Interesting take - I would definitely agree that Omicron cannot be explained by typical viral mutation which appears to explain Alpha/Beta/Delta. I am curious what comes next - will this last remaining Omicron variant become the source of further typical viral mutations? Do you find it odd that the original Wuhan clades didn’t seem to evolve as rapidly as Alpha/Beta/Delta (for almost a year we had Wuhan & then the named variants all passed through in 2021 and now we have the Omicron family) - do you think vaccines caused that pressure or was it immune escape or both or it’s anybody’s guess?
Well I think the biggest issue is that we don't know which direction Delta would have gone because of the abrupt emergence of Omicron. This is one of the reasons why I'm critical of such comments such as the lack of seasonality for COVID. Well, seasonality requires that the virus circulate among the population until competition between the two causes it to plateau in some way. Omicron didn't allow us to reach post-Delta variants that may lead to seasonality, and now we're dealing with sudden jumps between Omicrons which are likely to have been around at similar times to one another.
I'm not sure to typical level of mutation rates that should be seen, but as Brian pointed out the level of mutations seen in Omicron necessitates years of circulation, and the idea that Omicron somehow existed for a year or two within either animal reservoirs or immunocompromised individuals doesn't quite make sense. So some possible accelerated measure via serial passage may have caused it, and serial passage through different animals or cell lines may have led to the different Omicron sub-lineages, as Brian Mowrey alludes to.
I really don't think we can argue that the vaccines are doing this because in order to make such an argument we need to explain how the vaccines led to the Delta/Omicron jump, and it's one of the things that doesn't appear to be answered anywhere. It's why I've been critical of the OAS argument, because models such as ones used by GvB utilize the Delta/Omicron jump to substantiate OAS yet never finds a valid explanation as to why such a jump occurred through vaccination. Such a model should explain why the vaccines led to Omicron, or why South Africa, which apparently has low vaccination rates, were the ones to have the emergence of Omicron.
I'm not entirely entrenched into the lab hypothesis, but I don't find the other alternatives to be any better, and are actually worse explanations. So the lab hypothesis is the best thing out of the worst things that we have.
You’re assuming people are only getting sick from a forever-evolving virus. If these are indeed lab-made (and I believe them to be) think of other ways they can be finding their way into people.
Well, for now the main focus of lab origins would be both Wuhan and Omicron. As to the other variants, they follow an evolutionary path that we would consider viruses to normally follow (to a degree). The problem would be if we see continuous, abrupt strains emerging that show huge escape. That would point more towards something possibly intentional. It would be rather ironic if the releases are seasonal, rather than the actual virus.
Jul 16, 2022·edited Jul 16, 2022Liked by Modern Discontent
Very nice theory RE L452R immune recognition from Delta.
One thing to keep in mind RE the question of why they lost out initially is clonal interference, which is when more fit alleles in an asexual population don't win out if the numerically dominate allele is "fit enough." https://en.wikipedia.org/wiki/Clonal_interference Natural selection and clonal interference are opposing forces; the former only works if the latter is overcome by rendering the dominate allele no longer fit enough in the niche.
So the 4/5 spike model may have been more fit, but it was a numerical rarity in the initial viral swarm of the Omicron siblings that was in whatever matter "released." Conversely, BA.1 might have been a numerical rarity as well, but was so much more fit in an Omicron-naive landscape that it quickly overtook BA.2 and the others (this is what I imply in my fictional Origins scenario). (I regard BA.1 as clearly more transmissible than the others, don't care what the experts say on that one.)
So if BA.2 gets "first dibs" in the post-BA.1 landscape simply because of numerical superiority within the 2/4/5 family, it's not necessary that it's actually more fit. But once BA.2 has raised population adaptive immune response (the dirty "h. i." phrase that I won't say), it's substantially less fit than 4 and 5 and natural selection becomes the dominate force.
*edit: Alternately, there's some fitness detriment to the non-spike mutations in either 4/5 vs 2. So they had to wait until they had a leg up in the immune landscape. This is more of a stretch. BA.1 vs the 2 family has enough difference in non-spike mutations, esp. in Orf1, that the likelihood of different performance under the hood seems high, but not so much with 4/5 vs 2 which have so few changes to the internals. At most the P151S on 4's N protein might be disruptive since P changes are always radical. As a counter-argument, my own Omicron timeline describes BA.2 as evolving under high 3'-region pressure (everything after spike) and this would apply to 4 and 5 as well; but this could apply to fitness in the lab conditions and not real life transmission.
