5 ms·

Reducing the spread of existing variants reduces the number of replications the virus can make, which in turn reduces the occurrence of mutations.

jjcon 4y ago
But it is always going to continue to spread won’t it? A vaccine may slow it down which is good but my fear is that long term non-live vaccines like this could just make things worse when used with such a volatile virus.
- lazide 4y ago
  Why would a live vaccine be better?
  - dataflow 4y ago
    I feel like the parent wasn't trying to argue that injecting people with live vaccines (er, live virus?) would be better? Rather the idea seemed to be to stop making more vaccines for COVID - kind of like how we deal with colds now.
    - lazide 4y ago
      They were explicitly saying their concern was with non-live vaccines though?
      - dataflow 4y ago
        I obviously can't say for sure, but given the topic was the development of artificial resistance to vaccines, I would've thought the alternative they had in mind was natural resistance - i.e. getting infected naturally.
    - jfoster 4y ago
      There would be cold vaccines if it were possible to produce effective ones, so it's not an argument against producing a highly effective vaccine.
  - jjcon 4y ago
    Just in my non-expert head - a live vaccine is using the virus as it already exists to confer immunity - not trying to code against a ton of hypothetical variants which could select for more radical variants
    - lazide 4y ago
      Ah, that isn't how a live vaccine works though. They get attenuated (aka damaged/killed/broken) or similar but not the same viruses (aka cowpox used to be a live vaccine for smallpox), then introduced. The body reacts to the not-really-functional virus, but it isn't the same as if it was an actual infection. It still triggers the immune system, but mutations in any of the major receptors or the like will cause it to be less effective too.
- bsder 4y ago
  Precisely the reverse: attenuated virus (live virus) vaccines regularly allow mutation back to pathological forms. See: polio. This is because an attenuated virus is still replicating viral particles and every replication is a lottery ticket that the virus might mutate back. mRNA vaccines, by contrast, causes no viral replication so the virus doesn't get these lottery tickets. Of course, either type of vaccine is going to place evolutionary pressure on a disease to evolve an escape. That's just what happens. One side note: one of the things about mRNA vaccines is that they can be very specific. Now, that may not be great for Covid where we would like to be more general. However, that may be absolutely essential against Epstein-Barr where a chunk of the virus looks like nervous system proteins. A standard vaccine is likely to prime the immune system just like the virus and cause multiple sclerosis as a side effect. An mRNA vaccine, by contrast, could target only those sections of the E-B virus that look sufficiently different from the nervous system and prime the immune system without risking friendly fire.
peteradio 4y ago
That doesn't answer the question though, almost a non-sequiter.
- heavyset_go 4y ago
  It does answer the question. Evolution is the result of mutations propagating through reproduction. The more copies of a virus replicating, the higher chances of mutation causing a more deleterious and/or virulent variant of the virus. As the number of viral copies and replications approaches zero, the chances of a worse strain of the virus spreading also approaches zero. Vaccines reduce viral load and spread, thus reducing the chances of mutation and spread of worse variants. An example of this happening is the Spanish flu, which was a mutation of the common flu that was widespread and uncontrolled with vaccines at the time.
  - peteradio 4y ago
    Where does the worry come from regarding drug resistant bacteria why would that worry not have a viral analog?
    - heavyset_go 4y ago
      Drug-resistant bacteria are the result of misuse and incomplete use of antibiotics, and the environmental spread from waste of antibiotics. Also, bacteria can share genes horizontally, meaning resistance in one species can transfer to another quickly. Antibiotic resistance in bacteria is mainly from misuse in humans and animals, and disease spread between the two, along with ineffective waste treatment and the leaching of antibiotics into the environment[1]. About 80% of antibiotics sold in the US are used in agriculture[2], where they are given to animals not to treat infections, but to prevent them and to stimulate growth. Over 60% of infectious diseases in humans are spread from animals, and 75% of new diseases in humans are spread from animals[3]. Shooting a few micrograms of vaccines into humans' arms is nowhere near the scale of antibiotic use or accumulation in the environment. It's also possible to achieve herd immunity with vaccines, whereas antibiotics do not leave lasting immunity. To be effective, antibiotics must be taken when there's a bacterial infection, and their effectiveness diminishes as they leave the body. Are these "worries" consistent? Where is the worry that polio vaccination might create worse strains of polio? [1] https://en.wikipedia.org/wiki/Antimicrobial_resistance https://en.wikipedia.org/wiki/Antimicrobial_resistance [2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4638249/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4638249/ [3] https://www.cdc.gov/onehealth/basics/zoonotic-diseases.html https://www.cdc.gov/onehealth/basics/zoonotic-diseases.html
osigurdson 4y ago
I've often wondered if other viruses (below) could possibly mutate into a more dangerous form. Perhaps there is a reason why they cannot. https://en.wikipedia.org/wiki/List_of_virus_species https://en.wikipedia.org/wiki/List_of_virus_species
- heavyset_go 4y ago
  It can and does happen: https://en.wikipedia.org/wiki/Influenza_pandemic#Influenza_pandemics https://en.wikipedia.org/wiki/Influenza_pandemic#Influenza_p...
- Mikeb85 4y ago
  They can, they just usually don't, as more dangerous viruses kill their host before they can spread as far...
  - mlyle 4y ago
    Sometimes this can be an effect that causes viruses to mutate to be less virulent. On the other hand, faster replication is also often selected for, which often corresponds to more virulence. Both trends have been observed, depending on a whole lot of complex factors.
  - heavyset_go 4y ago
    It's wrong to say they usually don't, it's that the deadlier variants haven't lived long enough for us to remember them or have to worry about them at this moment. They still happen and can wipe out populations, and thus die out, as well. They can also reach an equilibrium where they maim many of their hosts, more than we'd like, without killing them all. Mutations are random, nothing really is preventing a virus from replicating rapidly and killing a lot of its hosts in the short term, it's just the long-term evolutionary advantage of such traits are small, because killing hosts quickly reduces replication, potentially. But that doesn't stop viruses and bacteria from mutating into something deadly and killing a lot, or all, of its hosts. However just that has happened throughout evolutionary history on Earth, and even in humans' history. We've seen plenty of pandemics wage war against humans and cause considerable casualties. There's also plenty of equilibria deadly viruses can reach with their hosts, where they kill a relatively large amount of hosts, but not enough to wipe them out.
maegul 4y ago
Key flaw with this is the presumption that the required mutations are not already present in the population. Even if they are rare, it is a facile process for natural selection to make said set of mutations dominant. If a small amount of recombination (I don't know if this is occurring with COVID-19) or novel mutation is required, again, it's a fairly straight forward affair unless we're close to an eradication scenario. "Life finds a way", as they say. I think the only reasonable response to the parent query is to address the core issue ... are there non-overlapping capabilities between "artificial" and "natural" antibodies apart from the speed and health-risk of their development/inoculation. In other words, is "artificial" immunity a better form of immunity in a way that "natural" immunity can never match? If so, seems like a pretty obvious case of "lock in". Without being an expert, I imagine it isn't a trivial question to answer, as the evolutionary capabilities of a pathogen are a key factor, and well, we're still wrestling with predicting protein folding.

