Viruses that cause a cytokine storm tend to kill the young and healthy but not kill people with weaker immune systems like children or the elderly.
Diseases like SARS-Cov2 kill the elderly, but leave kids and middle aged people alive.
I’m assuming there are viruses that kill kids but do not kill adults, but I can’t think of any offhand. Google isn’t helping either. The bacteria that causes diphtheria seems to mostly kill kids though.
So you could engineer an infectious pathogen that kills kids, healthy middle aged people, or the elderly if you wanted I would assume.
Or more accurately Nature provides different chinks in the armor of the various ages. So in principle one could design something to exploit one or another chink specifically.
Whether it could be done in practice depends on our state of bio-knowledge and bio-tech. Which seems generally inadequate to the task today. Modern science can wave its arms in the right general directions and has very specific knowledge of a few spots in the overall vast landscape of pathogens and immunity. But not enough to do the whole job.
Da Vinci could draw pictures of almost-plausible flying machines and explain roughly how they might work. An actual flying machine was several hundred years into the future.
Also, as I say, while there are viruses that disproportionately affect infants, the elderly or people, say 16-30, I’m not aware of any that disproportionately affect 35-45 year olds. Which makes sense; given that their immune systems are somewhere in-between the characteristics of other groups.
So I am not sure we could in fact assert that targeting middle-aged people with a virus is actually possible, though IANA virologist / epidemiologist.
It’s not a new idea that fixing up the errors that accumulate in DNA will be a rejuvenation treatment. There are other SF stories that have that idea, which has been around for at least 40 years or so. My idea was fixing up the epigenes. That is, things that are attached to DNA and change how the DNA works, but are not the DNA itself.
My understanding is that telomeres are just one small part and all these other changes (and thanks to @Riemann for the link to that paper about them) are far more important. Just fixing up the telomeres is not going to do much toward rejuv.
The thing with aging is that it’s a whole bunch of things that all tend to fail at about the same time. They all fail at about the same time because any specific thing that failed earlier would have strong evolutionary pressure against it. But the result of them failing at about the same time is that fixing, or even just effectively treating, any one of them would, by itself, have only a very small effect on lifespan.
Take someone who would have died at 80 of a heart attack. Give them a miracle medicine that cures all heart problems, and they’re still likely to die at 82 or 83 of a lung problem, or a blood problem, or an accident made worse by a weak skeleton, or…
However, if they all fail for similar reasons, then treating that underlying cause could be helpful. So, if the underlying issue is that the DNA in our cells starts to break down, preventing that could help in a lot of ways.
That is my understanding of why, say, the telomere issue exists. Those help prevent errors in DNA copying by essentially sacrificing a bit of themselves with every copy. Thus it makes sense that elongating them might prevent DNA degradation by that route.
That said, there are likely multiple things that lead to said degradation. Errors can build up over time due to just mutations caused by radiation or carcinogens, for instance.
But aging isn’t just genetic, either. Everything breaks down with time. Your body is constantly being damaged in small ways, and constantly repairing itself, but the repairs are never quite as good as the original.
The whole concept of ageing is due to the fact that selection pressures are weaker the further organisms get from the age of reproduction and survival expectancy* (that is, how long an organism might be expected to survive if ageing wasn’t a factor).
From the “selfish gene” point of view, getting fat, ugly and bald are pretty damn serious faults, but by the time we are in our 40s and 50s the selection pressure is much weaker. (Granted, “middle age spread” would not have been so prevalent in our history when food was not so plentiful), so they can persist in the gene pool, along with countless other serious problems.
In terms of actual organ failures, there’s nothing special about the 80s, and indeed no special time at all. People right now do suffer organ failures before 80, or, much more commonly, are afflicted with illnesses that could have been crippling or fatal prior to modern medicine.
And, no doubt, the other side of “at the same time” is not true either. That is to say, if we just prevented all the known causes of death, and got a human to 150 years old, there would be other damage and kinds of organ failure that right now we are unaware of, because no human lives long enough to experience them.
* The survival expectancy for humans in the modern world is now very high; IIRC it has been estimated as several thousand years. This would mean that there would be strong selection pressure against all forms of ageing prior to being a few centuries old. However, humans are a bit of a special case when it comes to natural selection, making things not so simple, and besides, we’d have to wait millenia to see any noticeable difference anyway.
Should also point out that, yes, elderly people are more at risk from Covid. But… the absolutely horrific death rates of elderly that we saw were a side-effect of North American culture. In China and many other less developed countries, elderly live with their children (or children live with their parents… depending on point of view). A virus targeting the elderly would have to be spread to the younger healthier members of society first, and did have a certain lethal percentage with them too.
In USA and Canada, and to a lesser extent in Europe, many elderly live in group homes, tended to by a group of nurses and attendants who go from one to the other person. This meant that (a) the disease more easily spread from person to person as they were all under the same roof and (b) staff contracted the disease and needed to stay home causing a shortage of people to help tend to elderly patients, so patients also did not get fed, hydrated, or their toilet needs attended to - aggravating the problems.
A capitalist aggravation was that many nursing home staff were part time (for ease of scheduling, issues with benefits eligibility, etc.) so the same person might work in multiple jobs in multiple homes, thus carrying the disease between them; also, being paid paltry wages, they could not afford to miss work unless they were completely debilitated, so they went to work even when slightly sick.
I doubt we know enough host specificity yet to change any old virus into something that will target humans. If we do, I’d expect the modified virus to have a lot of differences in code sequence from the progenitor virus. IOW, the synthetic virus would not look much like a typical Coronavirus. The coat protein gene would have to be redesigned so as to bind tightly to the altered RNA. That’s a tough problem, and not one that I don’t think we’re up to yet.
Yes, really we’re at the point where we can cut and paste pieces of DNA and then say “I think is is what it should do” with no way to verify it except the hard way.