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Toilet Duck

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Toilet Duck last won the day on May 29

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  1. Basically it’s the amount of variation in R (kind of!)...diseases with a high K number have lots of people who contribute to its spread, diseases with a low one have super-spreaders...COVID has a low K number meaning that not everyone is driving the R number. Control super spreading events and you can control R!
  2. Lads, ye have another letter/number to be arguing about as well...K! (Which has a big impact on R)...appears especially relevant for this virus and how we handle it.
  3. Both! Edit: I think there is a duty of care for employers to ensure that when employees return to work, it's under the safest conditions possible. For the next while, this will mean limiting people in the workplace and using alternative means to have meetings etc. Face-to-face interactions can be built into that (but not at 100%). I'd love to go back into the university, there's absolutely a loss of collegiality that happens when everyone is working remotely...but I wouldn't do it under unsafe conditions...thankfully my institution is very proactive in terms of adapting our workplace (thermal scanners, in house testing etc). It's a massive logistical challenge and I appreciate not every business can go to the lengths we do, but there are some straightforward precautions that can be implemented (for example, we don't wait for the HSE (our version of the NHS) contact tracing, we do our own as soon as a suspected case is identified).
  4. To be honest, I think the paper makes one huge assumption...namely "...generically it is often very difficult to infer epidemiological parameters from clinical data, without the results being informed more by the prior beliefs encoded in the model than by the data. The exception is when clinical data directly measure the quantity of epidemiological interest. This is the case for deaths with COVID-19 and for fatal disease duration. While not perfect, these data are far less compromised than the data on ‘cases’. Deaths are reliably recorded, clinical grounds for suspecting COVID-19 are clear, and good records are kept for fatal cases". I would argue that reporting of deaths is exceptionally noisy at the moment. Hospitals were fire-fighting at their peak of admissions and we see significant auditing of data and reporting of more fatalities well after they occurred as a result of this (not just in the UK, but everywhere). For me, the most robust measure of what the outbreak is doing is hospital admissions and ICU admissions, which are happening in realtime (and these are the triggers used for implementation of the public health measures). Irrespective of when the "peak" is modelled to have occurred, if people are streaming thorough your hospital door, you are going to have to do something about it. So, I think that the "measure of quantity of epidemiological interest" is not just fatalities, but also the rate of hospital/ICU admissions. I guess the above paper is what happens when a mathematician looks at something purely from a data perspective and doesn't necessarily consider all of the other evidence pointing towards what course of action should be taken (it's also only possible to do this analysis after the fact as realtime reporting of deaths is extremely unreliable). Suggesting that the lockdown wasn't needed will garner attention, but the timeline example I provided of how lockdown prevented breaching the capacity of the Irish health service doesn't solely rely on a model, it's just what actually happened (and what was predicted to happen based on the increasing number of patients arriving in hospital). But, look, this is just how I read the situation, you'll find other academics (better qualified than me) who have a different view. That's the odd thing about academia...it's an abstract pursuit that has very real implications for society. Reaching consensus is the only way to implement what the myriad scientific opinions actually think should happen. Mix in political policy considerations and it's an exceptionally complex (and dynamic) situation to manage. Geography and economics complicate things even further. In terms of whether this was the first wave or a second one, it's kind of immaterial. The threat to life and our health services was real, irrespective of whether the virus had circulated previously. For what it's worth, there was a particularly nasty RSV infection notified before Christmas and I suspect this is what most people caught (and not SARS-CoV-2). If they did, then two waves of this virus has led to less than 10% of the population developing antibodies to it, so most of the population is still susceptible. I had something nasty before Christmas (I was also in China at the end of November 😧), but in all honesty, I really don't think it was this virus (I guess I'll find out when I eventually get a serology test!). There are encouraging signs from countries that have opened up a bit more over the last few weeks (apart from Iran). Spikes in cases are in predictable locations and in theory, it's still possible to contain once numbers get really low again....just needs to be done correctly! (though if what @crazyfool1 has described is widespread, then someone needs to get a hold of things and quickly!).
  5. No worries!...however, the problem with immune responses to common coronaviruses is that they don't last very long! 6-12 months is the commonly accepted duration (so we repeatedly get infected with them...and most common colds are caused by rhinoviruses anyway). Honestly, I've no idea how this might impact of a second wave or "herd immunity". I would still be placing a lot of my effort into containment using testing and contact tracing. Data on mask wearing is firming up as well, not sure how long governments can stick to "guidance" rather than making them mandatory in confined spaces.
