Study: Recovered COVID-19 Patients Possess Robust Immunity To Virus

The Federalist ^ | 7/26/2021 | Shawn Fleetwood

[Signalman]

A newly released study conducted by Emory University suggests recovered COVID-19 patients possess long-term immunity to the respiratory virus months after infection.

Published in Cell Reports Medicine, the comprehensive study analyzed 254 individuals with mostly mild to moderate symptoms of SARS-CoV-2 infection over an eight-month period and found that patients possessed “durable broad-based immune responses” to the virus after recovering from an infection.

“The study serves as a framework to define and predict long-lived immunity to SARS-CoV-2 after natural infection,” said Emory Vaccine Center director Rafi Ahmed. “We also saw indications in this phase that natural immunity could continue to persist.” Ahmed served as a lead author on the study.

The study goes on to note that in response to an active infection in the body, the human immune system produces a multitude of neutralizing antibodies, while also activating certain T and B cells to establish immune memory. Ahmed denotes that these developments make a strong case for some form of lasting immunity to the virus.

“We saw that antibody responses, especially IgG antibodies, were not only durable in the vast majority of patients but decayed at a slower rate than previously estimated, which suggests that patients are generating longer-lived plasma cells that can neutralize the SARS-CoV-2 spike protein,” he said.

Moreover, the analysis also demonstrates that not only are recovered patients likely to possess lasting immunity to existing SARS-COV-2 variants, but that “SARS-CoV-2 infection also boosts antibody titers to SARS-CoV-1 and common betacoronaviruses.”

“While pre-existing exposure and antibodies against HKU1 and OC43 betacoronaviruses are common in adults, pre-existing SARS-CoV-1 exposure is rare and antibody levels to SARS-CoV-1 spike protein were very low (essentially negative) in the pre-pandemic healthy controls,” the study says. “However, SARS-CoV-1 spike-reactive antibodies increased significantly after SARS-CoV-2 infection.”

The report later goes on to conclude that taken together, the results of the study “suggest that broad and effective immunity may persist long-term in recovered COVID-19 patients.”

The study’s participants are expected to be evaluated by the Emory research team over the next few years as part of continued research on the matter.

[Renfrew]

To add another layer of correction. Sars 1 infected don’t have antibodies 17 years later/ They have memory T-Cells with record of the virus.

That provides a more uncertain level of protection. By analogy antibodies are cops on the street actively hunting for a perp. Memory T-Cells is a wanted poster on a billboard at the police station.

The most likely scenario is that T-Cells prevent the infection getting severe. You might still get infected again, but it won’t become more than a mild cold.

[T.B. Yoits]

To repeat. Yes, those who were exposed to SARS in 2003 have the antibodies against SARS COVID-19.

2aProtectsTheRest: A) No they don't, it's a different virus.

It's not a different virus. They're both SARS coronaviruses and yes, those exposed to SARS in 2003 do have antibodies. Multiple sources have confirmed it. Here's just one:
https://www.timesnownews.com/health/article/study-finds-antibodies-from-patients-infected-with-sars-cov-in-2003-cross-neutralised-sars-cov/665536

2aProtectsTheRest: B) There are 7,324 in the entire world who are known to have had and survived SARS 2003. That's 0.0000977% of the world's population. It doesn't help the other 99.99991% even if it were true. And it isn't.

It does help. It shows that natural immunity does work and does last longer than these experimental treatments which apparently need a "booster" after only six months. There were no reports of SARS 2003 survivors having enlarged hearts, blood clotting, and nerve damage. None were reported to have lost pregnancies either.

It also shows that a true vaccine against SARS would work instead taking these experimental treatments.

[roving]

Maybe you should put your tagline to use.

[2aProtectsTheRest]

"The most likely scenario is that T-Cells prevent the infection getting severe. You might still get infected again, but it won’t become more than a mild cold."

It really just depends. The cross-reactivity shown in the lab was outside the body and may not accurately represent a significant response in natural situations. Lab experiments are helpful tools, but more work would be needed to establish what the actual effect would be in the real world.

Macrophages and neutrophils would already be fighting SARS-CoV-2 virions in any healthy person. If some T cells join the fight, that's going to be helpful. The question the remains is: to what extent? Perhaps it's enough to completely halt infections in their tracks. Unlikely, given the lack of significant numbers of T cells and the lack of coordinated B cell lymphocyte action, but who knows. Maybe it reduces the severity of infection as you suggested. That's certainly possible. It may also be that actual cross-reactivity in the body is minimal and the T cells aren't even that involved.

The difficulty here is that challenge trials are unethical and the pool of SARS2003 survivors is so tiny that you'd have a hard time studying this any other way. It's interesting data, and with luck we'll see some useful long-lasting immune system reaction with COVID-19. So far, those who were previously infected with SARS-CoV-2 appear to have great immunity moving forward. That's great news.

[Renfrew]

Very good points.

My suspicion is that Covid may be more like the common cold coronaviruses than we think:
*first infection is severe, except in kids where it is just a cold
*reinfection occurs every few years, but those later ones are mild.

The only difference with Covid is that it is new, so most of us never got that first infection in childhood.

[fireman15]

Funny how all you anti-vax zealots

I have never been “anti-vax” in my entire life. Because of my position as one of the heads of a Hazmat team for many years... my guess is that I have had ten times as many vaccinations as you. I likely have had a hundred times the training for dealing with bio-hazards than you.

