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Michaelcycle13 t1_j8sxvlc wrote

Reply to comment by Rakshear in Scientists find people with Long Covid have 2 major cytokines of the immune system (IL-8, IFN-γ) reduced by 100% by sagdiyev1

GUY BELOW ME KNOWS MORE When a virus invades the host. The body's bacteria along with antibodies find and detect its existence. They then go to deploy Cytokine molecules from the Thymus gland to seek out and kill the viral matter through cells called "T cells", typically called "Killer T Cells". These cells engage the virus and begin to fight it. You usually experience symptoms like Fatigue, Fever, or other bodily dysfunctions during this time as your body is using natural processes to kill viral matter and protect itself.

In the above article it is stating that they are finding people with Long Covid don't have an overreactive immune system. But that they have an underreactive immune system. Specifically lessened Cytokine molecules aka T cells. T cells are the most crucial, when deployed they give the sensations of a "fever" and those other aforementioned bodily dysfunctions.

The Thymus gland produces Cytokine and T Cells. And it is fueled off of Vitamin C and Zinc. Vitamin C and Zinc are shown to be lessened in people with Long COVID. With insufficient nutrition the Thymus gland will have atrophy and shrink. This leading to a understrength baseline Immune System response in the future.

I'm now theorizing that our mild or asymptomatic infections are really red flags that our immune system was underprepared to fight off the virus. Or that our bodies did not have adequate antibodies or [gut] signaling bacteria to detect the existence of the virus for defense or deployment.

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discotititis t1_j8wcddm wrote

As someone who works in immunology, your explanation is very inaccurate. When an unknown virus invades the host, special cells known as dendritic cells (not antibodies or bacteria—antibodies can’t even be produced until B cells are activated) take up bits of the virus and travel to lymph nodes (not the thymus—the thymus is where T cells mature).

In the lymph node, a single T cell with a matching receptor recognizes the bit of the virus the dendritic cell is presenting. When it recognizes the virus, the T cell divides and multiplies. Certain kinds of T cells—killer T cells—destroy infected cells. Other kinds of T cells—helper T cells—activate B cells, which produce antibodies that neutralize virus. All the multiplication of T cells and activation of B cells occurs in the lymph nodes—it’s why doctors check to feel if they’re swollen when you’re sick to see if there’s an infection on.

Cytokines like IFNy and IL-8 (among others mentioned in this paper) are produced by a wide array of immune and non-immune cells when they recognize viral infection. (Not the thymus, though. Once again, the thymus is just where T cells develop.) They activate dendritic cells to take up bits of virus and travel to the lymph node. They also direct T cells to develop in a certain way and for B cells to produce the right kind of antibodies. They also encourage migration of other kinds of immune cells to the site of infection to eliminate the virus.

The authors here believe that immune exhaustion is the cause of long COVID. Once cells stop producing these necessary cytokines, the immune system simply cannot function as it should anymore. This exhaustion doesn’t come from initial underreaction, though—it’s overreaction of the immune system that causes it.

Tons of studies have proven that high levels of pro-inflammatory cytokines like the ones in this paper actually correlate with worse outcomes. The inflammation they cause, when unchecked, can be very damaging to tissues. On the other hand, lack of reaction at all is also very dangerous. The immune system has to walk a tight line between over- and underreaction or risk either scenario. Long COVID is essentially dysfunction of this balance, likely due to initial overreaction.

I recommend How the Immune System Works by Lauren Sompayrac as a great primer to immunology. Cause it doesn’t work like how this person is describing it.

TL;DR: This explanation is absolute BS and any doctor or scientist would laugh their ass off about any number of things in it. Bacteria and antibodies taking virus to the thymus? Doesn’t happen and goes against the entire logic of how the immune system works. The thymus dying? The thymus shrinks with age, but that doesn’t cause what we see in long COVID. It usually just causes a weaker immune system in old age.

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Michaelcycle13 t1_j8yc5hz wrote

I see I do appreciate your correction. I’m regurgitating personal at home research from online doctors I’ve watched explaining it and pubmed papers. It looks like I’ve completely messed up the initial signaling from the dendritic cells. I never did say that bacteria or antibodies carried the virus to the thymus to correct you. But that they served a role in signaling to the T cells for response of the immune system. Which is a true scientific statement that I would be happy to share the research on. I was however incorrect about the thymus being the origin of the production of cytokines. I appreciate the correction again. My explanation also was missing the functionality of the dendritic cells, lymph node, and B cell activations for the pathology of immune response. I’d love to ask you more questions because I am fascinated to hear more and to learn more!

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discotititis t1_j8ysyeh wrote

I’m on mobile so pardon my formatting.

> The body’s bacteria along with antibodies find and detect its existence.

