Professors Nick Loman, Alan McNally, and K K Cheng gave an insightful discussion on their expertise and views on coronavirus, and showed how Birmingham is playing an instrumental role in tracking the virus.
View the video on YouTube
Date of recording: 19/11/2020
Webinar speakers: AR - Professor Alice Roberts, KKC - Professor K K Cheng, NL - Professor Nick Loman, AM - Professor Alan McNally
Audience questions from: BK - Brian Kirkland, MB - Mahjabeen Begum, TM - Thelma Mattock, MH - Melanie Hopper, GM - Gavin Maggs, AB - Amy Barber
Video Length: 1:16:05
AR: … on mapping the virus. I’m Alice Roberts, Professor of Public Engagement at the University of Birmingham and I’m joined this lunchtime by three colleagues who are going to share their expertise and answer questions – Professor K K Cheng, Professor Alan McNally and Professor Nick Loman. This event is part of the Bringing Birmingham to You series which is staged by our alumni office, enabling Birmingham academics to engage with our global alumni community. We cover a great range of different subject areas in this series. Academics discuss and share their latest research and findings in a way which we hope opens that knowledge up to everybody and gives our alumni community a chance to meet and hear from some of the brilliant Birmingham people who are leading the way in science and in the arts and humanities. We’re really pleased today that some of our Rowbotham Fellows are joining us – welcome. So today our topic is ‘Mapping the Virus’. The spread of Covid is one of the biggest challenges humanity has faced in recent history and leading research teams at the University of Birmingham have played a key role in trying to understand the virus through genomic sequencing and mapping transmission rates, in order to forge a path through this difficult and uncertain terrain. Today, you know, it is absolutely clear in no uncertain terms the work of these colleagues of mine at the University of Birmingham will save lives and they’re here to share some of that work with you today. But before they do, I have a little bit of housekeeping to do. Firstly a reminder that we’re recording this webinar and it is going to be interactive, so we’re inviting you to submit your questions via the Q&A box. I know some have already submitted questions via email, thank you very much, and we’ll try to get to as many of them as possible during the webinar. Now you may be invited to pose your question directly to the panel and if you are then your mic will be turned on; we’ll do that for you. If you’d rather not ask your question directly or you’d like to remain anonymous, please let us know in that Q&A box and please, you know, feel free to use that chat function through the webinar as well.
… OK, time for some proper introductions then. Professor KK Cheng is a Professor of Public Health and Primary Care and he’s also the Director of the Applied Health Research Institute at the University of Birmingham. His main interests are epidemiology and prevention and control of non-communicable diseases, and also the development of primary care in China so he’s got a very interesting perspective there. During the pandemic, KK was among the first researchers in Western countries to advocate the importance of mask wearing. He’s been very vocal about that and very prominent on social media – mask wearing in the community to control the pandemic. KK, what are you focusing on right now?
KKC: Thank you. As you introduced, a feel a bit of a pretender because my main interest really has always been on non-communicable disease, but with the issue of masks, my colleagues from China rang me in January and said ‘why are you guys not wearing masks?’ and that started my interest in this area and I’ve done a bit of efficacy to argue for the case of masks. So I’m pleased at least now there’s a reasonably good uptake of mask wearing, although really in public transport, in supermarkets, there’s still some problems. So my main interest has moved on a little bit from that. But my preoccupation, it’s not really research, it’s within the university we’ve got a lot of students who when they came back from the summer holidays there was a bit of a spike in the campus so we did a little bit of public health work within the university to make sure that this problem doesn’t get out of hand. Thank you.
AR: Thank you, KK. We’ve also got with us Professor Alan McNally who is Professor in Microbial Genomics and the Director of the Institute of Microbiology and Infection at the University of Birmingham. Alan’s work focuses on the evolutionary genomics of pathogenesis and antimicrobial resistance in bacterial pathogens, but in April Alan was seconded to the Milton Keynes Lighthouse Lab as the Lead for Infectious Disease at the government’s first flagship Covid-19 testing facility and he’s currently heading up the new Covid testing lab at the University of Birmingham. So Alan, it’s been a busy year for you.
AM Yes, thank you, Alice. Yes it has. Yeah, I used to work in virology a long, long time ago, about 15 years ago when I was back as a postdoctoral researcher and I worked on avian influenza and it’s come back to haunt me I guess. I was asked if I would go and help set up the Lighthouse Lab in Milton Keynes, which was fantastic and then when I came back to Birmingham I was asked if we could set up a testing lab in the university, which is now up and running and we test all of the samples taken across the city of Birmingham, here in our lab, and we pass those onto Nick to do his thing as well. And actually at the moment I’m completely preoccupied with – we are requisitioning the university’s Great Hall at the moment so that we can test all of our students with rapid test kits, beginning on Wednesday the 2nd December, to allow them to travel home for Christmas. So I’m working round the clock on that at the moment.
AR Brilliant, thanks Alan. Onto our third panellist today, Professor Nick Loman works as Professor of Microbial Genomics and Bio-Informatics in the Institute for Microbiology and Infection at the university. He uses cutting-edge genomics and meta-genomics – that’s the genomes of everything that isn’t human; mostly pathogens – to approach the diagnosis, treatment and surveillance of infectious disease. Nick recently helped establish real-time genomic surveillance of Ebola in Guinea and his current work focuses on the development of novel sequencing and bio-informatics methods to help interpret genome and meta-genome data because, as you can imagine, there’s a lot of it in both clinical and public health microbiology. Now Nick, did you see Covid-19 coming?