jjcon 4y ago

But it is always going to continue to spread won’t it? A vaccine may slow it down which is good but my fear is that long term non-live vaccines like this could just make things worse when used with such a volatile virus.

lazide 4y ago
Why would a live vaccine be better?
- dataflow 4y ago
  I feel like the parent wasn't trying to argue that injecting people with live vaccines (er, live virus?) would be better? Rather the idea seemed to be to stop making more vaccines for COVID - kind of like how we deal with colds now.
  - lazide 4y ago
    They were explicitly saying their concern was with non-live vaccines though?
    - dataflow 4y ago
      I obviously can't say for sure, but given the topic was the development of artificial resistance to vaccines, I would've thought the alternative they had in mind was natural resistance - i.e. getting infected naturally.
  - jfoster 4y ago
    There would be cold vaccines if it were possible to produce effective ones, so it's not an argument against producing a highly effective vaccine.
- jjcon 4y ago
  Just in my non-expert head - a live vaccine is using the virus as it already exists to confer immunity - not trying to code against a ton of hypothetical variants which could select for more radical variants
  - lazide 4y ago
    Ah, that isn't how a live vaccine works though. They get attenuated (aka damaged/killed/broken) or similar but not the same viruses (aka cowpox used to be a live vaccine for smallpox), then introduced. The body reacts to the not-really-functional virus, but it isn't the same as if it was an actual infection. It still triggers the immune system, but mutations in any of the major receptors or the like will cause it to be less effective too.
bsder 4y ago
Precisely the reverse: attenuated virus (live virus) vaccines regularly allow mutation back to pathological forms. See: polio. This is because an attenuated virus is still replicating viral particles and every replication is a lottery ticket that the virus might mutate back. mRNA vaccines, by contrast, causes no viral replication so the virus doesn't get these lottery tickets. Of course, either type of vaccine is going to place evolutionary pressure on a disease to evolve an escape. That's just what happens. One side note: one of the things about mRNA vaccines is that they can be very specific. Now, that may not be great for Covid where we would like to be more general. However, that may be absolutely essential against Epstein-Barr where a chunk of the virus looks like nervous system proteins. A standard vaccine is likely to prime the immune system just like the virus and cause multiple sclerosis as a side effect. An mRNA vaccine, by contrast, could target only those sections of the E-B virus that look sufficiently different from the nervous system and prime the immune system without risking friendly fire.

