You couldn't design a virus to target an age group, could you?

This thread about conspiracy theories about covid reminded me of a CT I saw a few times last spring - the theory being that Covid was a virus designed by the Chinese government to target the elderly in China because old people cost too much money and it accidentally got loose into the rest of the world. Obviously a not very good bio-weapon given the fairly low mortality rate amongst even people 80+

It’s not actually possible to create a virus to target people of a specific age, right? They wouldn’t have a common genetic profile, after all.

Unless there was a mechanism that’d allow you to target something the group might have in common immunologically, say everyone with some immunity to smallpox from the vaccine that was given up until the early 70s or people who survived the 1957 flu pandemic?

I’m just wondering if the CT is 100% nutty or only 99% nutty.

Well, ace2 receptors (the kind Sars-Cov-2 likes to bind with) may increase with age, especially in the nasal epithelium…

The 1918 flu was noted for its surprising tendency to take out the healthy prime-of-life people.

Two theories seem to have gradually emerged:

a) Older people had some immunity from a moderately similar flu from a couple decades earlier; younger people did NOT

b) Healthy people’s powerful immune systems were doing them in. Reactions that would most often protect a person were instead inflaming lung tissue in particular and causing them to die from suffocation; people with less agile immune responses were paradoxically surviving better because their tissues were not swelling from immune responses. Or something of that general ilk. I won’t swear that I’ve got the details precisely correct.

AIUI, it’s more the “design” part than the “target” part.

That is to say, we cannot make entire viable viruses out of whole cloth yet. We broadly just modify existing strains, again AIUI.

But in terms of targeting age groups, sure, certain viruses are more deadly specifically for infants, elderly, or people in the prime of their lives (and immune system). Probably the hardest to specifically target would be 30-45 age group, as their immune system is in-between the characteristics of other groups.

Without actually testing it, I don’t see how it could be done with any level of certainty. There seems to be a default assumption that a new disease will hit the elderly and already sick the hardest, due to their immune systems being taxed already. But it wasn’t until cases came in that we knew for sure, even for COVID-19.

The H1N1 flu is an example, as the usual understanding is that flus follow the same general pattern stated above.

This was meant to say that the difficult part is more in designing (i.e. engineering a virus) than with having something that proportionally affects a particular age group more. Viruses can affect different groups in different ways, and, as the 1918 flu showed, it’s not necessarily the case that the most forceful immune response is the best.

Designing a virus may be easier with CRISPR than it was before, since that lets them target specific spots on a DNA strand. They wouldn’t be using the Cas9 protein (which just cuts the DNA at the targeted spot), but some other protein that makes the specific change they needed. This would let them modify an existing virus in specific ways.

As far as targeting an age group, it might be possible to target people who’ve had certain epigenetic changes. As you gets older, your DNA accumulates epigenetic changes, so they possibly could target people with certain epigenes that most everyone gets. Or perhaps target people who don’t have those epigenes. This might let them target the old or the young. It wouldn’t be super accurate, though.

BTW, I have a hypothesis that if they could restore someone’s epigenome to about what it was when they were in their 20s, it might be a big step in a rejuvenation treatment. Probably not the only thing needed for complete rejuvenation, but certainly major part of one. I may write an SF story about this someday. Well, OK, probably not.

Surely, COVID itself is proof that it’s possible for a virus to disproportionately affect the old. The difficulty is just, as others have said, the “design” part. With current or foreseeable tech, the only way to “design” a virus with certain properties would be to start with a whole bunch of viruses, test them all, then take the most promising ones, make a whole bunch of random changes to them, and repeat. And each one of those “test them all” steps would require exposing thousands of humans to each virus, and tracking them. There’s no way to keep that secret.

No, the default assumption is that a new disease will hit the young and the old and the sick. It’s very weird that COVID is benign in children. That doesn’t indicate an artificial origin, but it is odd.

So I guess the real question might be “is it possible to design a virus so that it doesn’t target an age group?” Because the weird thing about COVID is not that it’s so harsh on old people, but that it isn’t equally harsh on children under 5.

