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Thread: Disease and pandemics thread (because it's science)

  1. #2491
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    We should hear interim results from the Oxford vaccine soon, but in the meantime the Phase II/III results have been through peer review and have been published in The Lancet. Good immunogenicity in older people, and better tolerated in that age group too.

    Grant Hutchison

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    Interesting interim results from the Oxford/AstraZeneca vaccine this morning. 62% effective with two equal doses a month apart, but 90% effective with an initial half dose followed by a full dose a month later. The immune system is certainly a funny thing--I'll be interested to read what immunologists make of those results.

    Grant Hutchison

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    Quote Originally Posted by grant hutchison View Post
    Interesting interim results from the Oxford/AstraZeneca vaccine this morning. 62% effective with two equal doses a month apart, but 90% effective with an initial half dose followed by a full dose a month later. The immune system is certainly a funny thing--I'll be interested to read what immunologists make of those results.
    I think (without having read the paper) that I would also want to take a good look at the error bars.
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    Quote Originally Posted by Jens View Post
    I think (without having read the paper) that I would also want to take a good look at the error bars.
    I doubt if it's an error-bar issue. The p values are very tight, implying correspondingly tight confidence intervals around the quoted values.

    Grant Hutchison

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    In other news, the most recent Ebola outbreak in the DRC is officially ended, without killing us all. (Remember when people worried about that?) Stalwart efforts under adverse conditions must be applauded.
    Interestingly, vaccine was transported into remote regions using passive cool-boxes at dry-ice temperatures, with a useful storage time of one week, which is a good demonstration of how some of the Covid-19 vaccines may travel to their final distribution points.

    Grant Hutchison

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    Quote Originally Posted by grant hutchison View Post
    In other news, the most recent Ebola outbreak in the DRC is officially ended, without killing us all. (Remember when people worried about that?) Stalwart efforts under adverse conditions must be applauded.
    Interestingly, vaccine was transported into remote regions using passive cool-boxes at dry-ice temperatures, with a useful storage time of one week, which is a good demonstration of how some of the Covid-19 vaccines may travel to their final distribution points.
    Actually, I completely remember the first outbreak. I was young then, and I remember obsessively trying to get information (the Internet wasn't very well developed at that time) on how it was spreading and worrying that it was going to wipe us out.

    ETA: I should have checked before posting. It was the sixth or seventh, actually, the one around 1994-1995.
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    Quote Originally Posted by Jens View Post
    Actually, I completely remember the first outbreak. I was young then, and I remember obsessively trying to get information (the Internet wasn't very well developed at that time) on how it was spreading and worrying that it was going to wipe us out.

    ETA: I should have checked before posting. It was the sixth or seventh, actually, the one around 1994-1995.
    I vividly remember the first. I was a medical student at the time, and there seemed to be a sort of gathering momentum of novel viral haemorrhagic fevers at that time--Lassa, Marburg, then Ebola. And the BBC were running a pretty effective TV series at the time called Survivors, set in a post-apocalyptic Britain immediately after a pandemic has wiped out most of the population.

    (But I was actually referring to more recent events, on this forum, and the fact that those Ebola anxieties now seem a little outdated.)

    Grant Hutchison

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    The Oxford vaccine interim analysis has now been published in the Lancet. So that's the first peer-reviewed report of a Phase III Covid vaccine trial. The Science Media Centre has a lot of good commentary.