When we have experimental gene therapy injections with more death and serious injury associated than every other vaccine in the last 30 years combined... it upsets me because I fully support legitimate vaccines. Much of the public will never trust the government about vaccines ever again as the full extent of this massive failure become more and more apparent. And that is a terrible shame which will result in millions of deaths from preventable disease in the future.

In other news... the CDC is withdrawing its EUA for PCR tests that have been used to falsify millions of positive Covid results. The test in question cannot distinguish between the Flu and Covid. What a strange coincidence that supposedly that Flu deaths dropped to nothing while Covid deaths soared.

You continue hiding behind a false pseudonym to deflect criticism for spreading leftist nonsense. I will remind you for the umpteenth time that you really ought to at least comment on an occasional firearms thread... I know you don't know the difference between a cartridge and a bullet, a magazine and a “clip”, or smokeless and black powder, or any other firearms related matters... but really??? Give yourself a tiny bit of credibility... please!

Oh and yes I almost forgot... I found this picture of you looking rather dapper.

[2aProtectsTheRest]

The challenge with the common cold is that it’s actually caused by any one of over 200 different viruses from several different families. Most are actually caused by a rhinovirus. There are four viruses in the coronavirus family known to caused colds in humans. What we call the “common cold” is really just a collection of symptoms shared by infections with any of those over 200 different viruses.

It does seem that immunity from that first bout is holding up even when new variants arise, so that’s really good news. Hopefully that continues to be the case and this thing goes away the way SARS2003 and MERS2012 both did.

[TexasGurl24]

That’s not what you said above, and you have a history of misinterpreting what studies say anyway.

[ifinnegan]

“As for the rest, you’re admitting I’m right and then saying I’m wrong anyway? What kind of nonsense is this?”

Nonsense is you’re not able to read or think clearly.

“Or an epidemiological study with all 7,324 SARS2003 survivors.”

All?

[ifinnegan]

“... don’t have antibodies 17 years later/ They have memory T-Cells with record of the virus.”

Antibodies are expressed on the surface of the memory cells. They proliferate when encountering the antigen.

Soluble antibodies probably are present but too low to detect.

[2aProtectsTheRest]

What I said above is that they don’t have antibodies. And they don’t. You’re confused about the difference between T cells and antibodies, which are produced by B cells.

Demonstrating that there are some cross-reactive T cells in a lab is not the same as showing that they have antibodies against the new virus. My history is that of explaining the study data in plain English to help people understand it and put it in context. Not twist it into some pre-selected narrative. If you’re confused about the study you referenced, you may be about others as well.

[2aProtectsTheRest]

"Antibodies are expressed on the surface of the memory cells. They proliferate when encountering the antigen."

No, that's not how that works at all. Antibodies are not produced by T-cell lymphocytes. They're produced by B-cell lymphocytes.

You've got the wrong cells.

[TexasGurl24]

I didn’t say anything about antibodies clown. Why are you lying?

I posted the study link and an excerpt. Nothing more.

[TexasGurl24]

Oh, and your history is creatively interpreting studies to push people toward getting the vaccine.

You never did answer my question regarding the SPECIFIC antibody level that protects against re-infection.

You just posted a vague non-response instead of honestly saying “I don’t know.”

[ifinnegan]

You’re a moron.

You’re not a moron because you don’t know anything about the different types of antibodies there are. Most people wouldn’t know.

You’re a moron because you think you do when you know nothing.

[2aProtectsTheRest]

Is this how you always react when you’re wrong about something? You call people names?

https://www.cancercenter.com/community/blog/2017/05/whats-the-difference-b-cells-and-t-cells

No matter how many names you call me, you’re still wrong.

[Organic Panic]

I hear liberals refer to themselves as “survivors.”

When I had it I didn’t know. The doctors didn’t know much about it since we were one of the first west coast places hit (A large Chinese exchange school has students coming and going. When suddenly one day all the Chinese students started wearing masks). They just said it is a particularly bad flu and to rest. I did my usual illness routine, got a bottle of good whiskey, and slept it off. It was bad, but no worse then a cold. In fact... It just hit the lungs and not the usual sinus issues that happens when I get a cold. Everyone I know who got it had the same thing and some barely even felt anything.

[ifinnegan]

No I react like this to morons with hubris.

B cells and T cells have membrane attached antibodies with v(d)J derived antigenic determinant sites. B cells have two antigen recognition regions, T cells one referred to as T cell antigen receptor

[2aProtectsTheRest]

You’re still wrong. This time you’re confusing antigens with antibodies. Antigens are pieces of foreign substances or organisms which provoke an immune response. Antibodies are part of the immune response. They bind to the invading pathogen in such a way as to disable or kill it. Two different things.

The T cell antigen receptor is used to bind to pathogen major histocompatibility complex sites and initiate biochemical responses (including recruitment of CD4 and CD8 co-receptors) so the pathogen or infected body cell can be destroyed.

It does NOT carry an antibody. That would not make any sense. If it had an antibody attached to the antigen receptor, the T cell would not be able to bind to the MHC and would become useless. What you’re describing is more along the lines of an autoimmune disease.

[ifinnegan]

“This time you’re confusing antigens with antibodies.”

You’re a moron.

I am not confusing antigens with antibodies.

T cell antigen receptors are membrane associated antibodies with antigen recognition sites created via vdj rearrangement. B cell antigen receptors have two antigen recognition sites. T cell antigen receptors have one.

My use of the term antigenic determinant sites may have confused you and caused you to make your comment, and recognition rather than determinant would be better, but in the context of the phrase “vdj derived antigenic determinant” would not confuse anyone knowledgeable of molecular immunology.

(See how nice I can be you you?)