RE dispersion from South Africa, it doesn't seem that BA.2 was automatically spread alongside BA.1. Only some countries seemed to get BA.2 at about the same time as BA.1 in the figure I used from Yamasoba, D. et al. That's important for my argument against BA.2 turning out to have already been outside of South Africa all along before being sequenced / detected.
One other insight from the antigen map is that the Omicron siblings would have to reverse Delta (and other B.1-descendent circulating strains) mutations, as well as a plethora of non-spike mutations including synonomous ones. It's just not possible that Delta was in some vaccinated person and was like "screw this, I'm reinstalling to B.1!"
Thanks Brian, I always appreciate your insights. This was a lot of my thoughts scrambled together and me trying to piece it together, so I eventually just said "screw it!" and just put it into words and see what comes of it. I'm perfectly fine if this idea has more holes than Swiss cheese, but I wanted to at least solidify something for myself.
The clonal interference is interesting. In regards to Ba.4/Ba.5, a big issue with my hypothesis is that I've compared it to Delta via the L452R mutation, yet I don't have any quantitative data to compare the two. Pre-Delta variants had tropism for the lower airway and lungs, and so Delta with its L452R mutation is likely to just do it "better" than prior variants. The jump from Omicron losing that tropism means that something else is happening, so maybe the L452R mutation helped restore some of that functionality, but maybe not to the extent of Delta via other spike mutations. It's been months since I looked at studies of Ba.1 so I may have to return to some of those and try to figure that information out.
Your second and third paragraph was something I was trying to allude to via references to monoclonals. I'll admit my comment that "well, Ba.1 won out!" really doesn't cut it unless I have evidence to substantiate why Ba.1 was favored over Ba.2. I reference the antigenic maps but it's really improper for me to assume Ba.1 was more antigenically distant than Ba.2 just based on that alone. But essentially instead of having a slow walk through various mutations with Omicron it was like taking an Olympic pole vaulter and having a huge jump, and then instead of having another slow walk it was like playing hopscotch through all of the Omicrons.
I'll look back at the Yamasoba paper. I wonder if selection for Ba.2 or Ba.1 may have been due to population genetics such as HLA haplotypes in different countries. More confounding variables, but that's how it goes.
Could you clarify what you mean by the last paragraph? Maybe it's too early but I'm a little confused.
But thanks for your remarks Brian. I think after more research and dwelling on it further I may either try to formalize it further or if it's really not substantiated I'll toss it.
My guess for BA.2 is that is was an unlikely draw as far as what people traveling from South Africa would be carrying, and so only places with a lot of travel got it at first, namely north coastal Europe. It then had to spread from either there or SA. So places with less travel with SA initially got just BA.1.
The last paragraph is that once you subtract the B.1.1, the Omicron siblings don’t have any silent mutations from Delta. So they didn’t come from Delta. I think there was one or two mutations almost shared with Alpha, I lost my work on that one
So your suggestion is that there could be an argument of global spread at different timepoints? That would require a lot of reworking for my hypothesis, since it would need to find another explanation for the Omicron pipeline. The observational data does substantiate separate spread, but I suppose in my mind it makes more logical sense to have some Omicron Big Bang event and that they all just traveled together afterwards. More things to consider here.
And thanks for clarifying. I guess I was having a slow moment. Yes the whole Delta situation is one thing that I need an explanation for. This is one of the reasons why all hypotheses for Omicron deviates from selective pressure via circulation among humans (this includes the immunocompromised, as the lack of immunity essentially removes selective pressure), and yet OAS and the "virus of the vaccinated" does not make sense, yet it's becoming the argument that is used to justify our current predicament. It just feels like one of those hypotheses that just fits too well.
If they all traveled together, than the "movie" of sibling-to-sibling transition should be identical everywhere that got BA.1 in the winter. BA.2 should appear just as quickly post-BA.1 in the US / UK / Israel as it does in Denmark. imo...