    Grant Hutchison

  9. 2020-Dec-15, 07:35 PM
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    Quote Originally Posted by grant hutchison View Post
    Quote Originally Posted by Trebuchet View Post
    Grant, as a doctor, do you believe that herd immunity can be achieved other than through vaccination; in other words by enough people getting infected? I keep seeing different stories; such as that that was what Sweden was planning on.
    Anders Tegnell is on record saying that Sweden's aim was never to achieve herd immunity, in the sense of deliberately setting out to get everyone infected. I've no reason to doubt him. (Sweden, of course, is the subject of another set of mutual contradictory narratives.)
    In general, I think people became hypnotized from very early on by the naive calculation of the herd immunity threshold, (R0-1)/R0, which comes out to 2/3 of your population if R0=3. From that, they looked at the infection fatality rate, did a little arithmetic, and start yelling about hundreds of thousands of deaths. So from March to August this year, no-one has really been able to say the words "herd immunity" without becoming the focus of a toxic reflex twitter-storm.
    But we know that infection is not distributed at random throughout the population (which is a key assumption of the naive calculation); and we know that R doesn't really resemble R0 in any society in the world at present, because we've made huge social changes specifically to achieve that end. So we know that the 2/3 threshold is an overestimate.
    People who carry out more realistic modelling exercises of how populations actually behave are coming up with "effective herd immunity" levels as low as 20%. There's a recent preprint here, for instance. To that, we can add recent observations that there appears to be a degree of cross-immunity between common cold coronaviruses and SARS-CoV-2, which means that some individuals may be immune without having been infected with Covid-19.
    Now, there are already places in the world with seroprevalence of Covid-19 antibodies of 20%. (Bit of wiggle room there, however, in that we still don't know what level and kind of antibodies are protective, and we do know that some people may have cell-mediated immunity in the absence of antibodies.) And there is suggestive epidemiology--the way the case rate in Sweden is declining without any changes in disease control measures, and while still far short of that 2/3 seroprevalence everyone got so exercised about; the way London seems to have (so far) avoided becoming a UK hotspot as lockdown relaxes, despite being earliest and worst hit in the first wave.
    That said, there are places where seroprevalence is higher than 20%. If 20% was some sort of magic herd immunity wall, then that wouldn't have happened. But we'd need to model the social structure in those places to estimate the effective herd immunity threshold for those places, before we could truly understand the figures.

    So, basically, I don't know. What I do know is that it's complicated and messy, and that "60-70% for herd immunity" is a figure that only makes sense if you're planning to vaccinate a population at random, not if you're dealing with a real disease transmitting through a real population. I think we're seeing a little scintilla of evidence that in some settings "useful herd immunity" might already be occurring, while in other settings it very much isn't. And I know that, by any reasonable expectation, we're going to see a lot more cases this winter, so we're going to get more evidence, one way or another, of how close some societies are to helpful levels of seroprevalence developing in their populations.
    Worth revisiting this, I think (particularly the last sentence), given how much things have changed in both Sweden and London over the last few months. Sweden, in particular, saw case rates take off dramatically while their restrictions remained unchanged, and London has now kicked off big-style, after enjoying lower transmission than other parts of England. So the apparent damping of the pandemic in places that had experienced early high infection rates appears to have been a false dawn.
    The lull was very interesting, though. So what changed?
    1) The virus might have become more transmissible. (Despite recent worries in the UK about a new strain, there doesn't yet seem to be much evidence of that, but watch this space.)
    2) We may be seeing immunity acquired during the first wave starting to wane. (There's conflicting evidence from seroprevalence studies.)
    3) The nature of the herd may have changed.
    I think this last is probably a major factor, if not the major factor. As weather has got colder, people are gathering more indoors. And as the pandemic has worn on, people are starting to let their observance of existing restrictions slide.

    Grant Hutchison

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    In terms of 1.)

    No one has sampled viruses from every victim, have they?
    Could a more lethal strain lose some of its “crown” in a hot-spot, but when sampled after a length of time, look pretty much like all the rest? Maybe ALPHAFOLD could do a test...

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    Quote Originally Posted by publiusr View Post
    No one has sampled viruses from every victim, have they?
    COG-UK are maintaining genomic surveillance in the UK, and they're currently sequencing about 10% of positive samples.
    It's because of that surveillance that we now know we are dealing with a more transmissible strain in London, the south-east of England, and South Wales, probably accounting for the rapid surge in cases we're seeing in those areas.

    Quote Originally Posted by publiusr View Post
    Could a more lethal strain lose some of its “crown” in a hot-spot, but when sampled after a length of time, look pretty much like all the rest?
    I have no idea what this means. Sorry.

