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Can anyone with more knowledge on this topic than me (I’m no expert) assuage my fears: by giving human populations such artificial resistances (non-live vaccine

by jjcon 4y ago

Can anyone with more knowledge on this topic than me (I’m no expert) assuage my fears: by giving human populations such artificial resistances (non-live vaccines) we run the risk of selecting for viruses that are even harder for even our own immune systems to detect and destroy. Current Covid strains don’t seem all that bad, basically everyone I know has been infected now. Might we run the risk of making things worse at this point?

Kerrick 4y ago
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.
robbiep 4y ago
Evolution is climbing mount improbable. And natural selection (even in the face of in this case intelligently designed selectors) funnels organisms into potential dead ends which they can’t evolve out of - they’ve gone up the ‘north face’ and in order to reach fitness in the face of their selectors, they actually need to be on a completely different mountain. An antibody that dead ends all current evolutionary trends for an organism means that they can’t evolve out of the dead end natural selection has funnelled it down. So no, this isn’t a ‘might make it worse’, this is a ‘end of covid’ agent. That’s if the antigenic trigger can be made into a vaccine. More likely what the research is describing is that it is now possible to make a monoclonal antibody that can work as an infusion and is active against all known and future possible variants with the same efficacy.
- maegul 4y ago
  So, from the article: > Once the virus has bound to ACE2, it must complete a final step: fusing its outer membrane with the membrane of our cells. This throws the door open to infection. Using a novel live-cell imaging platform, Alex Kreutzberger, HMS instructor in pediatrics at Boston Children’s, and Tomas Kirchhausen, professor of cell biology in the Blavatnik Institute at HMS and professor of pediatrics at Boston Children’s, showed that SP1-77 blocks this step. > “SP1-77 binds the spike protein at a site that so far has not been mutated in any variant, and it neutralizes these variants by a novel mechanism,” noted Kirchhausen. “These properties may contribute to its broad and potent activity.” Questions: * If mutations at this site are possible, how would this be an evolutionary deadens in a way that the current evolutionary dynamics of the virus are not? * Surely a lack of mutations at this site, on their face, imply only that there is no evolutionary pressure on the site and its phenotypes, and, that mutations at this site are as viable as anywhere else? * Or, is it possible that the lack of mutations (presuming that this is very accurate) indicates an evolutionary pressure to maintain functionality that is sensitive to failure due to even minor mutations or deviations in functionality?
  - robbiep 4y ago
    > If mutations at this site are possible, how would this be an evolutionary deadens in a way that the current evolutionary dynamics of the virus are not? * Surely a lack of mutations at this site, on their face, imply only that there is no evolutionary pressure on the site and its phenotypes, and, that mutations at this site are as viable as anywhere else? * Or, is it possible that the lack of mutations (presuming that this is very accurate) indicates an evolutionary pressure to maintain functionality that is sensitive to failure due to even minor mutations or deviations in functionality?* the answer is that something that is so highly conserved across so many variations is mission critical. Mutations occur through replication everywhere, randomly. Highly conserved means that a change is a breaking change, severely impacting fitness, if no mutations have been observed elsewhere. Ie to extend the analogy, that point is the 'mountain' SARS-CoV-2 has decided to scale.
johnchristopher 4y ago
> by giving human populations such artificial resistances (non-live vaccines) we run the risk of selecting for viruses that are even harder for even our own immune systems to detect and destroy That'd be a valid question if we didn't ready have non-live vaccines with very good proven track records for polio, hepatitis, the flu, etc. > Current Covid strains don’t seem all that bad, basically everyone I know has been infected now. And here comes the covid denial argument. Relentlessly repeating the same loaded arguments again and again. > Might we run the risk of making things worse at this point? Yeah, but what about wind turbine's rare earth ? It's really polluting ! And what if climate change has more benefits than problems once we have adapted, uh ?
- jjcon 4y ago
  Where did I deny Covid? I simply asked if stronger vaccines could lead to stronger viruses and make things worse than they already are
  - johnchristopher 4y ago
    No, you did not simply ask that. You also said Covid is now not that bad and implied it's okay to be infected since everyone you know has been infected now.
    - jjcon 4y ago
      Assume good faith - its in the rules friend (https://news.ycombinator.com/newsguidelines.html https://news.ycombinator.com/newsguidelines.html) If that is what you took from my comment I apologize that isn't what I intended to convey at all. I did however intend to ask a question about the topic at hand (broader vaccines) in our current situation which is categorically improved relative to early covid
- ehvatum 4y ago
