Senolytic Self-experiments and COVID-19
There is evidence that the TOP2 receptor that the COVID-19 virus uses to enter cells is more prevalent in senescent cells. Also, clearing accumulated senescent cells from the immune system probably boosts immunity. Both effects should make it more difficult to contract COVID-19.
Therefore, I was wondering if anyone participating in the Forum has (a) engaged in senolytic self-experiments with D+Q and/or Fisetin, and (b) actually come down with the COVID-19 virus?
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You may be interested in this paper by Prof. Sinclair in which he discusses C-19.
https://www.preprints.org/manuscript/202004.0548/v1
There's a lot of information on immunity which you can hopefully skip through and still get at the meat of the discussion. It may be useful to have a copy of Kuby's Immunology nearby.
NMN cured my immune dysfunction in term of making me no longer allergic to peanut butter. I think this also means I'm better in resisting virus.
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JGC said:
There is evidence that the TOP2 receptor that the COVID-19 virus uses to enter cells is more prevalent in senescent cells.Abstract
Cellular senescence is often considered a protection mechanism triggered by conditions that impose cellular stress. Continuous proliferation, DNA damaging agents or activated oncogenes are well-known activators of cell senescence. Apart from a characteristic stable cell cycle arrest, this response also involves a proinflammatory phenotype known as senescence-associated secretory phenotype (SASP). This, together with the widely known interference with senescence pathways by some oncoviruses, had led to the hypothesis that senescence may also be part of the host cell response to fight virus. Here, we evaluate this hypothesis using vesicular stomatitis virus (VSV) as a model. Our results show that VSV replication is significantly impaired in both primary and tumor senescent cells in comparison with non-senescent cells, and independently of the stimulus used to trigger senescence. Importantly, we also demonstrate a protective effect of senescence against VSV in vivo. Finally, our results identify the SASP as the major contributor to the antiviral defense exerted by cell senescence in vitro, and points to a role activating and recruiting the immune system to clear out the infection. Thus, our study indicates that cell senescence has also a role as a natural antiviral defense mechanism.