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.