That is true. More things to consider and more variables. Maybe I'm wildly pontificating on something that may otherwise be a nothing burger 🤷♂️. I'll just need to find more evidence one way or another.
Like I said when the mostly harmless Omicron emerged in South Africa and began displacing the more dangerous variants:
“The WHO and world wish to thank South Africa for its willingness to serve as guinea pigs for experimentation. Their willingness to do so has saved countless lives.”
I really have no idea what happened in South Africa, but it just keeps adding to the level of uncertainty with everything going on. I'll admit I didn't give Omicron much thought for a few months, but given what's going on right now it seems extremely important to think about the origins of Omicron, as well as the origins of Wuhan.
First of all I am grateful for your very instructive posts (which in all honesty are way above my head).
That being said I am a bit confused by your BA.4 and BA.5 pipeline theory.
I guess what you say -sorry for over simplifying- is that Delta and BA.4/5 shared the same time and space and eventually BA.4 and BA.5 had to "wait" until previous immunity from Delta fades(?) and let them spread.
If that is true wouldn't that mean that mostly everyone in that shared space somehow gained immunity for Delta via infection or other means? Otherwise all 3 variants could have acted simultaneously infecting different sets of people, eventually separated geographically.
Wouldn't also mean that currently BA.4 and BA.5 should translate into a lot more of re-infections rather than covid first-timers?
I'll first start off my saying if this hypothesis seems like it has a bunch of holes, that's probably because it does. This is a working model that I just wanted to have in written format because I have so many thoughts going on in my head and I wanted to solidify it in some way.
My argument for Ba.4 and Ba.5 is that the L452R mutation is likely a pivotal mutation for the virus. It is involved with ACEII binding, greater fusogenicity, and targeting of the lungs. So loss of that functionality would cripple the virus.
Because Delta carried the mutation, there's a possibility that many people who were infected with Delta may have immunity via antibodies that target the epitope carrying the L452R mutation. Therefore, carry-over immunity from Delta may target Ba.4/Ba.5, and if so that would cripple the virus.
Essentially, a Delta immunity landscape may have selected against Ba.4/Ba.5. Going with your comment, it does raise questions as to why one person who had Delta would get Ba.1, while someone who didn't would get Ba.4/Ba.5. We would expect pockets to emerge within the population who did not get Delta. I don't have a concrete answer, but it could be that Ba.1 gained dominance because of the immunity landscape but many people could have gotten Ba.4/Ba.5 as well, and even Ba.2. We don't know because unless we did genomic sequencing for everyone who was sick then we would miss out on it.
As to PCR tests, the drop in the S gene from Ba.1 is also happening in Ba.4/Ba.5 because both carry the 69-70 deletion, so PCR would not be a proper way to differentiate the two in that regard (i.e. if someone had a PCR test done during the Ba.1 wave you wouldn't be able to tell if it was Ba.1 or Ba.4/Ba.5). This evidence isn't concrete, but I suppose this is a way I can rationalize it.
As for re-infections, Ba.4/Ba.5 wouldn't necessary lead to greater reinfections, but that the route that was taken was the route with the least immune pressure. The Omicron route appears to be a roundabout way of evading the immune system where we just happened to land in a somewhat similar spot as when Delta was circulating. It's hard to figure out whether re-infections would be happening more frequently because we don't know who hasn't gotten COVID at this point given the messaging that 40% of infections are asymptomatic.
Hopefully that answers some of your questions. Please let me know if there is anything that requires clarifying. Just remember that this is a working model with a lot of holes in it.
Also, if the posts are above your head there's no problem in asking questions. Sometimes my writing may not be clear, or maybe I haven't included information that I should have. It's always good to know why the information went over someone's head so I can get some perspective.
It's not about the clarity of your writing which I think it's adequate for the purpose and scope, it's just that I do lack the necessary knowledge and background to fully grasp these matters. So at the very least you could be content (sic!) that some of your readers are trying to understand things they never thought before as being of interest(*for them*). Obviously the last two years of arbitrariness did help with that too.
Very interesting, I hadn't thought of it that way, that all Omicron variants were in the population waiting for a time to express. This would make sense, particularly with all the funky things going in injected immune systems. It seems to me we aren't dealing with normal viral evolution interaction with healthy immune systems. Thank you MD.
