XE— a new sister lineage of Omicron— has peppered the headlines this week. And while it’s important for scientists to track every change of the virus, I don’t think the public needs to be anxiety-ridden every time this virus changes. This is what viruses do to survive, and we should anticipate this. In fact, Omicron mutating may be
What is the reasoning behind "we expect with high certainty a “flu-like drift” of SARS-CoV-2" ? It seems like everything you said (and I've read elsewhere) is that viral evolution hasn't fit any known models or patterns. Omicrons BA.1 and BA.2 are as different from each other as Alpha, Beta, Gamma, and Delta are from one another, so that isn't ladder like change yet. Is there something about a lot of recombinants that supports“flu-like drift” I'm missing?
Thanks for a great post, Katelyn, helping us understand where the uncertainties lie (and why they are uncertain). It's fascinating and inspiring that there is so much work worldwide and that so much of it is being shared - which points out the urgent need for the public to understand how science works. QUESTION: Is there an evidence base for the statement "viruses evolve to become more transmissible but less pathological?" (Meaning it's not "in their interest" to kill their host) It seems that by the time the host transmits the virus, the virus "doesn't care" what happens to the host. If true, then it seems there wouldn't *necessarily* be selective pressure on pathogenicity
My mental model is that these first few variants are like shrapnel from an evolutionary explosion. Isn't Omicron thought to have branched off pretty early? In which case we're bound to see stuff keep turning up...until it doesn't, because there's some evidence of convergent evolution and the space of mathematically possible variants is much larger than the space of variants that can actually occur in nature (and thrive). Is that a fair assessment?
Super interesting that "there are really only two antigenic spaces or areas of vulnerability this could happen: a virus that is closer to Beta, or a virus that is closer to Delta."
Are there implications here that our vaccine induced cellular immunity would be somewhat effective going forward into this space?
Great exposition! I take heart that this virus will reach an accommodation with us that is fairly predictable and manageable. It may not seem like it right now, but we really dodged a bullet with covid, it could have been far far, worse.
Not related to this post, but wondering if you would do a post on vaccines for children under 5? Moderna made a splash with their trial data and then there has been silence. What is going on?
Why do we want high transmissions and more contagion (eg. XE) when the evidence is piling up that there can be substantial side-effects from even mild and moderate COVID infections, and even those aren't fully understood yet? I want someone to explain this to me very clearly because I'm not digging what I'm seeing right now. This is going to have future health implications, especially if it's hitting all systems in a fairly slipshod manner (as preliminary studies seem to be suggesting).
"there are really only two antigenic spaces or areas of vulnerability this could happen: a virus that is closer to Beta, or a virus that is closer to Delta."
Is this because they are more likely to give rise to a more severe disease? Or is it something about the likelihood of these kinds of mutations occurring over a more Omicron like virus?
Not related to this post, but I wish you would put up a post talking up the post-exposure therapeutics, Paxlovid and the like. I have encountered dozens of people who do not know about this stuff in the past month, and most of them are people with college educations or graduate degrees, people who are vaxed, boosted and fairly well-informed. AND I'd say a third of them are 65+ or have a health problem that's a substantial risk factor.
I often read screeds by health professionals about how we need to get more people vaxed and boosted, improve ventilation in buildings, develop systems for evaluating current risk and adjusting precautions accordingly. All great points, BUT these same people don't say a word about Paxlovid, etc. I just don't understand it. Do they not realize how underutilized these treatments are? Are they afraid unvaccinated people will be even less likely to finally get vaxed if they know there are treatments that help high-risk people if they get infected? Are they all having a brain glitch?
"Our model predicts that COVID-19 is likely to become the leading cause of death in the US under many scenarios. For example, for a hypothetical SARS-CoV-2 variant with an R0 of 5, an IFR of 1%, and a 12-month duration of natural immunity, approximately 700,000 US COVID-19 deaths could be expected per year if a vaccine preventing 90% of infections were administered to 70% of the population. We observe that despite a high degree of vaccine efficacy – 90% reduction in risk of infection and 90% reduction in risk of death given infection– the region in which US COVID-19 deaths under endemic conditions rival influenza deaths (12,000 – 52,000 per year, according to the CDC50) is small and would require a significant reduction in IFR."
Katelyn, you really are more than a local epidemiologist. An "LE" wouldn't "call" with periodic valuable updates! Thank you.
Suggestion for a future post:
An update on your views of Long Covid.