  To be fair, you are stigmatizing someone for offering a correct observation (that the successive COVID variants have proven less debilitating and deadly) and for asking a question that must be on many people’s minds: can monoclonal antibody administration promote resistance analogous to bacterial antibiotic resistance? Be aware that live virus vaccines are certainly not monoclonal antibody injections. As well, rather than spending your mental energy developing excuses to dismiss, why not think on the subject at hand? You should wonder why this mouse model produces broadly neutralizing antibodies in response to COVID spike proteins while the human immune system does not. That’s a bit interesting to the subject of COVID, isn’t it? Certainly more so than windmills and politics.
HWR_14 4y ago
> by giving human populations such artificial resistances (non-live vaccines) we run the risk of selecting for viruses that are even harder for even our own immune systems to detect and destroy I can put your fears to bed. That shouldn't happen. How vaccines work is they teach a very specific signature to our bodies so it can be destroyed as soon as it appears. . Therefore, any selection pressure would just be to not have that signature. But, since that signature is only valuable because it is recognized, there's no great loss if it becomes meaningless. So no supervirus issues. This is different from overusing antibiotics, because the selection there is not on signatures, but instead a more general "robustness" to the poison (well, poison to the bacteria).
- throwawaylinux 4y ago
  Some of foremost vaccine companies and medical experts in the world all but promised the COVID vaccines would give immunity to the disease and prevent it being transmitted. So they really have far less of a grasp of vaccine effects in even that a very narrow situation than you would think. So I don't think you can just put this to bed with a few sentences starting with "it shouldn't happen"!
- jjcon 4y ago
  Are you saying that because the number of possible signatures is so vast and the vaccines so specific, even if they get slightly broader it isn’t going to make things worse because in the grand scale of things we aren’t really walling too much off?
  - DubiousPusher 4y ago
    I think what they are saging is that something that kills perfectly, every time does not generate selective pressure. The virus would have to lose the signature completely randomly. Whereas antibiotic resistance is something that could develop because antibiotics could be under doses so individuals survived partial exposure or perhaps they worked by a mechanisms which already had some resistance in the population. It's like, you can breed high lung capacity mammals by having them live in water but you would just kill the species if you jumped straight into holding them underwater for 20 minutes. Something has to be survivable to genetate selective pressure.
hammock 4y ago
Shorel 4y ago
I think it is the other way around. By cutting down the population of live covid virus particles in the wild, that is, living in human hosts, the possibility of a hard to kill variety to evolve will diminish by a very big probability. In fact, the new more dangerous varieties are theorized to have evolved in single individuals, who lack a strong immune system, and can't kill a single virus infection for months, and then the virus accumulates changes over these months before jumping onto the general population.
inopinatus 4y ago
> Current Covid strains don’t seem all that bad, basically everyone I know has been infected now The first observation is false, the second, very far from universal.
- mnw21cam 4y ago
  Indeed, there's still plenty of people ending up in hospital because of covid, including me three months ago.
- jjcon 4y ago
  In EU and US the majority of people have had covid and certainly nearly everyone has had covid or been vaccinated. The new strains are not as deadly as the original or the delta variant. That is factual.
  - inopinatus 4y ago
    "EU and US" is not even remotely approaching "universal": in total that is less that 10% of the world's population. Expand your horizons; this is not a parochial forum. For example, I was born in a country that is neither, and I live in another country that is neither. Besides which, there are numerous EU member states whose vaccination rate remains below the population immunity level. More broadly, the global chain of infection, and the consequences thereof (preventable suffering and death), has not (yet) been interrupted by a sufficient global reservoir of acquired immunities. Furthermore, "not as deadly" hardly corresponds to "don’t seem all that bad". Mustard gas is "not as deadly" as VX. Let's not move the goalposts. In the same vein, it would be a mistake to implicitly assume that future COVID variants will be less deadly.
    - jjcon 4y ago
      Broadly speaking we don't have great data (in scale or quality) outside of the US and EU which is why I spoke to that. Things get pretty speculative even inside those borders. > "not as deadly" hardly corresponds to "don’t seem all that bad". That is a simply a judgement call really isn't it? We live with all sorts of terrible things. Cars kill over a million people each year and while terrible, they really aren't "all that bad" I'm not trying to make light of something so serious only speaking in relative terms compared to what we've already been through. Also what is wrong with including vaccinated exactly? They have some level of immunity, that is what counts here right? >you expressed a common fear that vaccination development becomes counter-productive That is just false. I was asking if by developing such broad vaccines (as opposed to those that we have developed in the past) if we ran the risk of selecting for worse viruses. As best as I can tell the answer is no, but there isn't anything wrong with asking the question right?