NL I think we didn’t see it coming exactly how it did but it was absolutely a pandemic was on our radar and has been for quite some time and as you mentioned, we’ve been tracking Ebola around – latterly Zika – and I think it was just a matter of time until we found a global pandemic pathogen that would wreak this amount of both medical and economic damage. It’s certainly been something the WHO and other organisations have been warning against for some time. So I think people were slightly taken aback that it was a coronavirus but that was certainly well within the expectations of the source of pathogen that we might see emerge and cause this amount of devastation, frankly.
AR Thank you very much. I mean I think it’s interesting that it’s been up there on the risk register for so long and yet it does seem to have caught the entire world by surprise and I think, you know, whatever we’re doing now presumably will put us in good stead for the next one because this isn’t going to be the last one, clearly. I’m going to get onto the discussion then and as you can imagine, as soon as we made it public that we’d be doing this event today, we started to receive a lot of questions. Some of them we’ve been able to condense so there was some duplication and we’re also going to hear some live questions as well, so thank you for asking live questions if you’re going to be doing that today. But let me start with one of these questions that’s come in and it does get straight to the point. The question is, ‘what are the main reasons behind the disastrous record of the UK in this pandemic?’. Who’d like to start with that one? Alan? Oh, KK, we’ll start with you then.
KKC There’s a long list of reasons and I don’t want to rehearse all the reasons which are probably quite well known to the audience, but I think the root cause of the problem is that we probably underestimated the potential impact of the virus and we treated it for a little while like the influenza virus and therefore assuming that it’s not containable. But many countries in Asia, Australia, New Zealand, have shown that this is not true, that we can actually contain it while we wait for the vaccines to come on board. In this country we did not suffer from SARS and in 2003 SARS only had a tiny impact on us. For a number of years I’ve felt grateful about this because it’s quite horrendous, in 2003 in China, in some other countries like Canada, Singapore and so on, but in retrospect now actually I thought if we had a slightly bigger problem with SARS we’d have managed Covid differently I think. In early March we had a misconception that this dichotomy between health and economy as well, and the government differs on the basis because if you lockdown, the economy will die and so on, but we now know that actually the two are the same. Actually if you don’t control the virus, bad health means a bad economy.
AR Alan, would you like to comment on that particular question; why have we had such a disastrous record? Why are we continuing to have a disastrous record? You know, this is the second time that we’ve had a wave, we seem to be doing particularly badly again.
AM Well, I think Nick can answer better on why the second wave’s occurred, but I think from my own biased point of view, in 2005 I worked on avian influenza and the reason avian influenza never really became a problem in the United Kingdom is because we had an absolutely fantastic surveillance system, you know, a really comprehensive testing and surveillance system and for years we’ve under-funded things like Public Health England and NHS testing and surveillance systems and I think our inability to handle the number of tests that we had to do early absolutely had a profound impact on how bad the pandemic got in the United Kingdom. We just didn’t have the ability to test as much as we needed and that meant that we couldn’t get ahead of transmission chains and unfortunately we saw that again in September; we didn’t seem to be prepared for the fact that when schools and universities went back, there would be a huge increase in respiratory infections and a huge demand for tests and that again meant we didn’t get ahead of transmission by testing and isolating infected individuals. So I think testing played a big role in it as well.
AR And just to come back to you on that one, Alan, I mean could we have ramped up testing to the point where we could have dealt with that upsurge of infections at that time? Did we have the time to do that? If we’d thrown the cash at it, could we have done it?
AM I think we did throw the cash at it, if you look at the Lighthouse Labs. I think what I argued at the time, and the reason I went to the Lighthouse Lab was because I realised that they were going to be the only option, but at the time I argued very strongly that what we should do was create a network of labs across the country using universities, using medical schools, using university laboratories that they wouldn’t have got there immediately but within say a month they would have been able to get themselves up and running as validated, accredited testing labs, and clearly we didn’t go down that route and it meant that the Lighthouse Labs, because of their size, took maybe a month longer and so we were well into April/May by the time we had the testing capacity we needed, which was too late.
AR Are we switching over now? Are we starting to use that, you know, the capacity existed and we had the equipment sitting there in universities, are we starting to make use of that now?
AM Yes, we are. I mean the testing capacity has changed dramatically and testing capacity is very good now, you know, our lab is the first of a number of university labs that will come online into the national testing programme. We obviously now have the rapid tests like the lateral flow devices that are being used. I think our testing capacity is excellent at the moment. I still sometimes think we could do a little bit of work on the strategy behind their use but I think the capacity’s got much better.
AR Nick, is there anything you’d like to add there and particularly thinking about the second wave that we’re experiencing now and why we seem to be doing so badly once again?
