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.

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.