    Grant Hutchison

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    Quote Originally Posted by grant hutchison View Post
    COG-UK are maintaining genomic surveillance in the UK, and they're currently sequencing about 10% of positive samples.
    It's because of that surveillance that we now know we are dealing with a more transmissible strain in London, the south-east of England, and South Wales, probably accounting for the rapid surge in cases we're seeing in those areas.



    Grant Hutchison
    and which has caused a reversal of policy, cancelling what was to be a lax Christmas, or tier zero for a few days in the middle of tier 3, the strictest level. Too soon to know if this more easily caught strain has lower or higher morbidity. But not surprising.
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    Interesting correlations with vitamin D blood assay and severity of Covid infection. Higher lattitude peoples and darker skinned, plus winter sunshine levels reduce D levels. D is actually a hormone and it does have a role in the immune system. Long presentation available via MedCram.com, free although you have to join, and, I believe available on you tube. Many recent research studies quoted.
    sicut vis videre esto
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    Quote Originally Posted by profloater View Post
    Interesting correlations with vitamin D blood assay and severity of Covid infection. Higher lattitude peoples and darker skinned, plus winter sunshine levels reduce D levels. D is actually a hormone and it does have a role in the immune system. Long presentation available via MedCram.com, free although you have to join, and, I believe available on you tube. Many recent research studies quoted.
    I'm not inclined to sign up for MedCram (okay, I'm lazy), and I don't trust my ability to find trustworthy info on YouTube. However, I *did* come across the following paper on the Nature website.

    https://www.nature.com/articles/s41598-020-77093-z

    The abstract seems to make a strong case for ensuring you aren't Vitamin D deficient:
    The fatality rate was high in vitamin D deficient (21% vs 3.1%). Vitamin D level is markedly low in severe COVID-19 patients. Inflammatory response is high in vitamin D deficient COVID-19 patients.
    I wonder why this information hasn't been more widely publicized.
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    Quote Originally Posted by Extravoice View Post
    I wonder why this information hasn't been more widely publicized.
    Probably because of the concerns expressed, among other places, in a recent editorial in the British Medical Journal:
    The panel agreed that low vitamin D status was associated with more severe outcomes from covid-19. It is not possible, however, to confirm causality because many of the risk factors for severe covid-19 outcomes are the same as the risk factors for low vitamin D levels. The serum concentration of vitamin D falls during a systemic inflammation which may occur during severe covid-19 illness and it is difficult to know if low vitamin D status causes poor outcomes or vice versa.
    (My bold)

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    Ugh. The old correlation problem. How to tell which causes which?
    I suppose you could test people for vitamin D levels before they get sick, but thatís more complex and possibly ethically questionable.
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    Quote Originally Posted by grant hutchison View Post
    COG-UK are maintaining genomic surveillance in the UK, and they're currently sequencing about 10% of positive samples.
    It's because of that surveillance that we now know we are dealing with a more transmissible strain in London, the south-east of England, and South Wales, probably accounting for the rapid surge in cases we're seeing in those areas.

    I have no idea what this means. Sorry.

    Grant Hutchison
    What are the implications for the vaccine? The official word seems guarded so far.

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    Quote Originally Posted by Glom View Post
    What are the implications for the vaccine? The official word seems guarded so far.
    There are changes to the spike protein, which is what the virus uses to bind to cells, and what the current vaccines raise antibodies to. The important change with relevance to infectivity is in the receptor binding domain. (There's a deleted section elsewhere in the protein, too.) So far, people who know what sort of spike-protein sequences the vaccines produce seem to think this isn't enough of a change to make the new spike protein "invisible" to antibodies raised by vaccines. But we won't really know until we have a lot more people vaccinated--the proof, as always, is in the epidemiology, not in the laboratory.

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    If it did (purely hypothetically), would it mean back to square one for the pharma or could the vaccine in use now provide the basis for a quicker turnaround.