NL Yeah, I mean I think something that I lament is the strategy very early on was probably that this was going to be very difficult to contain and that the main thrust of the government’s strategy was to try and really try and protect the health service and prevent the NHS being overwhelmed. I think in retrospect, you know, it would have been better to at least attempt the so-called zero Covid strategy. You know, countries like China have gone for that strategy, South Korea, Australia and New Zealand, all very effectively have attempted to ensure every time you see a Covid case, it’s tracked down and those chains of transmission are eliminated by use of quarantine and isolation. That can be a really effective strategy. We’ve seen it now in many countries, it can be a really effective strategy but it only really works if the level of, you know, the incidence is pretty low. One of the things we found out quite early on with the genomic analysis was that we had a really very large number of introductions of Covid into the UK and I think people had a sense that Covid came in through half-term and skiing holidays, people returning, but the analysis showed it was actually a lot more widespread than that and actually it was past half-term, it was kind of early March we had a huge number of separate introductions of Covid distributed very evenly across the whole of the UK and conservatively we think at least 1,500 individuals returned and resulted in downstream transmission. That makes life very difficult because that’s 1,500 separate chains of transmission that all need to be tracked, traced and isolated and as Alan said, we just didn’t have the infrastructure to deal with that because, you know, it’s very hard to scale up that infrastructure. I think the other thing is that everyone’s pretty convinced that lockdown was a couple of weeks too late on that basis. I think what’s more disappointing is the situation over summer because the current analysis is basically showing we’ve had exactly the same problem again, we’ve had exactly similar, folk have gone off on holidays, they were encouraged to go off on summer holidays to keep the travel industry alive, keep the restaurant industry alive and hospitality, and we’ve imported a lot more again and we’ve ended up, as Alan said, the double-whammy of a lot more importations plus we’ve got the problem of it getting colder, everyone going inside and the schools reopening and again, it’s just overwhelmed the test, trace and isolate. So the test, trace and isolate is a brilliant idea but it doesn’t scale to huge numbers of cases and so that for me is the one thing that we could have addressed better.
AR Thank you, Nick. I’ve immediately got more questions of my own but I’m meant to be chairing this, not just asking my own questions. So I’d like to bring in one of our attendees then, Brian Kirkland. Brian, are you there and ready to ask your question?
BK Yes, I am here. Can you hear me?
AR We can. Go ahead.
BK Good. OK, I had a few questions but I’m going to ask one about the way the virus passes. It seems to pass very easily between people. We also know that at least half the people who have the virus don’t have any symptoms. These two characteristics suggest to me that actually it’s going to be around for quite a long time and it’s going to be very difficult to eliminate it. Do the panel agree with that? And do we know whether or not asymptomatic cases are as likely to pass on the infection as people with symptoms? And what about people who have been vaccinated and then come into contact with the virus, are they likely to be able to pass it on? I mean obviously we haven’t got the experience with this virus but we must have the experience from other viruses.
AR Thank you, Brian. I think probably that is a question for you first, KK. I mean this is an insidious virus isn’t it? I mean if it was all symptomatic it would be so much easier to track it surely?
KKC Absolutely, but Brian also asked a question whether we can eliminate it. I don’t think we can eliminate it as such. We tried very hard with smallpox and at the end we managed to eradicate it, with polio coming pretty close. But we’re not talking about elimination, we’re talking about really public health interventions, including vaccines that are going to come on board. We’re going to be able to contain it and limit the problems. We don’t understand immunology of this field very well. If we had Paul Moss, who is a Professor of Haematology on the call here, he would be talking to us about – because he leads the national consortium on immunology – and we don’t know actually long term if many people get infected and so on, you know, this virus is a coronavirus and there are four seasonal coronaviruses that only cause mild common cold like symptoms. So after a few years or a couple of decades, whether it will just become something like this pandemic virus that cause maybe minimal problems plus a bit of vaccination then we put it under control. But asymptomatic sharing of viruses is a major problem and if we ever talk about masks, that will be a key issue why we want people to wear masks.
AR So clearly then, KK, asymptomatic people are able to pass this virus on?
KKC Well yeah, absolutely, I think it’s extremely difficult to estimate the exact proportion but easily 40, 50% of the transmission could come from people who are asymptomatic or pre-symptomatic, you know, they are people who remain asymptomatic throughout but there are people also who one or two days before their symptoms occur are already shedding viruses.
AR Alan and Nick, do you want to comment on that question at all?
NL I completely agree. I mean this is going to be an endemic virus. It’s so widespread globally that it’s not going away any time soon and we do hope and expect that the use of vaccines will certainly reduce the amount of virus circulating but the idea of eliminating it globally – and remember that has to be both in human populations and in all the susceptible animal populations of which there are probably quite significant reservoirs, including the mink that are in the headlines at the moment. I think it’s going to take a long time and may not be possible to completely eradicate it. I just wanted to make a comment about endemic disease because I think there’s an assumption that a disease that becomes endemic and circulates for a long time in the population must become more benign, you know, must eventually adapt to humans and become not a big problem. There’s no actual reason that that’s the case. It could tick along at exactly the same kind of infection fatality rate as we have now, it could get worse, it could get better, but we track these mutations and we track what’s happening to the virus and I think it’s just worth saying that the idea of it becoming endemic is probably not a good thing, you know, there’s no reason to think just like so many other viruses that are endemic like HIV for example, Hepatitis, they don’t necessarily get any better in terms of how the infection goes for an individual. So you know, vaccines are clearly our way out of this.
AR Yeah, from an evolutionary point of view there’s no reason for it to adopt a more benign characteristic if it’s managing to spread through a population perfectly well as it is.
NL Exactly.
AR If it’s managing to, you know, cause the amount of fatality it’s causing but actually still get passed on..