I tried to hold models of both viral and terrain theories. I'm new to the terrain theory of illness. My brain is having trouble thinking at the moment, but I do recognize all the toxins that are in our environment as well, and a sick population is attempting to detox toxins.
Well, the problem is that Omicron itself has strange origins, and so I don't think it's that people's immune systems are damaged from the vaccine per se, but that Omicron and all of the sub-lineages were around, not needing to undergo selective pressure or evolution. It just needed to find its niches and just jump from one sub-lineage to another. So instead of a slow walk, there's a game of immunity hopscotch happening where we're just hopping from one sub-lineage to another. In fact, the jump from Ba.1 to Ba.2 probably wouldn't happen in a severely damaged immune landscape. If the Ba.1 sub-lineage was capable of dominating, the other ones wouldn't have a way to take hold unless the immune landscape became one that targeted Ba.1. Hope that makes sense.
Terrain theory is interesting. I don't ascribe to the argument that pathogens are just toxins from our bodies arising due to changes, but terrain theory is right in arguing that our bodies play a huge role in whether we get sick or not. It's finding a balance between not having ourselves run into a ton of different pathogens that can kill us, but to also understand that having a healthy, functioning body will help us fight off pathogens when we become unfortunate to come across them.
Yeah, that does make sense. 👍🏽 I had been thinking about the variants coming one after the other, so I appreciate your view that they are in the population and just waiting for the chance to express as symptoms. Actually that makes more sense than one after the other.
Yeah, perhaps keeping both terrain and viral theories in mind, since as you say the terrain of the body makes a huge difference with illness.
Any given variant or mutation may occur due to selective pressures or through curation, but Omicron specifically appears to have had some sort of Omicron big bang moment from a possible B.0 progenitor as Brian pointed out. That's why this situation is so unique, and can't quite be explained from the original pipeline.
Both are important, and it's how they work together to either help or hurt us in the end that's the important factor. We shouldn't worry about just the pathogen when our terrain is horrible through processed foods and lack of exercise.
Interesting take - I would definitely agree that Omicron cannot be explained by typical viral mutation which appears to explain Alpha/Beta/Delta. I am curious what comes next - will this last remaining Omicron variant become the source of further typical viral mutations? Do you find it odd that the original Wuhan clades didn’t seem to evolve as rapidly as Alpha/Beta/Delta (for almost a year we had Wuhan & then the named variants all passed through in 2021 and now we have the Omicron family) - do you think vaccines caused that pressure or was it immune escape or both or it’s anybody’s guess?
Well I think the biggest issue is that we don't know which direction Delta would have gone because of the abrupt emergence of Omicron. This is one of the reasons why I'm critical of such comments such as the lack of seasonality for COVID. Well, seasonality requires that the virus circulate among the population until competition between the two causes it to plateau in some way. Omicron didn't allow us to reach post-Delta variants that may lead to seasonality, and now we're dealing with sudden jumps between Omicrons which are likely to have been around at similar times to one another.
I'm not sure to typical level of mutation rates that should be seen, but as Brian pointed out the level of mutations seen in Omicron necessitates years of circulation, and the idea that Omicron somehow existed for a year or two within either animal reservoirs or immunocompromised individuals doesn't quite make sense. So some possible accelerated measure via serial passage may have caused it, and serial passage through different animals or cell lines may have led to the different Omicron sub-lineages, as Brian Mowrey alludes to.
I really don't think we can argue that the vaccines are doing this because in order to make such an argument we need to explain how the vaccines led to the Delta/Omicron jump, and it's one of the things that doesn't appear to be answered anywhere. It's why I've been critical of the OAS argument, because models such as ones used by GvB utilize the Delta/Omicron jump to substantiate OAS yet never finds a valid explanation as to why such a jump occurred through vaccination. Such a model should explain why the vaccines led to Omicron, or why South Africa, which apparently has low vaccination rates, were the ones to have the emergence of Omicron.
I'm not entirely entrenched into the lab hypothesis, but I don't find the other alternatives to be any better, and are actually worse explanations. So the lab hypothesis is the best thing out of the worst things that we have.
