Coronavirus

[bkp_duke]

What are the thoughts on taking an anti inflammatory like naproxen, acetaminophen, etc.? Or anything else?

My wife and I avoided them last night, and were willing to deal with up to 24h of fever and body aches because we didn't want anything to mute the immune response. I did, however, take a single Tylenol this AM for my headache because I need to be lucid for work.

Overall, I don't think they will be a substantial difference and if someone is miserable, I would rather they take an anti-inflammatory than not get the vaccine at all.

 

[Doggydogworld]

Remember, with mRNA vaccines, the cells of your body must take up the vaccine, then transcribe the mRNA into proteins, those proteins must be transported to the cell surface, and THEN once all that happens, you have to wait for the existing antibodies you have developed to bind to the expressed proteins and recruit macrophages, etc. to act as antigen-presenting cells to ramp up your plasma/B memory cells to divide and produce antibodies.

Compared to a traditional vaccine where you just inject the protein itself and it is readily available in between the cells for your body to start the immune process, instead of needing to transcribe, build, and transport the protein to the muscle cell membrane.

The immediate reaction at the injection site is most likely an immune response to the carrier fluid that the vaccine is suspended in, not the actual S-protein itself.

Which cells does the vaccine invade? And when do the invasions stop? Does it die out on its own or does your immune system have to kill it off?

 

[bkp_duke]

Which cells does the vaccine invade? And when do the invasions stop? Does it die out on its own or does your immune system have to kill it off?

Muscle cells, you want them because they are excellent at "presenting" to the immune cells. The "invasion" stops when the mRNA is used up.

 

[madodel]

Should COVID vaccines be mandated?
How Soon Could COVID-19 Vaccines Be Mandated? How Can We Overcome Setbacks from Initial Vaccine Rollout Failure? Though most of this video is concerned with how messed up the vaccine rollout has been to date and why that is making people fearful of the process.

 

[AlanSubie4Life]

It would be nice to understand all the reasons for why the US FDA doesn't do rolling approvals or make any attempt to approve the J&J vaccine in much less than 21 days. This is the same thing that happened for Pfizer/Moderna (though clearly it didn't cost that many lives since Pfizer and Moderna did not apparently have any significant vaccine available, in any case).

Obviously I am not the only person to ask why:

FDA Career Staff Are Delaying the Vaccine As Thousands of Americans Die

This article suggests that there is really no actual reason, and I wonder how much truth there is to it and how much complexity has been glossed over here.

Worth noting that if J&J has no significant inventory of vaccine, then it actually doesn't matter very much (just like it didn't matter much for Pfizer/Moderna, probably "only" costing a few thousand lives or maybe less depending on actual vaccine quantities). But that would be somewhat surprising, since they've had months to produce vaccine (at risk), but I think they also received $1 billion from the federal government via OWS to do risk production (no idea what the actual contractual arrangement is - but if there's a way for them to avoid risking that $1 billion from the feds, I'm pretty sure they would avoid it). I would think they would have at least a few million doses stockpiled at this point, even if they're having production ramp problems. But of course no one knows. (And of course, since the storage requirements are not strict for this vaccine, these millions of doses should NOT be sitting in storage - they should already be distributed to pharmacies and medical facilities with the storage capacity and capability. This should be done prior to approval, even if it's not legal (just change the law).)

 

[TEG]

When someone receives an mRNA vaccine (like Moderna or Pfizer), does the body have a somewhat random immune response in how it decides to build antibodies against the foreign spike proteins that start to show up in your body?

For instance, is medical science taking the resultant antibodies from various people to compare them to see if they recognize the same attributes of the spike proteins? Do we understand how similar or variable these responses can be?
I think perhaps the monoclonal antibodies that are created get based off of "best of breed" natural immune responses that were found? Would monoclonal antibodies taken from an actual COVID infection response be any better/worse than those taken from someone who just received vaccine?
Hopefully these questions make sense, and I am not misunderstanding even these points.

I am contemplating making a silly diagram showing a "normal" protein with a proper ACE2 key for normal "unlocking", and a bad foreign protein with a weird elongated key that seems to fit the same ACE2 lock, and showing how our antibodies would tell the difference between the two.
( Sort of a silly analogy, but trying to make this visually easier to understand mostly for my own learning. )

 

[EVNow]

Yeah, I've heard that. I wonder how good a predictor a reaction to the first dose is to prior COVID-19 infection.