NL Exactly and I think the selection for a virus is on transmissibility so, you know, if the virus wants anything it’s to infect more people. So whether you get sick or whether you die as a result is almost irrelevant for the evolutionary angle. In fact it’s quite interesting because our work has shown that there have been several mutations now that look to increase transmissibility but don’t have much of an impact on virulence or pathogenesis. One called 614-G, we showed in the UK data that that probably does increase the R, increases the transmissibility, but doesn’t have much of an impact on whether you need to have oxygen in hospital or whether you die.
AR I think it’s absolutely fascinating and extremely useful to our strategies, obviously, the amount of detail we know about this virus, Nick, and so much of that is down to genomics. When you talk about the number of introductions into Britain, presumably that entirely depends on being able to effectively genotype all those different strains that entered the country.
NL Yeah, exactly. In the UK we’re part of a networked called ‘COG’ – Coronavirus Genomics UK Consortium – and Birmingham is a really big part of that Network where we’re just really trying to sequence the genomes of as many viruses as we can. Currently the total is well over 100,000 and that’s more than half of the global total of the viruses that have been sequenced, so the UK is really at the vanguard of this. It’s interesting because these viruses, they’re pretty similar to each other but there are very small differences that we can detect, you know, a handful of mutations between any given virus from a patient in the UK, tells us an awful lot about the evolutionary trajectory and it will allow us as we introduce more treatments and more vaccines, to see almost instantly whether we’re putting a selection pression, we’re influencing the evolution of that virus by introducing those vaccines. That is probably for me the most exciting thing that we’re about to learn about the virus, you know, how adept is it at evading a vaccine? How much opportunity has it got to mutate and to escape our interventions, or is it a bit of a lame duck in that regard? We literally will not know that until we introduce those vaccines.
AR Great. Well we’ve got more questions coming in I can see but I’m going to go to one of our previously submitted questions, which is about interventions. So obviously, you know, we’re having to assess what we’re doing as we go along here and do this very, very quickly. Are there problems with the way that we appraise evidence of intervention measures? Can I come to you, Alan, first with that one.
AM I’m going to ask if we can go to KK on that first!
AR OK, that’s fine! KK, do you think there are any issues then with the way that we’re – because obviously, you know, it has to be evidence based – how quickly are we able to collect evidence and really know if the interventions that we’re putting in place are the right ones?
KKC Can I use the example of masks to illustrate what I’m going to talk about because I think it’s a sad example of how we actually misinterpret what we mean by ‘evidence based medicine’. In the last 30 years, this concept ‘evidence based medicine’ has been established as the base of clinical decisions. Specifically we have come to rely on evidence from clinical trials in guiding treatments rather than on clinical experience of doctors. A few decades ago, experienced doctors would say ‘well, I’ve always treated them like this’, then they treat them like that. But now, thankfully, in the health service it doesn’t happen like that. But so they’re serviced quite well in healthcare but in this pandemic, the fact that there hasn’t been clinical trials that have been done to test if people wear masks would reduce transmissions via the mechanism of source control, was actually used as a main reason for not recommending mask wearing. And there was obviously also the worry that if the government recommended masks early on then the public would panic buy and worsen the problem of mask shortage for healthcare workers. But as we’ve said about asymptomatic transmission, since February we know that virus shedding happens in effected people who are pre-symptomatic or asymptomatic and we know from mechanistic studies that if we put a piece of cloth in front of the mouth and nose, it will actually reduce the risk of infection arising from droplets coming out of our airways. And we’ve seen this demonstrated vividly in this infrared imaging, using infrared cameras we can see droplets actually coming out of our mouth when we speak and we put a mask on, it dramatically reduces that. So it’s not clinical trials, it’s really mechanistic evidence that for a long time, for two or three months if you watched the 5pm Downing Street press conferences, every few days the Minister or scientific advisor would be asked ‘what about masks?’ and they always said ‘there’s no evidence’ and the WHO adopt a similar approach like that in this pandemic. That’s the only point when I disagreed with the WHO. I think they’ve done a splendid job, but on masks I wrote something in the BMJ questioning the guidance. So this very dogmatic thing of evidence based medicine means clinical trials has actually damaged our efforts.
AR Thank you very much. I mean yeah, certainly the hegemony of the RCT, you know, the randomised control trial, is absolutely the gold standard if we want to assess an intervention and we’ve got plenty of time to do it and, you know, time to sit on our laurels waiting for the results to come back. But actually we’ve got to look at other forms of data when we’ve got an epidemic – a pandemic – unfurling before our very eyes. Do either of the other two panellists want to respond to that Alan?
AM Yeah, I wasn’t avoiding the question I just thought KK was much better placed to answer it. But no, I agree entirely. I mean I got so frustrated, you know, there was all of this – as KK said, we were doing lots of assumptions around influenza and lots of assumptions about what might or might not prevent transmission. We got bogged down with whether or not Covid was airborne or aerosol and actually it was very clear that we had to minimise person to person contact to reduce Covid and it took ages for us to come to the decision to say ‘OK, we’re going to minimise restrictions on people’s activities, we’re going to close bars, we’re going to close restaurants’, when it was absolutely clear that how this virus spread was when two people get in close proximity to each other but we got so bogged down in trying to find evidence for it and it was very frustrating that everything was about modelling flu rather than just looking at what was happening in other countries.