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    Well, mRNA vaccines are new territory, so new regulatory standards would need to be agreed. But an mRNA vaccine candidate can be formulated within days of a genome being published, so there's no problem there. And the delivery systems, manufacturing lines and storage solutions are already in place. So the bottleneck would be clinical safety and efficacy tests.
    There, we have a precedent in the seasonal flu vaccines--once you have a licenced flu vaccine, then small changes to the specific influenza protein in your vaccine, to match the currently prevalent strains, merely requires a supplement to the licence, and no new clinical data. It makes sense that you don't need to go through the entire testing process again when all that has changed is a small number of amino acids in the presented antigen. (And we could never keep up with the constant changes in seasonal flu if we had to reapprove every new flu vaccine in Phase III trials.)
    I'd guess that the same consideration would apply to Covid, except that with the current vaccines the change would be to a small number of RNA base pairs. But, as I say, these are novel vaccines, so there may be potential issues I don't understand.

    People have been debating the potential of "vaccine escape" in Covid for a long time. Coronaviruses are more stable than many viruses, and mutate relatively slowly, but we've seen many strains come and go during this pandemic (the strain currently driving the pandemic is not the one that originally came out of China, for instance, but one that appeared in Europe). So at some point it could potentially develop enough protein changes to escape from current vaccines. The higher its prevalence, the more quickly that will happen, because there are more virions in circulation. So I'd guess knowledgeable people already have draft contingency plans on their hard drives.

    Grant Hutchison

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    Quote Originally Posted by Extravoice View Post
    Ugh. The old correlation problem. How to tell which causes which?
    I suppose you could test people for vitamin D levels before they get sick, but that’s more complex and possibly ethically questionable.
    I don't think it's ethically questionable unless you deliberately infect them after doing the test.
    As above, so below

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    Quote Originally Posted by Jens View Post
    I don't think it's ethically questionable unless you deliberately infect them after doing the test.
    One ethical problem is that hypovitaminosis D is a risk for other disease conditions. So once you identify that someone has low Vitamin D, you can't ethically conceal that from the subject or withhold treatment. There's admittedly a large grey area, with doctors arguing about what exactly is the normal range for Vitamin D, and at what point disease risk becomes elevated above the background noise.
    One way of moving forward would be to treat all the extreme low values you find, and then follow up everyone who's in some agreed acceptable range, with or without supplementation. You then look for a "dose response" curve--do those with blood levels at the upper end of the normal range fare better than those at the lower end of the normal range?

    Grant Hutchison

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    Quote Originally Posted by grant hutchison View Post
    Well, mRNA vaccines are new territory, so new regulatory standards would need to be agreed. But an mRNA vaccine candidate can be formulated within days of a genome being published, so there's no problem there. And the delivery systems, manufacturing lines and storage solutions are already in place. So the bottleneck would be clinical safety and efficacy tests.
    There, we have a precedent in the seasonal flu vaccines--once you have a licenced flu vaccine, then small changes to the specific influenza protein in your vaccine, to match the currently prevalent strains, merely requires a supplement to the licence, and no new clinical data. It makes sense that you don't need to go through the entire testing process again when all that has changed is a small number of amino acids in the presented antigen. (And we could never keep up with the constant changes in seasonal flu if we had to reapprove every new flu vaccine in Phase III trials.)
    I'd guess that the same consideration would apply to Covid, except that with the current vaccines the change would be to a small number of RNA base pairs. But, as I say, these are novel vaccines, so there may be potential issues I don't understand.

    People have been debating the potential of "vaccine escape" in Covid for a long time. Coronaviruses are more stable than many viruses, and mutate relatively slowly, but we've seen many strains come and go during this pandemic (the strain currently driving the pandemic is not the one that originally came out of China, for instance, but one that appeared in Europe). So at some point it could potentially develop enough protein changes to escape from current vaccines. The higher its prevalence, the more quickly that will happen, because there are more virions in circulation. So I'd guess knowledgeable people already have draft contingency plans on their hard drives.

    Grant Hutchison
    I like this post. Thank you.

