maybe one of these has something you're looking for:

The National Institute of Cancer helped sponsor this one. Can't say I've read many abstracts or papers discussing the infection of T-cells themselves, but I haven't checked it exhaustively.

SARS-CoV-2 may affect the immune response via direct inhibition of T cell receptor: Mechanistic hypothesis and rationale


During co-evolution with their hosts, many viruses have evolved a membrane fusion mechanism to facilitate host cell entry. Examples are human immunodeficiency virus type 1 (HIV-1) and severe acute respiratory syndrome coronaviruses 1 and 2 (SARS-CoV-1 and SARS-CoV-2). These viruses can also infect immune cells (e.g., T cells), providing one of the possible mechanisms for the T cell lymphopenia observed in patients with these infections. Previously, we hypothesized and confirmed in vivo that like HIV-1, SARS-CoV-1 can use its fusion domain not only to enter the T cell but also to directly inhibit T cell receptor signaling. Here, based on the analysis of available structural and clinical data, we hypothesize that SARS-CoV-2 may use a similar "disarm the alarm" strategy to suppress immune responses. We also discuss the implications of this hypothesis for better understanding coronavirus disease 2019 (COVID-19) pathology, developing effective COVID-19 vaccines and improving clinical outcomes for COVID-19 patients.

I've been reading a number of papers on the anti-idiotype antibody subject and have noticed some interesting things. The following paper mentions "cancer" 42-times and "vaccine" 45-times.

The Promise of Anti-idiotype Revisited


And there's the relationship to what's going on with SARS-CoV-2

Development of ACE2 autoantibodies after SARS-CoV-2 infection


Activation of the immune system is implicated in the Post-Acute Sequelae after SARS-CoV-2 infection (PASC) but the mechanisms remain unknown. Angiotensin-converting enzyme 2 (ACE2) cleaves angiotensin II (Ang II) resulting in decreased activation of the AT1 receptor and decreased immune system activation. We hypothesized that autoantibodies against ACE2 may develop after SARS-CoV-2 infection, as anti-idiotypic antibodies to anti-spike protein antibodies.

Many patients with a history of SARS-CoV-2 infection have antibodies specific for ACE2. Patients with ACE2 antibodies have lower activity of soluble ACE2 in plasma. Plasma from these patients also inhibits exogenous ACE2 activity. These findings are consistent with the hypothesis that ACE2 antibodies develop after SARS-CoV-2 infection and decrease ACE2 activity. This could lead to an increase in the abundance of Ang II, which causes a proinflammatory state that triggers symptoms of PASC.

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I was meandering through papers on NAD+, Sirtuins, and Niacin, as relates to cancer and these vaccines; (looking for potential 'smoking-gun' studies); when the fact of Niacinamide being the preferred NAD+ precursor during cancer-treatment, due to it not requiring Glutamine in the synthesis of NAD+, got me off those search-terms and onto the Glutamine metabolism track.

Papers found so far lead me to hypothesize that if these vaccines are destabilizing Glutamine metabolism, that is sufficient to answer at least some of the cancers. Interestingly, one paper revealed a Glutamine deficiency in advanced hospital Covid-cases. Competition for Glutamine between T-cells and Tumor-cells is well documented.

One question is what if we're mass-vaccinating into a Glutamine-deficient aged-population; with its preexisting propensity for cancer metabolism? At one end, they're not making it out of the hospital or nursing home. At the other, with weakened or altered T-cell signaling due to viral infection, T-cells lose the competition for Glutamine. Another question goes back to the related NAD+ metabolism. What if we're mass-vaccinating into a NAD+ deficient and/or a Niacin-deficient population? There's no 'discounting' for any of these considerations prior to shots being administered. What good is it to have our scientists find the commonality of Glutamine deficiency in advanced Covid cases and not notify everyone in headlines and covers of grocery store magazines?

Excerpts from an article by Dr. Thomas Levy:

The involvement of niacin in preventing cancer and chemotherapeutic side effects is not commonly recognized, but decades of research has established that niacin deficiency is common in cancer patients and cancer patients require larger amounts of niacin to correct deficiency. [4]

Generally, studies indicate that NAD functions as a preservative protecting cellular DNA from mutation and also preventing mutated cancer cells from surviving. Niacin deficiency promotes cancer by decreasing genomic stability, increasing the chances both for mutation and survival of mutated cancer cells.

Studies indicate that niacin deficiency delays DNA repair, promotes accumulation of DNA strand breaks, chromosomal translocations, telomere erosion typical of aging, and promotes cancer. Rat model studies indicate that most of these aspects of genomic instability are all minimized by the recommended levels of niacin. [5] Niacin deficiency also increases levels of the tumor suppressor p53. [6] Studies in mice indicate that mild niacin deficiency can cause an increased incidence of ultraviolet-B induced skin cancer. [7]

This review of 183 studies does a nice job of bringing together NAD+, PARP enzymes, Sirtuins, DNA repair, Cytotoxicity, and T-cell considerations.

NAD+-consuming enzymes in immune defense against viral infection


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Do you think this could be possible mechanism of action? Toll - Like Receptors, that need to be turned off so mRNA can get into the cell, but (who would'v thought?) TLRs have other uses also ... ? https://www.ukcolumn.org/article/stabilising-the-code (Thank you for being a voice of reason for so long.

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thanks - read that one and a linked reference https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC8071766/

so much 'high-strange' in that one it's hard to believe there's any confidence

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An interesting find today, from 2014 - https://www.nature.com/articles/nrd4278

Figure 5, seems like theorized auto-targeting by mRNA transfection of preexisting tumor tissue due to capillary fenestration.

It's one of the studies in the gigantic "Literature References" doc released by Pfizer a few days ago at https://phmpt.org/pfizers-documents/

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