  6. Honestly, it would be speculation...it is entirely possible of course, but I wouldn't pin all my hopes on it!
  7. 😜 Though if you had a cold recently, it might help...course, you don't know whether that cold you had over the winter was a coronavirus, or a rhinovirus, or a respiratory syncytial virus or an adenovirus or any number of other causes of the common cold...so, I wouldn't attach any certainty to it!
  8. Howdy, Had a quick read of the paper, very interesting stuff indeed! It starts to solidify ideas that have been floating around for a while (I wondered at the outset whether the relative resistance of children to this virus was rooted in their frequent exposure to other common coronaviruses... certainly more frequent and recent exposure than many adults...somewhere in this thread or one of the previous ones is a comment from me on them being little coronavirus factories!...I'm sure there are a bunch of other reasons too, especially pre-existing conditions and also how mature and immature immune systems respond to things). Cross reactivity with immune responses elicited by common colds is certainly a complication that was considered in the evaluation of the serology tests and it is tempting to speculate (and now with more precise information) that it plays a role in determining whether you develop mild/asymptomatic disease, or more serious symptoms. I joked to a colleague recently that the Jenner Institute should look a bit more closely at their name for the solution to the problem (ok, joked is a bit strong, it's a very nerdy observation!...but Edward Jenner's approach to vaccination for smallpox was to use cowpox (which is where the word vaccine comes from), a related but less deadly virus...obviously a vaccine that doesn't cause any disease is the best approach, but maybe if we all got a dose of common coronavirus, we could ride this one out). The paper doesn't prove this would work of course, and their data on common cold history is patchy (self-reported data almost always is), but they do see significant cross-reactivity between the immune response to other coronaviruses and those elicited in patients who caught this one but didn't need to go to hospital (and previous mouse work on SARS suggested the same thing happened with that virus as well). So, very interesting data, certainly sheds some light on what is currently being colourfully referred to as "immunological dark matter" (this isn't a real term by the way, but I know what he means by it...something certainly seems to make some individuals intrinsically immune to SARS-CoV-2) and it might also help us at least partly explain how infection progresses differently in different individuals...what it means for where we currently are is too early to say though.
  9. Very interesting! I work with a group that has been developing tests using exhaled breath condensate for cancer detection (It works very well!). I actually reviewed a submission by them to use this approach for detecting coronavirus (since they wanted to work with the virus in the university, it had to pass through our biosafety committee) and they are testing it at the moment. It's a different approach to this one in that it actually runs a rapid PCR, so it detects viral nucleic acids, whereas this one is based on resonance (which would be even quicker), so validation of the accuracy of this test is the key to it working, but it's exactly the type of game changer we need!. I guess the key question once accuracy is proven is whether you are infectious if you are below the detection threshold...if not, game on!
  10. Howdy, apologies for the delay, Wednesday mornings are busy, we have our lab meeting! So, in theory, inter-vaccine interference can influence how one vaccine impacts on another, but in general, these things are tested as part of the vaccine development and it's not a widespread phenomenon. Many vaccines can be combined safely and routinely are. All sorts of things can influence how well a vaccine works (interference from the actual virus you are trying to protect against, drugs, even the immunological makeup of the individual). The antibodies that we make are generally "polyclonal" i.e. they are directed at different parts of the virus (and even those generated via vaccination tend to be like this), so while potential for interaction exists, it's more likely that the immunological response elicited would just add to the pool of antibodies targeting coronaviruses. This can be a good thing, for example, repeated flu vaccinations with different strains builds up a pool of anti-influenza immunity in an individual (this is exactly why swine flu turned out to be less dangerous than it might have been since high risk populations had loads of prior flu shots). So, if the Oxford vaccine is safe and protects against potentially fatal complications and another more protective vaccine comes along later, then I wouldn't be too worried about getting the new one. My suspicion is though that in the timeframes outlined, access to both would be unlikely. High risk individuals would be more likely to get the first vaccine, with the rest of us getting the newer one later on. That's a scenario that would work though, since high risk individuals would have protection from serious disease, which would be bolstered by herd immunity in the general population gained via the next vaccine.