NL Yeah, I agree with that, Alan, but I also think, you know, the infectious disease model has got a very hard time over Covid but actually in retrospect, quite a lot of the models were extremely good I think. I think the other thing that is notable is that the modelling of different, what they call NPIs – non-pharmaceutical interventions – is actually extremely good. So we can quite precisely understand what the effect on the R number will be with different restrictions, you know, so if we open restaurants and pubs versus closing schools, dare I say universities, mixing in households, all of those openings or closings have an impact on the R number that is actually quite well understood. I think what we saw over summer is we got, you know, the R was consistently a bit below 1, which is obviously where everyone wanted it, and the real problem was you basically want to open up, you want to have fewer restrictions, you obviously want kids to go back to school – I certainly did want the kids to go back to school! – and we want those things to happen but of course you can’t have everything. If you allow everything, the R number inevitably goes up over 1 and I think that’s where we’ve had a problem, you know, using the evidence which was that we’ve basically done things that we knew wouldn’t work, that we couldn’t control the epidemic and have the freedoms that we felt that we needed as a society. So I kind of lament the fact that we haven’t had that conversation more openly as a society, like we’ve all had the opportunity to contribute our thoughts about what’s most important to keep open and what’s not important and to influence that. That always has felt like a top-down imposed decision and I think it’s actually a question for all of us to contribute our thoughts to. So I think that’s one of our problems.
AR Yeah, we’ve got lots more questions coming in which I’m going to move onto but I completely agree with you, Nick, and from the perspective of public engagement with science there hasn’t been enough dialogue and there hasn’t been enough engagement with communities about doing this together and a very obvious example of that is the way that schools were reopened with very – I mean a few schools managed to do engagement with their parents, with their families, and work out ways of minimising risk. Most schools didn’t do that at all and were just told from the top ‘you just open, we’re not giving you any extra resources. Tell everyone it’s safe, get them back in’ and there was no engagement at all. Anyway, anyway, moving onto more questions. We’ve had a lot of questions obviously, you wouldn’t be surprised, about vaccines and I think we’ve got someone who is going to ask a live question about vaccines. So Mahjabeen Begum, are you there? Mahjabeen, are you there? Go ahead, ask your question.
MB Hi, can you hear me? Hi.
AR Yes we can.
MB Hi, thank you for having me. Yeah, obviously we’ve heard recently in the news regarding the Pfizer and BioNTech vaccine and it’s been heralded as a success. I just wanted to know what your panellists thoughts were and how confident they were really regarding its efficacy, bearing in mind obviously we do have some of the population now spiralling anti-vaccine conspiracy theories and things like that. So it’s just giving us some context I think in relation to what their thoughts were regarding this vaccine really. That’s all, thank you.
AR Thank you very much. So how effective is this vaccine going to be then. Who wants to start with that one? I’m going to pick on someone then. Alan?
AM Yeah, look, I think I would say the same as any scientist, whether they’re vaccinologists or an epidemiologist. We’re all kind of sitting waiting to see what the data actually looks like but what we’ve seen is a couple of press releases with snippets of data that look very exciting but none of us really know how any of the vaccines have performed in the clinical trials yet and I think, you know, as that data starts to come into the public domain we’ll know more. Clearly, you know, the snippets of information that we’re being fed suggest there’s more than just a small reason to be hopeful about these. The data looks clear that certainly in the vaccinated groups there were fewer cases of Covid disease. We don’t know if that actually means there are fewer cases of Covid infection and of course that’s important because we come back to the point of asymptomatic transmission. But there’s reasons to be hopeful and, you know, I think even at the moment if we have a vaccine that prevents disease, we’d still all take that, you know, because it’s one more weapon in our arsenal of being able to prevent Covid deaths. So I think that’s about as much as we can say at the moment.
AR Nick, I think you’d like to comment on that question as well.
NL Yeah, I mean I agree and I think the good thing is there’s lots of reason to be optimistic about vaccines because there are so many in different phases of testing and the early results from the MRNA vaccines does, on the face of it, look extremely promising. I think it’s inevitable we’ll look back in a year’s time and some of these vaccines that looked great in Phase III maybe weren’t so good in reality, but we’ve got so many candidate vaccines being developed, I’m feeling extremely confident that we’ll have at least a few good options next year. I also think it’s really interesting that two of these vaccines that you mentioned reported recently are these MRNA type vaccines which, you know, this would be I think - I‘m not a vaccinologist but I think this would be the first example of MRNA vaccines making it out into general use and that to me as someone who’s interested in the genome is incredibly exciting because it gives a very clear route for vaccines to Covid to any mutations that we encounter in coronavirus, and also other viruses, being able to go from a very clear link from the genome sequence and the genes that are important in immune responses, to a vaccine through the delivery systems that have been developed is incredibly exciting. So I really hope that they do work out but if they don’t, in the end there are some more conventional type vaccines. I think everyone has high hopes for the ChAdOx1 from Oxford. I think that’s one that people are expecting to work well and I suspect we’ll find out about that quite soon as well.
AR KK?
KKC Normally when there’s a public euphoria, the optimism is usually misplaced but in this case I don’t think it is. I think really it’s something to rejoice on. The government has placed an order for, I think, 7 vaccines on several different platforms and the two MRNA vaccines with the early results showed an extremely promising 94.5/95% efficacy. The Oxford one is probably due to report any time but no-one knows because, well, you know, no one knows, the committee will be looking very carefully. But the question mentioned the important thing at the end whether it works would depend heavily on the uptake. At least in this country I don’t think there’s a lot of mad anti-vaccine people and I’m very pleased about that. We must make sure that when we are asked to go forward for vaccines, we take it on board and we really go and get ourselves vaccinated because the population effectiveness depends heavily – apart from the efficacy – depends heavily on the uptake rate as well.