by jjcon 4y ago

Kerrick 4y ago

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.

robbiep 4y ago

Evolution is climbing mount improbable. And natural selection (even in the face of in this case intelligently designed selectors) funnels organisms into potential dead ends which they can’t evolve out of - they’ve gone up the ‘north face’ and in order to reach fitness in the face of their selectors, they actually need to be on a completely different mountain. An antibody that dead ends all current evolutionary trends for an organism means that they can’t evolve out of the dead end natural selection has funnelled it down. So no, this isn’t a ‘might make it worse’, this is a ‘end of covid’ agent. That’s if the antigenic trigger can be made into a vaccine. More likely what the research is describing is that it is now possible to make a monoclonal antibody that can work as an infusion and is active against all known and future possible variants with the same efficacy.

maegul 4y ago
So, from the article: > Once the virus has bound to ACE2, it must complete a final step: fusing its outer membrane with the membrane of our cells. This throws the door open to infection. Using a novel live-cell imaging platform, Alex Kreutzberger, HMS instructor in pediatrics at Boston Children’s, and Tomas Kirchhausen, professor of cell biology in the Blavatnik Institute at HMS and professor of pediatrics at Boston Children’s, showed that SP1-77 blocks this step. > “SP1-77 binds the spike protein at a site that so far has not been mutated in any variant, and it neutralizes these variants by a novel mechanism,” noted Kirchhausen. “These properties may contribute to its broad and potent activity.” Questions: * If mutations at this site are possible, how would this be an evolutionary deadens in a way that the current evolutionary dynamics of the virus are not? * Surely a lack of mutations at this site, on their face, imply only that there is no evolutionary pressure on the site and its phenotypes, and, that mutations at this site are as viable as anywhere else? * Or, is it possible that the lack of mutations (presuming that this is very accurate) indicates an evolutionary pressure to maintain functionality that is sensitive to failure due to even minor mutations or deviations in functionality?
- robbiep 4y ago
  > If mutations at this site are possible, how would this be an evolutionary deadens in a way that the current evolutionary dynamics of the virus are not? * Surely a lack of mutations at this site, on their face, imply only that there is no evolutionary pressure on the site and its phenotypes, and, that mutations at this site are as viable as anywhere else? * Or, is it possible that the lack of mutations (presuming that this is very accurate) indicates an evolutionary pressure to maintain functionality that is sensitive to failure due to even minor mutations or deviations in functionality?* the answer is that something that is so highly conserved across so many variations is mission critical. Mutations occur through replication everywhere, randomly. Highly conserved means that a change is a breaking change, severely impacting fitness, if no mutations have been observed elsewhere. Ie to extend the analogy, that point is the 'mountain' SARS-CoV-2 has decided to scale.

johnchristopher 4y ago

> by giving human populations such artificial resistances (non-live vaccines) we run the risk of selecting for viruses that are even harder for even our own immune systems to detect and destroy That'd be a valid question if we didn't ready have non-live vaccines with very good proven track records for polio, hepatitis, the flu, etc. > Current Covid strains don’t seem all that bad, basically everyone I know has been infected now. And here comes the covid denial argument. Relentlessly repeating the same loaded arguments again and again. > Might we run the risk of making things worse at this point? Yeah, but what about wind turbine's rare earth ? It's really polluting ! And what if climate change has more benefits than problems once we have adapted, uh ?

jjcon 4y ago
Where did I deny Covid? I simply asked if stronger vaccines could lead to stronger viruses and make things worse than they already are
- johnchristopher 4y ago
  No, you did not simply ask that. You also said Covid is now not that bad and implied it's okay to be infected since everyone you know has been infected now.
  - jjcon 4y ago
    Assume good faith - its in the rules friend (https://news.ycombinator.com/newsguidelines.html https://news.ycombinator.com/newsguidelines.html) If that is what you took from my comment I apologize that isn't what I intended to convey at all. I did however intend to ask a question about the topic at hand (broader vaccines) in our current situation which is categorically improved relative to early covid
ehvatum 4y ago
To be fair, you are stigmatizing someone for offering a correct observation (that the successive COVID variants have proven less debilitating and deadly) and for asking a question that must be on many people’s minds: can monoclonal antibody administration promote resistance analogous to bacterial antibiotic resistance? Be aware that live virus vaccines are certainly not monoclonal antibody injections. As well, rather than spending your mental energy developing excuses to dismiss, why not think on the subject at hand? You should wonder why this mouse model produces broadly neutralizing antibodies in response to COVID spike proteins while the human immune system does not. That’s a bit interesting to the subject of COVID, isn’t it? Certainly more so than windmills and politics.