If the argument made by the article linked to in the OP here (full disclosure: I’m the OP! But not the article’s author) is correct, then a virus which is wholly novel to almost all of humanity will disproportionately target the old since their immune systems don’t do the generic response as well as the young, and they don’t have any specific responses (antibodies, memory cells, etc) for a novel pathogen. If you wanted to target the young, you’d pick something that’s highly virulent but not novel, like measles (but without the vaccine availability.)

And if the argument in that article is not correct, I’d love to understand why!

(note: SARS-CoV-2 meets the test for novelty for the vast majority of humanity. The number of people who have been exposed to similar viruses - SARS and MERS - is very small, though survivors of those diseases would likely have had a better go against SARS-CoV-2.)

I think the point is, as everyone else has pointed out, the difficulty of the “design” part. We really don’t know that much about genetics, and the interesting part is we don’t fully understand what genes will actually do. Particularly, many genes can have multiple effects and making a change in one place risks side effects in unrelated areas. We can’t even design effective vaccines against some diseases, and not for lack of trying.

Biology is complex, and the only way to be sure your design works is to test it.

I agree with your larger point about designing a virus in the manner suggested by the conspiracy theories being beyond current capabilities.

As for this part, though:

I recall some discussion earlier in the pandemic about why we thought we could create a vaccine for this virus so easily, when HIV has eluded us for decades despite tons of effort. And the answer that was generally given is that 1) vaccines basically just pre-train your immune system to recognize the virus 2) for most people, our bodies can successfully clear covid 3) no one could naturally clear HIV - it would hang around even after the immune system was fully ramped up. Therefore, giving the immune system early warning to recognize HIV wasn’t sufficient. In short, for classes of viruses where our immune system could fully win if it were ramped up early, we can develop vaccines. For ones where the virus can hide from our immune system, a vaccine is much harder to do.

No doubt, this is simplified, but it gives some guidance on why there remain classes of viruses where we can’t seem to develop vaccines, despite the level of effort.

It would have to get into the cell nucleus, but it is at lease conceivable that a virus could be built to look for short telomeres. These are the endcaps on genes and they shorten as we age.

I always thought it was more that HIV specifically targets the immune system, rather than hiding from it.

Chicken pox/Shingles(varicella zoster) can hide from our immune system, but there’s a highly effective vaccine for it, for example.

I’m no expert, but I thought HIV effectively hid from your immune system via rapid mutation and also targeted it.

Those two specific coronaviruses are novel to the vast majority of humans, but there are other coronaviruses that are much more common. Last I heard, somewhere around 15% of cases of “common cold” were due to coronaviruses.

I’ve actually wondered if part of the wide variation in response to COVID (the majority being asymptomatic, another large fraction having only minor symptoms, but a few suffering serious ailment or death) might be due to difference in prior exposure to those other coronaviruses. Maybe the people who never suffered any symptoms are those who had prior exposure to other coronaviruses, and so their immune systems were able to adapt more quickly?

A I’m sure you’re aware, this is not just sci-fi, it’s an area of active research.

And here’s a more recent review if you have access, I don’t at the moment.

https://www.nature.com/articles/s41580-019-0204-5

While there are a handful of coronaviruses that cause common colds, it was my understanding that they just aren’t similar enough to SARS-CoV-2 to have created any protection (whereas SARS and maybe MERS were.) That said, I wouldn’t be surprised if there’s a lot more study to be done on the topic.

A couple things to be aware of:

  1. covid-19 is close enough to the virus that caused “vanilla” SARS that we essentially just needed to tweak some existing vaccines that were in development. (“Tweak” might be doing a disservice to the work involved but you catch my drift).

  2. There is a vaccine for HIV currently in phase 1 trials.

So the question really becomes why a HIV vaccine has taken ~40 years and covid only ~15.
But, AIUI (I’m getting to use “AIUI” a lot in this thread) the science of synthetic vaccine development has advanced a great deal in the last 20 years. So probably if you just swap the dates of when these viruses became an epidemic in humans, the time delay before the creation of a vaccine would also be swapped.

Elizabeth Moon has a series where the regen is done by targeting the genes in this manner.

I always wondered about restoring the telemeres at the ends of the DNA as a means of regen, no idea if the shortening telemeres causing the DNA errors is still considered a large part of aging.