AR Thank you very much. I had a question which had come in earlier as well which follows up on Mahjabeen’s question – thank you very much for your question, Mahjabeen – which is about when we might – I mean this is looking into the future, this is crystal ball time, I’m sorry about this – but when might we be able to start vaccinating at scale? Do you have a feel for that because, you know, sometimes you hear people saying, you know, with confidence that we’ll be doing this by the middle of next year. Do you think that’s reasonable? What do you think, KK?
KKC The two American ones, American/German ones, is going through FDA approval anytime soon I think and they will fast track it no doubt. The Oxford one, as soon as the results come out I think MHRA will probably look at it very, very quickly. I wouldn’t be surprised if the first person receives a vaccine outside of a trial in this country before Christmas. But on mass scale I think we’re talking about spring sometime, so gradually over spring and logistically it’s not a small issue but I’m confident that by March or April a lot of people who are the most vulnerable will probably have got it.
AR Thank you very much. And we’ve kind of strayed into this territory where we’ve mentioned the fact that even if a vaccine is available, it doesn’t mean that everybody is going to have that vaccine, which I find quite extraordinary that you wouldn’t be rushing out to grab it. We seem to have rising levels of miscommunication and misinformation about anti-vaccination generally and I don’t know whether this is home grown or coming from the States but it certainly seems to be on the rise and I wondered if any of you had a perspective on that – how to combat it and how damaging it could be. Nick, I’m going to pick on you.
NL Yeah, I mean clearly anti-vac sentiments have been increasing over the years and I think it all dates back to unfortunately the Wakefield debacle over the MMR, but that’s certainly become a cause célèbre for many people and it’s absolutely – I mean for those of us who work in infectious disease and public health, it’s just awful because vaccines are and have been one of the singular triumphs of modern medicine and responsible for saving so many lives and so much suffering and to see them impugned is just distressing for all of us. More generally though, you know, I’m someone like Alan and I think KK as well, who spend a lot of time – and yourself, Alice – spend a lot of time on social media, and particularly Twitter, and what has been really noticeable is the shift in narrative about Covid-19 over the course. I think at the start in January/February/March there was a general level of concern, there was a general appetite for information and science and I think most people were on the same page in terms of this being a pretty dangerous virus that we didn’t want firstly to come to the UK and secondly to infect a lot of people. Over the summer we’ve really noticed that narrative shifting to this idea of Covid denial and the idea that certain new terms like ‘casedemic’, so there are lots and lots of cases but actually no-one’s really getting very ill and no-one’s dying. That kind of narrative has strengthened and grown over the past few months and clearly this is partly an artificially constructed narrative with perhaps some powerful folk behind these narratives driving them forward and it’s very similar to the political situation with other political issues that we’ve seen. There’s not much to say about that other than the fact that it’s just a very noticeable phenomenon and it’s a really difficult thing for us as scientists who enjoy interacting with the public and talking about science, it’s made our lives really quite difficult and t’s really damaged I think morale for those of us who I think are trying to help. So I’ll just say that really.
AR Well I hope it doesn’t damage morale too much and don’t stop, please don’t stop because I think one of the things that we really have to do is still be out there as scientists talking about the science and making sure that we don’t just have this flood of misinformation and anti-science out there. Alan, would you like to speak to this particular point?
AM Yeah, I mean I’ve been on the receiving end of some terrible utterable beatings on social media over the last month. I think the thing – and I can understand it from a human nature point of view. I think what’s happened over the last couple of months is people have stopped listening to expert opinion and instead they’ve started to seek out a voice or a narrative that they feel more comfortable with and that’s been the big challenge. A lot of the narrative around Covid isn’t nice to listen to, the reality of it, and people then naturally have searched and searched for a narrative that suits what they want to hear and you know, I agree with you 100%, despite some of the abuse I’ve been subjected to, the way I see it is if I can get through to a couple of people and convince them that actually this is the message you should be listening to, then I think I’ve succeeded. I’m not going to get through to everyone but I think it is really important that we continue to try and get the right information out.
AR Thank you. I mean yeah, it is getting that information out and communicating feeds into this whole issue of life and death which is incredibly important. We have got a question from one of our attendees here which is about what we might learn from the virus in the future and how it might change the way that we treat disease more widely actually. So I’m hoping that Thelma is there to ask her question. Thelma, are you there? Thelma Mattock. There she is.
TM Hello, the panel. There have been many theories as to how this virus originated. In your view, was the virus man-made in a lab and did it actually originate in Wuhan or some other place? Thank you.
AR Oh, KK, what do you think about that? Where did this virus come from? Is it manufactured?
KKC I think a group of eminent scientists have looked at this question and there’s absolutely no evidence that it’s man-made and it is – well, I’m not a virologist, but I don’t think we have the capacity to make a virus like that.
AR Nick?
