical-professionals/transplant-medicine/news/order-is-everything-new-procedure-for-heart-liver-transplant-averts-rejection-risk/mac-20519014
@TransitBiker

@noyes @TransitBiker

I’ll take a guess as to why we might not transplant with concurrent liver, and why not the liver first… currently.

Why, in the beforetimes, would the procedure not include these two key components?