What is the reasoning behind "we expect with high certainty a “flu-like drift” of SARS-CoV-2" ? It seems like everything you said (and I've read elsewhere) is that viral evolution hasn't fit any known models or patterns. Omicrons BA.1 and BA.2 are as different from each other as Alpha, Beta, Gamma, and Delta are from one another, so that isn't ladder like change yet. Is there something about a lot of recombinants that supports“flu-like drift” I'm missing?
Thanks for a great post, Katelyn, helping us understand where the uncertainties lie (and why they are uncertain). It's fascinating and inspiring that there is so much work worldwide and that so much of it is being shared - which points out the urgent need for the public to understand how science works. QUESTION: Is there an evidence base for the statement "viruses evolve to become more transmissible but less pathological?" (Meaning it's not "in their interest" to kill their host) It seems that by the time the host transmits the virus, the virus "doesn't care" what happens to the host. If true, then it seems there wouldn't *necessarily* be selective pressure on pathogenicity
My mental model is that these first few variants are like shrapnel from an evolutionary explosion. Isn't Omicron thought to have branched off pretty early? In which case we're bound to see stuff keep turning up...until it doesn't, because there's some evidence of convergent evolution and the space of mathematically possible variants is much larger than the space of variants that can actually occur in nature (and thrive). Is that a fair assessment?
Super interesting that "there are really only two antigenic spaces or areas of vulnerability this could happen: a virus that is closer to Beta, or a virus that is closer to Delta."
Are there implications here that our vaccine induced cellular immunity would be somewhat effective going forward into this space?
Great exposition! I take heart that this virus will reach an accommodation with us that is fairly predictable and manageable. It may not seem like it right now, but we really dodged a bullet with covid, it could have been far far, worse.
Not related to this post, but wondering if you would do a post on vaccines for children under 5? Moderna made a splash with their trial data and then there has been silence. What is going on?
Why do we want high transmissions and more contagion (eg. XE) when the evidence is piling up that there can be substantial side-effects from even mild and moderate COVID infections, and even those aren't fully understood yet? I want someone to explain this to me very clearly because I'm not digging what I'm seeing right now. This is going to have future health implications, especially if it's hitting all systems in a fairly slipshod manner (as preliminary studies seem to be suggesting).
"there are really only two antigenic spaces or areas of vulnerability this could happen: a virus that is closer to Beta, or a virus that is closer to Delta."
Is this because they are more likely to give rise to a more severe disease? Or is it something about the likelihood of these kinds of mutations occurring over a more Omicron like virus?
Not related to this post, but I wish you would put up a post talking up the post-exposure therapeutics, Paxlovid and the like. I have encountered dozens of people who do not know about this stuff in the past month, and most of them are people with college educations or graduate degrees, people who are vaxed, boosted and fairly well-informed. AND I'd say a third of them are 65+ or have a health problem that's a substantial risk factor.
I often read screeds by health professionals about how we need to get more people vaxed and boosted, improve ventilation in buildings, develop systems for evaluating current risk and adjusting precautions accordingly. All great points, BUT these same people don't say a word about Paxlovid, etc. I just don't understand it. Do they not realize how underutilized these treatments are? Are they afraid unvaccinated people will be even less likely to finally get vaxed if they know there are treatments that help high-risk people if they get infected? Are they all having a brain glitch?
Hi, I just read this article, and it's pretty grim. https://www.medrxiv.org/content/10.1101/2022.03.29.22273146v1.full-text The following paragraph really got my attention:
"Our model predicts that COVID-19 is likely to become the leading cause of death in the US under many scenarios. For example, for a hypothetical SARS-CoV-2 variant with an R0 of 5, an IFR of 1%, and a 12-month duration of natural immunity, approximately 700,000 US COVID-19 deaths could be expected per year if a vaccine preventing 90% of infections were administered to 70% of the population. We observe that despite a high degree of vaccine efficacy – 90% reduction in risk of infection and 90% reduction in risk of death given infection– the region in which US COVID-19 deaths under endemic conditions rival influenza deaths (12,000 – 52,000 per year, according to the CDC50) is small and would require a significant reduction in IFR."
This thing is keeping all of us guessing ... what a strange disease it's been.
Katelyn, one point to ponder: The coronaviruses are not the influenza virus. Different families, different mutation paths.
How are the rapid antigen tests holding up under omicron, BA.2, etc.? I've heard rumors they're giving a lot of false negatives.
Brilliant information - thank you!
Thank you for this post!