You’re assuming people are only getting sick from a forever-evolving virus. If these are indeed lab-made (and I believe them to be) think of other ways they can be finding their way into people.
Well, for now the main focus of lab origins would be both Wuhan and Omicron. As to the other variants, they follow an evolutionary path that we would consider viruses to normally follow (to a degree). The problem would be if we see continuous, abrupt strains emerging that show huge escape. That would point more towards something possibly intentional. It would be rather ironic if the releases are seasonal, rather than the actual virus.
Very nice theory RE L452R immune recognition from Delta.
One thing to keep in mind RE the question of why they lost out initially is clonal interference, which is when more fit alleles in an asexual population don't win out if the numerically dominate allele is "fit enough." https://en.wikipedia.org/wiki/Clonal_interference Natural selection and clonal interference are opposing forces; the former only works if the latter is overcome by rendering the dominate allele no longer fit enough in the niche.
So the 4/5 spike model may have been more fit, but it was a numerical rarity in the initial viral swarm of the Omicron siblings that was in whatever matter "released." Conversely, BA.1 might have been a numerical rarity as well, but was so much more fit in an Omicron-naive landscape that it quickly overtook BA.2 and the others (this is what I imply in my fictional Origins scenario). (I regard BA.1 as clearly more transmissible than the others, don't care what the experts say on that one.)
So if BA.2 gets "first dibs" in the post-BA.1 landscape simply because of numerical superiority within the 2/4/5 family, it's not necessary that it's actually more fit. But once BA.2 has raised population adaptive immune response (the dirty "h. i." phrase that I won't say), it's substantially less fit than 4 and 5 and natural selection becomes the dominate force.
*edit: Alternately, there's some fitness detriment to the non-spike mutations in either 4/5 vs 2. So they had to wait until they had a leg up in the immune landscape. This is more of a stretch. BA.1 vs the 2 family has enough difference in non-spike mutations, esp. in Orf1, that the likelihood of different performance under the hood seems high, but not so much with 4/5 vs 2 which have so few changes to the internals. At most the P151S on 4's N protein might be disruptive since P changes are always radical. As a counter-argument, my own Omicron timeline describes BA.2 as evolving under high 3'-region pressure (everything after spike) and this would apply to 4 and 5 as well; but this could apply to fitness in the lab conditions and not real life transmission.
RE dispersion from South Africa, it doesn't seem that BA.2 was automatically spread alongside BA.1. Only some countries seemed to get BA.2 at about the same time as BA.1 in the figure I used from Yamasoba, D. et al. That's important for my argument against BA.2 turning out to have already been outside of South Africa all along before being sequenced / detected.
One other insight from the antigen map is that the Omicron siblings would have to reverse Delta (and other B.1-descendent circulating strains) mutations, as well as a plethora of non-spike mutations including synonomous ones. It's just not possible that Delta was in some vaccinated person and was like "screw this, I'm reinstalling to B.1!"
Thanks Brian, I always appreciate your insights. This was a lot of my thoughts scrambled together and me trying to piece it together, so I eventually just said "screw it!" and just put it into words and see what comes of it. I'm perfectly fine if this idea has more holes than Swiss cheese, but I wanted to at least solidify something for myself.
The clonal interference is interesting. In regards to Ba.4/Ba.5, a big issue with my hypothesis is that I've compared it to Delta via the L452R mutation, yet I don't have any quantitative data to compare the two. Pre-Delta variants had tropism for the lower airway and lungs, and so Delta with its L452R mutation is likely to just do it "better" than prior variants. The jump from Omicron losing that tropism means that something else is happening, so maybe the L452R mutation helped restore some of that functionality, but maybe not to the extent of Delta via other spike mutations. It's been months since I looked at studies of Ba.1 so I may have to return to some of those and try to figure that information out.
Your second and third paragraph was something I was trying to allude to via references to monoclonals. I'll admit my comment that "well, Ba.1 won out!" really doesn't cut it unless I have evidence to substantiate why Ba.1 was favored over Ba.2. I reference the antigenic maps but it's really improper for me to assume Ba.1 was more antigenically distant than Ba.2 just based on that alone. But essentially instead of having a slow walk through various mutations with Omicron it was like taking an Olympic pole vaulter and having a huge jump, and then instead of having another slow walk it was like playing hopscotch through all of the Omicrons.