  11. Hi Nobby, yes, our case numbers are actual cases, not projected cases (I did see 8000 per day quoted somewhere for the UK and was confused as I thought it was closer to 2k and holding firm). If all of those are in high risk settings and not as a result of community transmission, then testing and contact tracing can (in theory) contain them. I was a little shocked at the level of training contact tracers in the UK were reported to have received (about 30 mins, a FAQ, a script and an instruction to look at videos on YouTube), whereas my own institution has trained about half of the contact tracers in Ireland and it was a week of face-to-face (socially distanced!) training. But whether that is actually the case or whether this was for extra bodies to bolster the system was not entirely clear from the reporting. I’m sure there must be some properly trained folk involved at some level. you are correct though, loads of things that would be happening still aren’t, so mostly it’s lower risk activities that are opening up again. I took the little one out for a ride on her bike yesterday. Our local park was packed, but it was of clusters of either families or 3/4 friends sitting on the grass a good 10-20 feet from each other. I saw nothing risky and found it uplifting to see people getting back to some sort of normality in a low risk way. The beach is also packed, but everyone is leaving plenty of space for each other, and queuing at shops etc is well organised, less browsing, and people are moving through quickly. So, at the moment, I don’t see vast amounts of high risk activity that could lead to a massive resurgence...unless containment in high risk settings is mismanaged. Personally, I’d leave the schools closed for the sake of a few weeks, and heaving pubs/clubs/gigs are still a way off. But now is the time to take stock of what we know about this specific virus and adapt our public heath plans from the influenza-driven protocols we used the outset, to coronavirus-specific plans to continue easing back to normal.
  12. Howdy, I honestly don’t know if the virus is “weakening”, but there is certainly a lot less of it about at the moment (which may explain lower viral loads)...I still think summer will have some impact on it (just based on what happens to other coronaviruses and respiratory viruses in general). There’s lots of people out and about now, but I do see significant changes in behaviour (there’s always some idiots, but many are being fairly sensible) so I too am optimistic (have been for a while, though to be fair, it’s my default position!...not based on blind optimism, but borne of a belief that if things are bad, we can always do something and change them). Really the key is having a robust surveillance system now...post-suppression you get the chance to go back to containment if you do it correctly, so that’s where the effort should be focussed and where clear information helps the public to play a role too. Still a good way to go, but there is definitely light at the end of the tunnel! edit: when looking at infection rates, there’s some important things to consider...look at the % positive tests, I haven’t paid close attention to the UK, but here, with similar numbers of tests per week, the % positive is steadily dropping. Also, where the positive cases are. Clusters in healthcare settings still pose a risk, but it’s not the same as chasing a virus that is rapidly spreading through the community. Again, haven’t seen breakdowns for the UK, but here, community transmission was all but extinguished a couple of weeks ago and the 50 or so cases per day we still get are in high risk settings...it was the same in most other places, so if not now, then soon it will be the same in the UK. Different countries have different capacities to deal with cases. France reckons 4000 cases per day is manageable for them, so, the UK will have a number in mind too. Again, if hospital admissions/ICU admissions are below trigger points, then things will open back up (and you can make your own personal assessment of risk and do things you are comfortable with, while avoiding things you think are too risky). If it starts to spread freely again and ICU admissions spike because of that, then a step back will occur. I was on a conference call with a doctor from London about 5 weeks ago (he had picked up COVID from a patient), but he said their hospital admissions had fallen off a cliff (ICU still had a fair few people in, but not full and admissions were way down). So, if that was the case on the ground in London 5 weeks or so ago, I’d expect it to be significantly better by now.