NL Yeah, we don’t – I mean that’s probably a very strong reason why it’s not man-made. As far as we know we wouldn’t be able to do it. The idea of constructing a virus essentially from de novo is an impossibly difficult task. So, you know, I think the question is are there any indications for example in the genome of artefacts that would suggest that there’d been some genetic engineering or any kind of changes that were man-made. All the analysis that we’ve seen and that we’ve done has said this is what a coronavirus that is circulating in the wild, in an animal reservoir, most likely a bat reservoir with potentially and intermediate host before it got to the human populations, this is exactly what it would look like. And that’s the most parsimonious explanation, that this is not the first time this has happened, this is not the first time a coronavirus has entered a human population. Of course SARS is a great example of a kind of fairly recent introduction, again from an animal population. There are a few things that we can say from the genomes that are kind of categorically true, that are kind of objectively true. One of the things that we’re really good at is dating viruses. So if we take a lot of different viral genome sequences that we’ve collected and we know when they were collected, we can estimate what’s called the ‘evolutionary rate’. The evolutionary rate is simply a clock – how many mutations do we see occurring over a given timescale? – and interestingly most viruses have a very stable clock and so the clock rate for SARS-CoV-2, which is the virus that causes Covid-19, is about two mutations a month and so what that means is with almost to the day precision, we can say what was the ancestor? When did the ancestor of all the cases that are circulating globally now, when did that exist? Over time that estimate’s got more and more refined and we basically put it into the middle of November last year and our confidence in that number is incredibly high. So the interesting thing about that is that that correlates entirely with the narrative of where the virus came from, so somewhere around Wuhan – not necessarily the seafood market actually but certainly the first cases were detected in Wuhan – and in fact the first confirmed case was recently said to be November the 17th. So there’s nothing there that’s suspicious and what I like about the genomics is it means that I can tell people with absolute confidence, if they say ‘you know, I think I had Covid last summer because I had very similar symptoms’ or ‘I went to China, I went to Wuhan’ or wherever, there is basically no chance that anyone had Covid before about that date because every virus that we’ve seen dates back to that individual. That’s a very useful thing to know. There is still a question mark about whether it could have escaped from a lab. It’s not impossible but it’s not the most likely explanation. There are lots and lots of animals with a huge reservoir of coronaviruses, particularly in that particular region of China. We know they’re out there, we know there are plenty of opportunities for humans to come into contact with them, either directly or indirectly, and so there’s no reason to search for an alternative explanation.
AR Thank you, Nick. Well it teed up Thelma’s question saying it was going to be something about how we treat other diseases in the future; it was actually about where this one came from. But we have got a questioner who is keen to ask a question about how coping with this pandemic and the aftermath of it might change how we treat diseases in the future. I think she’s there to ask her question now. Melanie Hooper. Melanie, are you there?
MH I am, can you hear me?
AR Yes. Sorry, Melanie Hopper.
MH Thank you. Yes, so my topic is to do with chronic illness, as a chronic illness advocate. There’s two parts, so the first one is to do with whether you see the current focus on long Covid becoming a positive step towards understanding and treating conditions such as ME that’s so far been severely under-funded and under-researched, despite the prevalence. The second part is whether you think this will kind of help fast track treatment of viruses such as Epstein-Barr which has a correlation with conditions like Multiple Sclerosis.
AR KK, would you like to take that one?
KKC It’s a very difficult one I think. I agree with you, there are certain conditions that are not as well researched as others. Well you know, cancer and heart disease are very well researched but some of the maybe less common ones, but nonetheless cause huge morbidity and mortality for those that are affected. Long Covid is a new condition and we don’t know the pathogenesis particularly well. We know that it probably affects 1 in about 20 of those who have got symptoms; that’s an estimate, and I’m pleased that more and more research now, the government is funding quite a lot of research into looking at this problem, we have a cohort of patients who were discharged from hospital and now also interestingly are looking at people who did not quite get sick enough to go to hospital but are more in the community. I think those research, it will probably – I hope you are right, Melanie, that it will actually throw light on how we manage some of the conditions which might at the end be related. For example, there’s some evidence that long Covid might behave something like an auto-immune condition with some auto-antibodies to some of our own body tissue. So it may actually work in a funny way to create some new knowledge about treatment of some auto-immune diseases.
AR Thank you. Alan, you’d like to comment on that as well.
AM Yeah, I think it’s an excellent question. I think at the moment we’re in the phase with Covid and SARS-CoV-2 where we are currently trying to put out an enormous fire. I think what we’ll see in the next couple of years is more fundamental, what I call ‘classical virology research’ and it will be around things like long Covid and the pathogenesis and what exactly are the different pathologies and infection. I would absolutely hope that there will be a big funding push towards that. There will be lots of people studying it and that hopefully will spill into the other kind of long term chronic conditions that come from viral infections that you mentioned. I think what’s really needed is if you think about what’s happening at the moment around Covid, you know, Covid is now the most tested foreign infectious disease we’ve ever had in this country, essentially. If you think about the number of people in the country that have been tested for Covid and we have this enormous bank of data now that we can cross-reference back to, you know, and if people do start to develop chronic conditions over the next 5, 10 years, we can correlate it all back to the testing we’ve done and we can really get to the heart of how big an issue long Covid’s going to be. Chronic disease and chronic indifference happen all the time. I think we’ve got a really quite unique opportunity to cross-reference that back to viral infection.
AR Thank you very much. We’ve got another question now from Gavin. Gavin, are you there? Here he is. Ask your question.
G I am. Yes, thank you. Afternoon panel, I’ve found it very interesting. I was wondering if there’s a way of combining all the various disciplines that we have within the university, acknowledging that we don’t have vaccinology – if that’s a word – to create a sort of Centre for Viral Resilience or a way of trying to reduce the impact of this happening again that’s not just the scientists who are on the call, but social policy, education, psychology and the like. How would we as Birmingham, can we do that?