I'll look back at the Yamasoba paper. I wonder if selection for Ba.2 or Ba.1 may have been due to population genetics such as HLA haplotypes in different countries. More confounding variables, but that's how it goes.
Could you clarify what you mean by the last paragraph? Maybe it's too early but I'm a little confused.
But thanks for your remarks Brian. I think after more research and dwelling on it further I may either try to formalize it further or if it's really not substantiated I'll toss it.
My guess for BA.2 is that is was an unlikely draw as far as what people traveling from South Africa would be carrying, and so only places with a lot of travel got it at first, namely north coastal Europe. It then had to spread from either there or SA. So places with less travel with SA initially got just BA.1.
The last paragraph is that once you subtract the B.1.1, the Omicron siblings don’t have any silent mutations from Delta. So they didn’t come from Delta. I think there was one or two mutations almost shared with Alpha, I lost my work on that one
So your suggestion is that there could be an argument of global spread at different timepoints? That would require a lot of reworking for my hypothesis, since it would need to find another explanation for the Omicron pipeline. The observational data does substantiate separate spread, but I suppose in my mind it makes more logical sense to have some Omicron Big Bang event and that they all just traveled together afterwards. More things to consider here.
And thanks for clarifying. I guess I was having a slow moment. Yes the whole Delta situation is one thing that I need an explanation for. This is one of the reasons why all hypotheses for Omicron deviates from selective pressure via circulation among humans (this includes the immunocompromised, as the lack of immunity essentially removes selective pressure), and yet OAS and the "virus of the vaccinated" does not make sense, yet it's becoming the argument that is used to justify our current predicament. It just feels like one of those hypotheses that just fits too well.
If they all traveled together, than the "movie" of sibling-to-sibling transition should be identical everywhere that got BA.1 in the winter. BA.2 should appear just as quickly post-BA.1 in the US / UK / Israel as it does in Denmark. imo...
That is true. More things to consider and more variables. Maybe I'm wildly pontificating on something that may otherwise be a nothing burger 🤷♂️. I'll just need to find more evidence one way or another.
Like I said when the mostly harmless Omicron emerged in South Africa and began displacing the more dangerous variants:
“The WHO and world wish to thank South Africa for its willingness to serve as guinea pigs for experimentation. Their willingness to do so has saved countless lives.”
I really have no idea what happened in South Africa, but it just keeps adding to the level of uncertainty with everything going on. I'll admit I didn't give Omicron much thought for a few months, but given what's going on right now it seems extremely important to think about the origins of Omicron, as well as the origins of Wuhan.
First of all I am grateful for your very instructive posts (which in all honesty are way above my head).
That being said I am a bit confused by your BA.4 and BA.5 pipeline theory.
I guess what you say -sorry for over simplifying- is that Delta and BA.4/5 shared the same time and space and eventually BA.4 and BA.5 had to "wait" until previous immunity from Delta fades(?) and let them spread.
If that is true wouldn't that mean that mostly everyone in that shared space somehow gained immunity for Delta via infection or other means? Otherwise all 3 variants could have acted simultaneously infecting different sets of people, eventually separated geographically.
Wouldn't also mean that currently BA.4 and BA.5 should translate into a lot more of re-infections rather than covid first-timers?
What am I missing?
Thank you.
I'll first start off my saying if this hypothesis seems like it has a bunch of holes, that's probably because it does. This is a working model that I just wanted to have in written format because I have so many thoughts going on in my head and I wanted to solidify it in some way.
My argument for Ba.4 and Ba.5 is that the L452R mutation is likely a pivotal mutation for the virus. It is involved with ACEII binding, greater fusogenicity, and targeting of the lungs. So loss of that functionality would cripple the virus.
Because Delta carried the mutation, there's a possibility that many people who were infected with Delta may have immunity via antibodies that target the epitope carrying the L452R mutation. Therefore, carry-over immunity from Delta may target Ba.4/Ba.5, and if so that would cripple the virus.