Different vaccine, different country.

My brother had some fever after the first Oxford vaccine. Not my sister-in-law. He had a Covid earlier.

Yet to take the second shot.

On a different note, new report says the second shot after 3 months is better for the Zeneca / Oxford vaccine.

 

[bkp_duke]

Different vaccine, different country.

My brother had some fever after the first Oxford vaccine. Not my sister-in-law. He had a Covid earlier.

Yet to take the second shot.

On a different note, new report says the second shot after 3 months is better for the Zeneca / Oxford vaccine.

Linky please. Everything I've read has shown the mRNA vaccines (Pfizer and Moderna) are producing the most robust, longest-lasting immune response. The AstraZenica vaccine was good for a traditional vaccine, but at 70% effective after 2 doses, it is a distant 3rd in efficacy.
UPDATED Comparing COVID-19 Vaccines: Timelines, Types and Prices | BioSpace

 

[bkp_duke]

When someone receives an mRNA vaccine (like Moderna or Pfizer), does the body have a somewhat random immune response in how it decides to build antibodies against the foreign spike proteins that start to show up in your body?

For instance, is medical science taking the resultant antibodies from various people to compare them to see if they recognize the same attributes of the spike proteins? Do we understand how similar or variable these responses can be?
I think perhaps the monoclonal antibodies that are created get based off of "best of breed" natural immune responses that were found? Would monoclonal antibodies taken from an actual COVID infection response be any better/worse than those taken from someone who just received vaccine?
Hopefully these questions make sense, and I am not misunderstanding even these points.

I am contemplating making a silly diagram showing a "normal" protein with a proper ACE2 key for normal "unlocking", and a bad foreign protein with a weird elongated key that seems to fit the same ACE2 lock, and showing how our antibodies would tell the difference between the two.
( Sort of a silly analogy, but trying to make this visually easier to understand mostly for my own learning. )

No, it's a pretty specific immune response actually, based upon the epitopes of the Spike protein. It will be a polyclonal antibody response, but they will be similar (not exact) in most individuals. There's not much value and looking at the antibody structure (which is insanely hard to do and involves either nano-meter level MRI tech on purified, high-dose samples, or X-Ray crystallography).


You probably want to look at the diagrams from this article:
What is the ACE2 receptor, how is it connected to coronavirus and why might it be key to treating COVID-19? The experts explain

 

[EVNow]

Linky please. Everything I've read has shown the mRNA vaccines (Pfizer and Moderna) are producing the most robust, longest-lasting immune response. The AstraZenica vaccine was good for a traditional vaccine, but at 70% effective after 2 doses, it is a distant 3rd in efficacy.
UPDATED Comparing COVID-19 Vaccines: Timelines, Types and Prices | BioSpace

What I meant was for AstraZeneca the second shot after 3 months is better than after 1 month.

Not comparing to mRNA - but more to point out I don’t know when my brother will decide to take the second shot.

 

[bkp_duke]

What I meant was for AstraZeneca the second shot after 3 months is better than after 1 month.

Not comparing to mRNA - but more to point out I don’t know when my brother will decide to take the second shot.

Gotcha, completely went over my head in my vaccine-induced delirium.

 

[HG Wells]

Gotcha, completely went over my head in my vaccine-induced delirium.

DELIRIUM ?
So when my wife gets her second shot on monday there's a chance I could get her to sign the commitment papers ?

 

[bkp_duke]

DELIRIUM ?
So when my wife gets her second shot on monday there's a chance I could get her to sign the commitment papers ?

The delirium is from being tired (lots travel and work in the past week). The shot and immune response just pushed me over the line.

 

[TEG]

You probably want to look at the diagrams from this article:
What is the ACE2 receptor, how is it connected to coronavirus and why might it be key to treating COVID-19? The experts explain

Still not finding quite what I am looking for. Anything that starts talking about "normal" processes with angiotensinogen II tends to start to get too complex on the background for that.
I sort of want a simplified comparison about how angiotensinogen II interacts with ACE2 compared to COVID-19. Seems like it gets used a lot differently. One is like using ACE2 as a cleaver, and the other is like use ACE2 like a doorknob.
I guess it is a multi-function appendage on the cells.