HWR_14 4y ago

> by giving human populations such artificial resistances (non-live vaccines) we run the risk of selecting for viruses that are even harder for even our own immune systems to detect and destroy I can put your fears to bed. That shouldn't happen. How vaccines work is they teach a very specific signature to our bodies so it can be destroyed as soon as it appears. . Therefore, any selection pressure would just be to not have that signature. But, since that signature is only valuable because it is recognized, there's no great loss if it becomes meaningless. So no supervirus issues. This is different from overusing antibiotics, because the selection there is not on signatures, but instead a more general "robustness" to the poison (well, poison to the bacteria).

throwawaylinux 4y ago
Some of foremost vaccine companies and medical experts in the world all but promised the COVID vaccines would give immunity to the disease and prevent it being transmitted. So they really have far less of a grasp of vaccine effects in even that a very narrow situation than you would think. So I don't think you can just put this to bed with a few sentences starting with "it shouldn't happen"!
jjcon 4y ago
Are you saying that because the number of possible signatures is so vast and the vaccines so specific, even if they get slightly broader it isn’t going to make things worse because in the grand scale of things we aren’t really walling too much off?
- DubiousPusher 4y ago
  I think what they are saging is that something that kills perfectly, every time does not generate selective pressure. The virus would have to lose the signature completely randomly. Whereas antibiotic resistance is something that could develop because antibiotics could be under doses so individuals survived partial exposure or perhaps they worked by a mechanisms which already had some resistance in the population. It's like, you can breed high lung capacity mammals by having them live in water but you would just kill the species if you jumped straight into holding them underwater for 20 minutes. Something has to be survivable to genetate selective pressure.

hammock 4y ago

Shorel 4y ago

I think it is the other way around. By cutting down the population of live covid virus particles in the wild, that is, living in human hosts, the possibility of a hard to kill variety to evolve will diminish by a very big probability. In fact, the new more dangerous varieties are theorized to have evolved in single individuals, who lack a strong immune system, and can't kill a single virus infection for months, and then the virus accumulates changes over these months before jumping onto the general population.

inopinatus 4y ago

> Current Covid strains don’t seem all that bad, basically everyone I know has been infected now The first observation is false, the second, very far from universal.

mnw21cam 4y ago
Indeed, there's still plenty of people ending up in hospital because of covid, including me three months ago.
jjcon 4y ago
In EU and US the majority of people have had covid and certainly nearly everyone has had covid or been vaccinated. The new strains are not as deadly as the original or the delta variant. That is factual.
- inopinatus 4y ago
  "EU and US" is not even remotely approaching "universal": in total that is less that 10% of the world's population. Expand your horizons; this is not a parochial forum. For example, I was born in a country that is neither, and I live in another country that is neither. Besides which, there are numerous EU member states whose vaccination rate remains below the population immunity level. More broadly, the global chain of infection, and the consequences thereof (preventable suffering and death), has not (yet) been interrupted by a sufficient global reservoir of acquired immunities. Furthermore, "not as deadly" hardly corresponds to "don’t seem all that bad". Mustard gas is "not as deadly" as VX. Let's not move the goalposts. In the same vein, it would be a mistake to implicitly assume that future COVID variants will be less deadly.
  - jjcon 4y ago
    Broadly speaking we don't have great data (in scale or quality) outside of the US and EU which is why I spoke to that. Things get pretty speculative even inside those borders. > "not as deadly" hardly corresponds to "don’t seem all that bad". That is a simply a judgement call really isn't it? We live with all sorts of terrible things. Cars kill over a million people each year and while terrible, they really aren't "all that bad" I'm not trying to make light of something so serious only speaking in relative terms compared to what we've already been through. Also what is wrong with including vaccinated exactly? They have some level of immunity, that is what counts here right? >you expressed a common fear that vaccination development becomes counter-productive That is just false. I was asking if by developing such broad vaccines (as opposed to those that we have developed in the past) if we ran the risk of selecting for worse viruses. As best as I can tell the answer is no, but there isn't anything wrong with asking the question right?