This is not true. Yes, there have been some studies that show that commensal bacteria are important for signaling to T cells. However, they do not activate T cells. T cell activation only occurs upon recognition of an antigenic peptide presented upon the MHC molecule of a dendritic cell in the lymph node. Signaling from commensal bacteria only has an effect once T cell activation occurs, when it can affect the differentiation of a T cell down different lineages. T cells can only then activate B cells, which produce antibodies. Antibodies for previously unknown viruses do not exist in the body yet—that’s why it takes so long to mount an immune response because it takes some time for a T cell with the correct receptor to recognize the virus as presented on a dendritic cell.

The initial recognition of a virus, though, occurs from innate immune cells that can recognize patterns present in lots of viruses. In response, these innate immune cells produce cytokines that begin the process of inflammation and activate dendritic cells to take up virus and travel to the thymus. These cytokines can affect the differentiation of T cells down different lineages (killer, helper types 1, 2, and 17, regulatory, follicular). These cytokines also affect the type of antibody produced, as different antibodies have different properties for better neutralizing different kinds of microbes.

Notice how the thymus isn’t involved in any of this. It’s very important but it doesn’t really play a role in the basics of the immune response.

I really wouldn’t rely off random internet doctors for immunology research, sorry. Way too many conspiracy theorists online. Research papers are also going to be way too advanced at this stage. Sompayrac is your best bet. I’ll even sell you my copy. Even Cells at Work (on Netflix) is going to be more accurate and helpful.

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Michaelcycle13 t1_j8yu7yq wrote

Haha we're saying the same thing about the commensal bacteria aspect. I never did say that commensal bacteria activated the T cells as you so put. I'd love to hear more from you. I'm a Long Covid struggler who's on the mend. A lot of people don't know what is going on, medical professionals especially, however, everyone has their theories.

I think through discourse like this we're only going to improve in knowledge and learn more. Obviously I do not have a background in immunology as you say you have. I've also been looking into starting a Long Covid Collaboratory podcast where we bring in other people struggling to share stories, share what helped us, and discuss symptoms. Would you ever be interested in saying some words?

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Rakshear t1_j8t12xo wrote

Thank you , I sincerely appreciate it.

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SanaFraley t1_j8takft wrote

A lazy immune system makes sense, but the lack of thymus being an attributor does not. I still have most of my thymus noted on my CT with contrast as "favored residual thymic tissue" as a 30 year old, yet still abysmally low specs and long covid.

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Michaelcycle13 t1_j8ty619 wrote

That’s good! I believe that it can be misleading to assume that because your thymus appears healthy on a CT scan that your immune system is functioning to par. Be sure you have the vitamin C, D, and Zinc in optimal ranges. There are other residual effects from the virus as well such as gut dysbiosis which is cause a number of continuous downstream effects if gone untreated. I did not mean to say any thymus dysfunction is the explanation for long Covid in it’s entirety. There is malabsorption of vitamins, nutrients, and amino acids; gut permeability, organ inflammation, dysfunction in Short Fatty Chain Acid synthesis, neurotransmitter synthesis, and a likely overgrowth of bad bacteria and yeast.

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SanaFraley t1_j8v3ork wrote

I definitely don't think my immune system is performing normally. Just was specifically mentioning the thymus part cause they said its rare for people to have an intact thymus when most by 30 went through a full involution.

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Michaelcycle13 t1_j8vms3r wrote

I see. That’s fully understandable. I don’t believe my immune system is performing well either. May I ask, what was your attributed “long Covid” infection like?

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SanaFraley t1_j8wnsv5 wrote

I don't fully understand your question. If you mean my acute infection, it was bad, 91% spo2 bilateral delta pneumonia. If you mean my long covid symptoms....2 years of pure hell....burning hands/feet, blurred vision, sob, chest pains, brain fog, dysmotility. To name a few.

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Michaelcycle13 t1_j8ya4e5 wrote

I was meaning long Covid. And sorry to hear about these symptoms Man. I’m about to begin a long Covid podcast and we’re aiming at just bringing on people with long Covid for quality collaboration, and discussing our long Covid stories. At the least you make a friend in the community and have some meaningful helpful conversations, at the most you help others through the spread of awareness and knowledge and we blow the lid off this misunderstood illness

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FSAaCTUARY t1_j8vj1vu wrote

So less symptoms mean more likely to get long covid?

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Michaelcycle13 t1_j8vm4ds wrote

There is an uncanny correlation between this exact phrase you uttered. It’s based by no scientific basis, some speculative research articles are floating around out there that mention this exact same hypothesis. While I would say it is probable it is not entirely purely 100% accurate. There seems to be a heavier hit to highly cardio active individuals as well.

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