SARS-CoV-2 disrupts timing of immune response (Tells body early “all clear” message)

Medical Xpress / Charité - Universitätsmedizin Berlin / Nature ^ | Oct. 25, 2021 | Andreas Diefenbach et al

[ConservativeMind]

Once an infection is under control, the body normally uses a biochemical messenger known as TGFβ to downgrade its immune response. In severe COVID-19, however, this messenger is released at the very beginning of the infection, thus blocking the early control of the pathogen by the innate immune system. The early production of the immune-dampening TGFβ messenger appears to be a hallmark of COVID-19 and has not been observed in other types of pneumonia. Correction of the immune system's faulty timing may therefore offer a new strategy for preventing severe disease.

The innate immune response is the first line of defense against pathogens entering the body. Though non-specific (i.e., the same for all pathogens), the innate immune response is ready to spring into action at any time. If this first line of defense fails to render the pathogen harmless, the second step is to activate the body's adaptive immune response—including both antibody-producing B cells and T cells—which targets and eliminates specific pathogens. However, the adaptive immune system must first acquire the ability to recognize these pathogens, and so its activation takes some time.

The innate immune system is therefore critical to the body's ability to mount an immediate response against invading pathogens. If the pathogen in question is a virus, this response primarily involves the activation of 'natural killer' ('NK') cells, which are able to identify specific infection-related cell surface changes and thus to recognize virus-infected cells. NK cells can then eliminate these virus-infected cells using cellular toxins. For the first time, the Berlin-based team of researchers was able to show that NK cells also play a role in the early control of SARS-CoV-2. However, their ability to eliminate SARS-CoV-2-infected cells was impaired by the early release of TGFβ.

[ConservativeMind]

This hasn’t been seen before in this type of virus—almost like it’s man-made…

[Prince of Space]

Positively evil.

[RummyChick]

So what about autoimmune people. Do they have faulty tgbf responses and that is why the body attacks itself

[RummyChick]

Hmmm..well maybe

https://pubmed.ncbi.nlm.nih.gov/16137611/

[BenLurkin]

"We are this close to getting away with it."

[dfwgator]

"I'm crushing your head!"

[neverevergiveup]

So what about autoimmune people. Do they have faulty tgbf responses and that is why the body attacks itself

TGF-beta has a lot of effects, and is involved in many biological responses. Whereas there is likely a role played by TGF-beta in the immune response to Covid, I highly doubt that it is the defining arbiter of pathological immune responses in the context of Covid infection.

Journal editors want 'stories'. They like nice neat 'stories' that link the presented data to a paradigm that explains 'everything' about x, y, or z. This is hardly ever the case, but to get published investigators package their data into 'explains it all' dogma. The editors love this, and reward it - thus ensuring that this approach to science is perpetuated.

[ConservativeMind]

The story clearly states it only does this to the innate immune system.

All subsequent immune reactions are normal.

[Arcadian Empire]

The destructive effects of the Fauci-Daszak-Wuhan coronavirus are going to be uncovered, along with the destructive effects of the poisons labeled COVID vaccines, for years.

[A Formerly Proud Canadian]

Ping

[metmom]

Ping

[rdcbn1]

Very early on there was a report that the Sar-cov-2 virus had a unique DNA sequence that seemed to have “jumped” from the HIV virus. There were corresponding NIH/NIAID research papers from a few years prior that had located and isolated the DNA sequence of the HIV virus that allowed it to remain hidden from the immune system . The sequences were suspiciously similar. Fauci was the guy who funded the HIV research. Just sayin’