Some other interesting diagrams:
A molecular trap against COVID-19 | Science

Identification of an existing Japanese pancreatitis drug, Nafamostat, which is expected to prevent the transmission of new coronavirus infection (COVID-19) | The University of Tokyo

ACE inhibitors appear to be safe and beneficial for COVID-19, say researchers

Examining the envelope protein of SARS-CoV-2

I am still struggling with the lock and key analogy.
I am thinking of it more like COVID-19 still "broke in" to the cell, but it found a handle it could grab onto to get the leverage it needed to do that.

Oddly reminded me of some kids toy from my past... Some sticky spiky balls you would throw at things and see if it sticks... It could roll along. Sortof like this:

So COVID sort of rolls its' way into the cells? Instead of bouncing off, it grabs an ACE2 handle and bends its' way into the cell?
Seems like a Ninja warrior challenge to reach out and grab onto the ring so you it can swing over to the goal.

The other thing I keep thinking about how this isn't like a steel door on a safe, hard to get through. This is all a bunch of squishy stuff, right? So sort of like when two bubbles bump into each other and merge.

 

[dhanson865]

Habitual use of vitamin D supplements was significantly associated with a 34% lower risk of COVID-19 infection

Deficiency was associated with higher risk of ventilation and death:

* Mechanical ventilation HR 6.12 p less than 0.001
* Death HR 14.73 p less than 0.001

 

[TEG]

Well, I am just one data point, but I have been taking 5050IU Vitamin D daily since COVID started and somehow managed not to catch it after living with 2 people having active cases recently.

 

[cwerdna]

Meanwhile, at least two months ago, this guy over at chevybolt.org who isn't a doctor and says he was previously infected by COVID-19 asserted that he's invulnerable. Then he went onto cite 11 years (I've never heard his comparison before) to which someone else replies, that's wrong.
Corona virus and oil crash
Corona virus and oil crash

I wonder how many other people out there who've recovered from COVID-19 infection have similar thinking: they're invulnerable or will be so for 11+ years? Sigh...

The above "invulnerable" to COVID-19 guy today at Corona virus and oil crash said "If people wanted to shame me for not wearing a mask, it wouldn't work because I can't spread the disease."

 

[alloverx]

In Victoria Australia they made some recent changes to hotel quarantine procedures due to 1 hotel person getting the virus
- All (non-medical?) staff to use face shield and surgical mask instead of planned N95 usage. Previously had surgical mask only.
- When delivering food to rooms (& testing), stagger the times so no doors on same floor open at same time.
- Spread out (leave some rooms empty) for large families as they suspect a previous case might have came from large infected family.
Note the current hotels do not have shared air between rooms/corridors.

 

[JRP3]

Covid cure? New Israeli Covid drug which cured 30 cases of disease hailed by scientists as 'huge breakthrough'

The EXO-CD24 substance was developed at the Ichilov Medical Centre in Tel Aviv and successfully completed its first phase of clinical trials on Friday.

The treatment was given to 30 patients with coronavirus, whose conditions ranged from moderate to severe.

Twenty-nine of the patients were then discharged from the hospital in the following three to five days, while one patient took slightly longer to recover.

A protein known as CD24 is delivered to the lungs by exosomes in the drug, which helps to rebalance the immune system and prevent it from overreacting to the virus.

 

[heltok]

Habitual use of vitamin D supplements was significantly associated with a 34% lower risk of COVID-19 infection

View attachment 634378

Deficiency was associated with higher risk of ventilation and death:

* Mechanical ventilation HR 6.12 p less than 0.001
* Death HR 14.73 p less than 0.001

I take 10k IU EoD, so I’m in the Vit-D-camp. But these studies are always tricky to do. People who supplement are likely more health oriented and have a higher level of conscientiousness than average. And people who are a lot in the sun likely are in better shape and exercise more and thus sleep better.

It’s like the old studies, women who take estrogen live longer, but women who are given estrogen supplementation in studies live shorter (women who pay for estrogen themselves have more money).

Not saying that Vitamin D doesn’t help, just that it’s hard to know from these studies. And just because we don’t know doesn’t mean that we should not act.