Essentially, a Delta immunity landscape may have selected against Ba.4/Ba.5. Going with your comment, it does raise questions as to why one person who had Delta would get Ba.1, while someone who didn't would get Ba.4/Ba.5. We would expect pockets to emerge within the population who did not get Delta. I don't have a concrete answer, but it could be that Ba.1 gained dominance because of the immunity landscape but many people could have gotten Ba.4/Ba.5 as well, and even Ba.2. We don't know because unless we did genomic sequencing for everyone who was sick then we would miss out on it.
As to PCR tests, the drop in the S gene from Ba.1 is also happening in Ba.4/Ba.5 because both carry the 69-70 deletion, so PCR would not be a proper way to differentiate the two in that regard (i.e. if someone had a PCR test done during the Ba.1 wave you wouldn't be able to tell if it was Ba.1 or Ba.4/Ba.5). This evidence isn't concrete, but I suppose this is a way I can rationalize it.
As for re-infections, Ba.4/Ba.5 wouldn't necessary lead to greater reinfections, but that the route that was taken was the route with the least immune pressure. The Omicron route appears to be a roundabout way of evading the immune system where we just happened to land in a somewhat similar spot as when Delta was circulating. It's hard to figure out whether re-infections would be happening more frequently because we don't know who hasn't gotten COVID at this point given the messaging that 40% of infections are asymptomatic.
Hopefully that answers some of your questions. Please let me know if there is anything that requires clarifying. Just remember that this is a working model with a lot of holes in it.
Also, if the posts are above your head there's no problem in asking questions. Sometimes my writing may not be clear, or maybe I haven't included information that I should have. It's always good to know why the information went over someone's head so I can get some perspective.
It's not about the clarity of your writing which I think it's adequate for the purpose and scope, it's just that I do lack the necessary knowledge and background to fully grasp these matters. So at the very least you could be content (sic!) that some of your readers are trying to understand things they never thought before as being of interest(*for them*). Obviously the last two years of arbitrariness did help with that too.
Very interesting, I hadn't thought of it that way, that all Omicron variants were in the population waiting for a time to express. This would make sense, particularly with all the funky things going in injected immune systems. It seems to me we aren't dealing with normal viral evolution interaction with healthy immune systems. Thank you MD.
I tried to hold models of both viral and terrain theories. I'm new to the terrain theory of illness. My brain is having trouble thinking at the moment, but I do recognize all the toxins that are in our environment as well, and a sick population is attempting to detox toxins.
Well, the problem is that Omicron itself has strange origins, and so I don't think it's that people's immune systems are damaged from the vaccine per se, but that Omicron and all of the sub-lineages were around, not needing to undergo selective pressure or evolution. It just needed to find its niches and just jump from one sub-lineage to another. So instead of a slow walk, there's a game of immunity hopscotch happening where we're just hopping from one sub-lineage to another. In fact, the jump from Ba.1 to Ba.2 probably wouldn't happen in a severely damaged immune landscape. If the Ba.1 sub-lineage was capable of dominating, the other ones wouldn't have a way to take hold unless the immune landscape became one that targeted Ba.1. Hope that makes sense.
Terrain theory is interesting. I don't ascribe to the argument that pathogens are just toxins from our bodies arising due to changes, but terrain theory is right in arguing that our bodies play a huge role in whether we get sick or not. It's finding a balance between not having ourselves run into a ton of different pathogens that can kill us, but to also understand that having a healthy, functioning body will help us fight off pathogens when we become unfortunate to come across them.
Yeah, that does make sense. 👍🏽 I had been thinking about the variants coming one after the other, so I appreciate your view that they are in the population and just waiting for the chance to express as symptoms. Actually that makes more sense than one after the other.
Yeah, perhaps keeping both terrain and viral theories in mind, since as you say the terrain of the body makes a huge difference with illness.
Any given variant or mutation may occur due to selective pressures or through curation, but Omicron specifically appears to have had some sort of Omicron big bang moment from a possible B.0 progenitor as Brian pointed out. That's why this situation is so unique, and can't quite be explained from the original pipeline.
Both are important, and it's how they work together to either help or hurt us in the end that's the important factor. We shouldn't worry about just the pathogen when our terrain is horrible through processed foods and lack of exercise.