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    One recent paper quoted by MedCram in the “Covid update” free episode compared high dose vit D fortnightly with low dose daily, and the low dose was more effective in correlation terms. The presenter prof Seheult, emphasises correlation because causation is hard to establish but the epidemiology quoted is rather impressive. Since it is free and easy to find on YouTube, I think it is worth watching. And not just for Covid,
    Last edited by profloater; 2020-Dec-21 at 10:55 AM. Reason: Typo
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    https://m.youtube.com/watch?v=Mdc7T2UTHBI
    I’m posting the link having realised that actually there are several covert related updates from MedCram.
    sicut vis videre esto
    When we realize that patterns don't exist in the universe, they are a template that we hold to the universe to make sense of it, it all makes a lot more sense.
    Originally Posted by Ken G

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    For Grant or others more expert than I:
    My cousin developed Covid symptoms and tested positive after taking her cat to the veterinarian, whose office closed with a Covid outbreak the next day. My cousin didn't actually go into the office but the cat was there for most of a day. When the cat got home, my cousin naturally cuddled it and it slept with her.
    My cousin thinks she may have gotten the virus from the cat's fur. She and her husband have otherwise been being very careful, staying in to the point of having all their food delivered. Does her supposition seem likely? It's not something I've heard of before.

    Location is Southern California.
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    Quote Originally Posted by Trebuchet View Post
    For Grant or others more expert than I:
    My cousin developed Covid symptoms and tested positive after taking her cat to the veterinarian, whose office closed with a Covid outbreak the next day. My cousin didn't actually go into the office but the cat was there for most of a day. When the cat got home, my cousin naturally cuddled it and it slept with her.
    My cousin thinks she may have gotten the virus from the cat's fur. She and her husband have otherwise been being very careful, staying in to the point of having all their food delivered. Does her supposition seem likely? It's not something I've heard of before.

    Location is Southern California.
    I'm no expert, but I wonder if the virus could have been transmitted not on the cat's fur, but in their breath (it is a respiratory virus).
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    Quote Originally Posted by Trebuchet View Post
    For Grant or others more expert than I:
    My cousin developed Covid symptoms and tested positive after taking her cat to the veterinarian, whose office closed with a Covid outbreak the next day. My cousin didn't actually go into the office but the cat was there for most of a day. When the cat got home, my cousin naturally cuddled it and it slept with her.
    My cousin thinks she may have gotten the virus from the cat's fur. She and her husband have otherwise been being very careful, staying in to the point of having all their food delivered. Does her supposition seem likely? It's not something I've heard of before.

    Location is Southern California.
    We can only know that it is possible, we will never know how it happened. Too many variables, unless we measure her strain and the strain from the clinic and see if we can rule it in or out, and nobody is going to do that for every situation. This virus, for whatever reason is easily transmitted.
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    Quote Originally Posted by Trebuchet View Post
    For Grant or others more expert than I:
    My cousin developed Covid symptoms and tested positive after taking her cat to the veterinarian, whose office closed with a Covid outbreak the next day. My cousin didn't actually go into the office but the cat was there for most of a day. When the cat got home, my cousin naturally cuddled it and it slept with her.
    My cousin thinks she may have gotten the virus from the cat's fur. She and her husband have otherwise been being very careful, staying in to the point of having all their food delivered. Does her supposition seem likely? It's not something I've heard of before.
    First thing is, there's no way in which the cat (or anyone else) could catch Covid and become infective in the space of a day. So we can rule out the normal "chain of respiratory infection" transmission.
    I guess it's possible that the virus survived on the cat's fur--we know it survives on skin for up to nine hours. And by grooming themselves and then licking humans on their hands or faces, cats are quite effective little disease transmission engines.
    But presumably some human contact was involved during the visit to the veterinarian's office, unless the cat walked in from the car park carrying its own documentation. Isn't good old human-to-human spread more likely?

    Grant Hutchison
    Last edited by grant hutchison; 2020-Dec-21 at 10:00 PM.

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    At the vet office next to my wife's hairdresser, they have half a dozen designated parking spaces, spread apart. A masked employee comes out and collects the leashed dog or cat in its carrier, takes them inside for the appointment, and brings them back. I assume it was something like that but don't know.
    Googling pretty consistently says "no" to getting Covid from pet hair.
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