  13. Hi Chef, I think there a combination of factors at play (and to be completely honest, everything that follows is a guess, I have no data to support any of it, it's just what I think may be happening). If you think about it, with suppression, we have moved back to where we were at the beginning of the outbreak. Except that we weren't testing at the rate that we are now (the state of the testing regime may be questionable in some places, but it's certainly an order of magnitude better than it was at the outset). So, I suspect that in most countries that have exited lockdown, levels of infection in the community are significantly lower than they were in the few weeks leading up to lockdown. Hence, we are probably back to where we were in January, with isolated pockets of infection cropping up in different places. The difference between now and then is that we have seen what happens, are taking it a bit more seriously and have far superior testing capacity to contain any hotspots that pop up. It's what we should have been doing in January/February this year but we didn't think it could happen to us (typical eh!). It looks like there is a lot of cases in some places, but I suspect there were far more before we put restrictions in place a couple of months ago, we just weren't looking as hard for them. The seasonality/impact of warmer weather has always been suspected but nobody really knew if it would play out that way. It still may play a role, just can't say for sure yet. Also, most places that have exited lockdown, still have restrictions on things that have the potential to be super spreading events. Where clusters occur, they are in exactly the places you would predict (meat processing plants, warehouses, care homes, hospitals, clubs etc) where people are in close proximity and under conditions where shedding lots of virus is probable. So, allowing people back out, having social distancing guidelines in place, practicing good hand hygiene and avoiding super-spreading events has the potential to keep this contained and suppressed (and I still think source control with masks where close proximity is unavoidable should be mandatory rather than suggested). I know people are saying "but we had fewer cases when we locked down", however the key to opening back up again isn't the absolute numbers of cases, it's the trajectory of infections and the rate of hospital admissions (and ICU admissions) that are the triggers, so case numbers can be misleading as we are currently (probably) below where we were when we locked down (since we were testing a lot less back then) and if hospital capacity isn't threatened, then places will open back up again. To give you an example of this in practice, in Ireland, we locked down at 70 ICU admissions. Capacity is about 400 and the projection (based on the trajectory of infections) was that with the 2 weeks it takes from infection to hospital admission, that ICU numbers would double within a week and double again in two weeks...meaning that we would be close to capacity within 2 weeks, so the place needed to shut down. That's exactly what happened, within a week ICU numbers were over 160, within 2 weeks they were at 384. But having closed the country down 2 weeks previously, the didn't go higher than that so capacity was never breached. They opened back up again when ICU admissions dipped below 70 again (so the date for relaxing lockdown got pushed out further a couple of times until this was the case). With 3 weeks between each phase, it's easier to keep an eye on what the infection rate is doing and move to the next phase (or stay where you are/go back should the trajectory of infections start to climb steeply again). The UK is using exactly the same triggers, there is just higher capacity (due to the higher population...per capita it's slightly less, but it's in the same ballpark). So, if infection rates are falling, hospital admission are falling and ICU admissions are below the trigger points, then irrespective of the headline case numbers, opening back up is what will happen....until the triggers are breached again and restrictions have to be reimposed. But, we have more data now on what might drive higher case numbers, so it can be a bit more nuanced than it was first time and hopefully we can avoid full scale lockdown again. Sorry, I'm rambling! Edit: Oh, and the "it plays itself out in 70 days" thing...it does if you do something about it. Nobody has let it rip through their population (even the Swedes), so I suspect it would take longer than 70 days without some kind of public health intervention....and the fatality rates would be just like the models predicted (since nothing that has happened so far has proven the models wrong).
  14. I need to work on the old brevity alright! 😁
  15. @stuartbert two hats @jparx @crazyfool1 Apologies for the delay! I was in a grants committee meeting...just about to have lunch, but I'll have a quick go at answering! So, the oxford vaccine...it's basically an engineered adenovirus (another virus that causes the common cold, weakened for use in the vaccine). It has the spikes of this new coronavirus inserted into it, so should elicit an immune response to this virus. It's not an entirely "traditional" vaccine in that old school vaccines either use dead versions of the same virus, weakened (attenuated) versions of the same virus, or they use parts of the same virus (subunit vaccines) that you are trying to protect against. In that sense, it's a newer approach to vaccine development (one they have been working on building a platform for in order to make all sorts of vaccines). The data from the pre-clinical study suggested exactly as our dual-hatted friend has outlined...doesn't stop you from getting infected, but does stop you developing pneumonia and decreases the amount of virus in the lungs. So, on the surface, it looks useful and could protect against more serious disease. This is why the further trials are going ahead and if it stopped people from dying, it would have the added bonus of facilitating herd immunity without the risk of trying it naturally. A word of caution though...the pre-clinical study was small, extrapolating from that to how it will function in humans is not guaranteed. Also, pneumonia is only one reason people who develop COVID die. There are other fairly frequent causes of death (coagulation problems especially) and many many organs other than the lungs have receptors for this virus, so how it protects against these other possible complications is currently unknown (I need to read through the paper again to see if they addressed this). It's promising, but many a vaccine (or drug) has failed at phase 3. The good thing is that there are a bunch of other vaccines at advanced stages too (and some of those are more "traditional" vaccines), so if this one doesn't make it, there's a chance one of the others will (actually, more than one possibly will and people will end up getting different vaccines along the line to meet demand). The antibody test that is being offered for sale is the Abbott one that PHE are using. It was designed to work on blood drawn by a healthcare professional, so hasn't been validated for use as a finger prick test. It could still work, they just don't know how accurate it is yet if blood is collected in this manner. I believe that is what they are now validating (i.e., compare the results of tests with blood drawn in different ways to see if you get the same result). If there's no difference in accuracy, then I'd expect it to be available for sale again.
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