That is not how senescent cells work. They turn over on a fast timescale. If covid induces a bunch of senescent cell development (which indeed makes sense), those senescent cells should generally be cleared out on a timescale of weeks. Any long-term effects would need to be mediated by something else.
But some of those SnCs probably won’t be cleared, and that extra burden of SnCs (especially if it’s much higher than what intrinsic aging produces during a short period of time) might be what’s causing long covid.
At this point, I have yet to see any compelling evidence that any SnCs stick around over a long timescale, despite this being a thing which I’d expect to have heard about if anybody had the evidence. Conversely, it sure does look like treatments to remove senescent cells have to be continuously administered; a one-time treatment wears off on roughly the same timescale that SnCs turn over. That pretty strongly suggests that there are not pools of long-lived SnCs hanging around. And a noticeable pathology would take a lot of SnCs sticking around.
The paper you linked to seems to claim that SnCs do stick around.
In old mice, baseline SnC levels are about 5-fold higher, and SnC removal rate is slower than in young mice (p=0.038).
This suggests that middle-aged mice should also have some baseline SnC level, although perhaps not as much as old mice. Also, the level of SnCs didn’t return to baseline in the old mice even at the 40 day mark.
“Baseline” does not mean they stick around. It means that background processes introduce new SnCs at a steady rate, so the equilibrium level is nonzero. As the removal rate slows, that equilibrium level increases, but that still does not mean that the “baseline” SnCs are long-lived, or that a sudden influx of new SnCs (from e.g. covid) will result in a permanently higher level.
Even if the original SnCs are eventually eliminated (which isn’t entirely clear), it sure looks like they should increase the SnC baseline anyway. It’s not just background processes that can produce new SnCs, but SnCs themselves produce new, secondary SnCs too. So, it’s not unlikely that adding a bunch of SnCs to the baseline pool of SnCs (whose size increases with age) could further increase the size of this pool. And that would be a net increase in biological age.
This might not be a problem for young mice which can eliminate SnCs fairly quickly, but it seems to be a big problem for old mice. Middle-aged mice probably lie somewhere in between. I’d also expect that overweight, obese, or otherwise messed-up, middle-aged mice would fare worse.
It’s not just background processes that can produce new SnCs, but SnCs themselves produce new, secondary SnCs too.
Imagine that each new SnC produced 3 new SnCs within a day, and also that SnCs had a 50% chance of being removed each day. In that case, there will be 4*0.5 = 2x as many SnCs tomorrow as there is today, leading to exponential runaway growth, immediately exploding in the number of SnCs and dying.
On the other hand, imagine that they only produce 1 new SnC within a day, and also that they had a 66% chance of being removed each day. In that case there will be 2*0.33 = 0.66x as many SnCs tomorrow, leading to quickly returning to the equillibrium caused by outside production.
You’d need some sort of fine-tuning where the production and removal are extremely close to each other to not either have explosive growth or rapid equillibration.
It’s probably too early to compare the amount of senescence that’s produced by SARS-CoV-2 versus other viruses, but what is known is that several viruses (including influenza) do induce the development of senescent cells in several tissues.
I’d say that unhealthy-for-their-age young and middle-aged people and otherwise healthy-but-middle-aged people might want to be more cautious. Healthy-for-their-age young people probably don’t need to worry.
Covid is airborne aging via SARS-CoV-2-induced senescent cell development.
Even non-elderly people might age faster, especially if they’re overweight or obese.
That is not how senescent cells work. They turn over on a fast timescale. If covid induces a bunch of senescent cell development (which indeed makes sense), those senescent cells should generally be cleared out on a timescale of weeks. Any long-term effects would need to be mediated by something else.
But some of those SnCs probably won’t be cleared, and that extra burden of SnCs (especially if it’s much higher than what intrinsic aging produces during a short period of time) might be what’s causing long covid.
At this point, I have yet to see any compelling evidence that any SnCs stick around over a long timescale, despite this being a thing which I’d expect to have heard about if anybody had the evidence. Conversely, it sure does look like treatments to remove senescent cells have to be continuously administered; a one-time treatment wears off on roughly the same timescale that SnCs turn over. That pretty strongly suggests that there are not pools of long-lived SnCs hanging around. And a noticeable pathology would take a lot of SnCs sticking around.
The paper you linked to seems to claim that SnCs do stick around.
This suggests that middle-aged mice should also have some baseline SnC level, although perhaps not as much as old mice. Also, the level of SnCs didn’t return to baseline in the old mice even at the 40 day mark.
“Baseline” does not mean they stick around. It means that background processes introduce new SnCs at a steady rate, so the equilibrium level is nonzero. As the removal rate slows, that equilibrium level increases, but that still does not mean that the “baseline” SnCs are long-lived, or that a sudden influx of new SnCs (from e.g. covid) will result in a permanently higher level.
Even if the original SnCs are eventually eliminated (which isn’t entirely clear), it sure looks like they should increase the SnC baseline anyway. It’s not just background processes that can produce new SnCs, but SnCs themselves produce new, secondary SnCs too. So, it’s not unlikely that adding a bunch of SnCs to the baseline pool of SnCs (whose size increases with age) could further increase the size of this pool. And that would be a net increase in biological age.
This might not be a problem for young mice which can eliminate SnCs fairly quickly, but it seems to be a big problem for old mice. Middle-aged mice probably lie somewhere in between. I’d also expect that overweight, obese, or otherwise messed-up, middle-aged mice would fare worse.
Imagine that each new SnC produced 3 new SnCs within a day, and also that SnCs had a 50% chance of being removed each day. In that case, there will be 4*0.5 = 2x as many SnCs tomorrow as there is today, leading to exponential runaway growth, immediately exploding in the number of SnCs and dying.
On the other hand, imagine that they only produce 1 new SnC within a day, and also that they had a 66% chance of being removed each day. In that case there will be 2*0.33 = 0.66x as many SnCs tomorrow, leading to quickly returning to the equillibrium caused by outside production.
You’d need some sort of fine-tuning where the production and removal are extremely close to each other to not either have explosive growth or rapid equillibration.
How does this compare to other contagious diseases?
EDIT: for aging in particular.
It’s probably too early to compare the amount of senescence that’s produced by SARS-CoV-2 versus other viruses, but what is known is that several viruses (including influenza) do induce the development of senescent cells in several tissues.
Then this doesn’t seem like a counterargument to “to elderly people it would be effectively the same as any other serious stressor” to me.
The counterargument would apply to “It wouldn’t be relevant to non-elderly people....”
Ah, yes. I think young people should probably take the long term effects of viruses more seriously in general.
I’d say that unhealthy-for-their-age young and middle-aged people and otherwise healthy-but-middle-aged people might want to be more cautious. Healthy-for-their-age young people probably don’t need to worry.