peteradio 4y ago

That doesn't answer the question though, almost a non-sequiter.

heavyset_go 4y ago
It does answer the question. Evolution is the result of mutations propagating through reproduction. The more copies of a virus replicating, the higher chances of mutation causing a more deleterious and/or virulent variant of the virus. As the number of viral copies and replications approaches zero, the chances of a worse strain of the virus spreading also approaches zero. Vaccines reduce viral load and spread, thus reducing the chances of mutation and spread of worse variants. An example of this happening is the Spanish flu, which was a mutation of the common flu that was widespread and uncontrolled with vaccines at the time.
- peteradio 4y ago
  Where does the worry come from regarding drug resistant bacteria why would that worry not have a viral analog?
  - heavyset_go 4y ago
    Drug-resistant bacteria are the result of misuse and incomplete use of antibiotics, and the environmental spread from waste of antibiotics. Also, bacteria can share genes horizontally, meaning resistance in one species can transfer to another quickly. Antibiotic resistance in bacteria is mainly from misuse in humans and animals, and disease spread between the two, along with ineffective waste treatment and the leaching of antibiotics into the environment[1]. About 80% of antibiotics sold in the US are used in agriculture[2], where they are given to animals not to treat infections, but to prevent them and to stimulate growth. Over 60% of infectious diseases in humans are spread from animals, and 75% of new diseases in humans are spread from animals[3]. Shooting a few micrograms of vaccines into humans' arms is nowhere near the scale of antibiotic use or accumulation in the environment. It's also possible to achieve herd immunity with vaccines, whereas antibiotics do not leave lasting immunity. To be effective, antibiotics must be taken when there's a bacterial infection, and their effectiveness diminishes as they leave the body. Are these "worries" consistent? Where is the worry that polio vaccination might create worse strains of polio? [1] https://en.wikipedia.org/wiki/Antimicrobial_resistance https://en.wikipedia.org/wiki/Antimicrobial_resistance [2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4638249/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4638249/ [3] https://www.cdc.gov/onehealth/basics/zoonotic-diseases.html https://www.cdc.gov/onehealth/basics/zoonotic-diseases.html

osigurdson 4y ago

I've often wondered if other viruses (below) could possibly mutate into a more dangerous form. Perhaps there is a reason why they cannot. https://en.wikipedia.org/wiki/List_of_virus_species https://en.wikipedia.org/wiki/List_of_virus_species

heavyset_go 4y ago
It can and does happen: https://en.wikipedia.org/wiki/Influenza_pandemic#Influenza_pandemics https://en.wikipedia.org/wiki/Influenza_pandemic#Influenza_p...
Mikeb85 4y ago
They can, they just usually don't, as more dangerous viruses kill their host before they can spread as far...
- mlyle 4y ago
  Sometimes this can be an effect that causes viruses to mutate to be less virulent. On the other hand, faster replication is also often selected for, which often corresponds to more virulence. Both trends have been observed, depending on a whole lot of complex factors.
- heavyset_go 4y ago
  It's wrong to say they usually don't, it's that the deadlier variants haven't lived long enough for us to remember them or have to worry about them at this moment. They still happen and can wipe out populations, and thus die out, as well. They can also reach an equilibrium where they maim many of their hosts, more than we'd like, without killing them all. Mutations are random, nothing really is preventing a virus from replicating rapidly and killing a lot of its hosts in the short term, it's just the long-term evolutionary advantage of such traits are small, because killing hosts quickly reduces replication, potentially. But that doesn't stop viruses and bacteria from mutating into something deadly and killing a lot, or all, of its hosts. However just that has happened throughout evolutionary history on Earth, and even in humans' history. We've seen plenty of pandemics wage war against humans and cause considerable casualties. There's also plenty of equilibria deadly viruses can reach with their hosts, where they kill a relatively large amount of hosts, but not enough to wipe them out.

maegul 4y ago

Key flaw with this is the presumption that the required mutations are not already present in the population. Even if they are rare, it is a facile process for natural selection to make said set of mutations dominant. If a small amount of recombination (I don't know if this is occurring with COVID-19) or novel mutation is required, again, it's a fairly straight forward affair unless we're close to an eradication scenario. "Life finds a way", as they say. I think the only reasonable response to the parent query is to address the core issue ... are there non-overlapping capabilities between "artificial" and "natural" antibodies apart from the speed and health-risk of their development/inoculation. In other words, is "artificial" immunity a better form of immunity in a way that "natural" immunity can never match? If so, seems like a pretty obvious case of "lock in". Without being an expert, I imagine it isn't a trivial question to answer, as the evolutionary capabilities of a pathogen are a key factor, and well, we're still wrestling with predicting protein folding.