AR So an inter-disciplinary approach and can universities start to forge those links between disciplines.
G Yeah.
AR Alan?
AM Yeah, I mean I think Birmingham’s a good example of how that’s happened. I mean I hadn’t worked on virology for 15 years and here I am knee-deep in the pandemic and you know, Nick clearly has done more recent stuff on virology, but if you look across the university campus, every discipline we have has got involved in Covid, whether it’s Covid research or the fight against it, and that goes from the social scientists to Law and Policy researchers to, you now, epidemiology, public health research. So we kind of have done that. I think talking about creating new centres and institutes, you know, maybe in the long run we’ll think about this. Actually there was a conversation at university level the other day about putting together a sort of degree course around pandemic preparedness and infectious diseases that would bring in all of the people that could contribute to it across the university. I think the one thing I think about this pandemic, if there’s any positives to be had in a horrible situation, is that as an infectious disease researcher it’s made me rethink what infectious disease research means and it doesn’t just mean playing around with bugs in a lab. It means what are the societal impacts, how does it affect policy, how does it affect the economy, and so I think there will be a move towards more inter-disciplinary infectious disease research as a result of what’s happened over the last 10 months or so.
AR Thank you. Do either of the other two of you want to comment on that?
KKC Maybe just very briefly.
AR Yes, KK.
KKC I think after the pandemic, I think there are many issues which this pandemic has exposed and the disciplines that Gavin mentioned in terms of helping us to rebuild better or having this awful thing, a ‘new n normality’, how we have actually a better society will be something that’s truly multi-disciplinary. I think it would be great if the – I think there will be plenty of interest in the university for colleagues to work together to do something like that.
AR Thank you. Here’s one of the pre-submitted questions. This one kind of feeds into some of the misinformation that we’ve heard about already. Are there lots of false positive tests for Covid? Alan, he’s got his head on the desk! [laughing]
AM This has plagued me since March and, you know, the amount of misinformation that circulates around testing is phenomenal. And why people would want to think that a test isn’t good or doesn’t work, I just can’t even fathom why people would want to press that narrative. But very clearly, the test works. It works brilliantly and we have millions and millions of testing data points now so that we can absolutely, with precision, pinpoint what the cut-off is for real infection. That cut-off for real infection, it’s a CT value and basically the test that we use in the UK, we have to amplify not just one gene of the virus, we have to amplify two genes independently at what’s called a CT value under 35. So that is essentially we know with absolute certainty that there’s virus in that sample. Now one thing we don’t know is does that mean that person’s infectious? We don’t know that. Clearly they’re probably symptomatic because they’ve decided to go and get a test. You would imagine therefore they’re not feeling great in some way, but we don’t know if that means they’re infectious or not. But there’s no casedemic, there are no false positive – there will always be the odd false positive PCRs but the rise we see in Covid is not because of really bad testing. The testing in the UK is excellent. I could bore people with the amount of documentation I’ve had to produce just for the government to say that our lab is good enough to do the testing.
AR Thank you, that is a definitive answer, although you did use a slightly strange statistic there. Can you change it into percentages for us? If there any false positives, what kind of a percentage do they make up of the..
AM The best data for that is the longitudinal survey that’s been conducted by the Office for National Statistics who are continuously monitoring people’s infectious status and from that data, the false positive rate seems to be around about 0.08%.
AR That’s a pretty good test then.
AM [Nodding]
AR OK, so we can put that one to bed. Basically if you get a positive Covid test, you’ve got Covid. You haven’t got some other coronavirus, it’s not a cough or a cold virus, it is actually Covid.
AM The specificity of the test is exceptional as well. It’s not a false result.
AR Thank you very much. Oh go on then, Nick, you can jump in on that one too.
NL I would just say one thing that’s been really difficult to communicate well and I think perhaps the BBC and the media have not done a great job is when we look at these two waves if you like, the case curve at the start around March peaking in April and now, those are not comparable waves because we had almost no testing at the start and so the way that we found out about cases were people that were admitted to hospital were pretty much the only people that were getting tested back in March and April. Now we have very, very extensive testing because of the efforts of Alan and colleagues and so I think there’s a natural discrepancy between the original, it looked like there were very few cases but lots and lots of deaths at the start, and now there are lots and lots of cases but relatively fewer deaths and that is entirely explained by the change in the testing. There’s so much more testing goes on now but that’s led to people saying that the virus has got less virulent, we’re much better at treating it. It’s not really that; it’s purely that mismatch between tests and cases but the infection fatality rate has sadly stayed more or less the same but reduced a bit we think.
AR Just picking up on some of the comments here in the chat and I have to ask off the back of that last question, what about false negatives? Alan?
AM So, false negatives, I think they’re a far bigger issue than false positives. We control for them as much as we can. Where false negatives will tend to occur is if the swab hasn’t been taken particularly well – false negatives, sorry – so if the swab isn’t taken very well there’s a chance you may not pick up enough virus to detect it. We control for that as much as we can. There’s an inbuilt control in the PCR that also detects a gene found in humans, so we can tell if there’s human material on the swab and if we find that and we don’t find virus, we have slightly more confidence that that’s not the case that actually the swab’s been taken OK. The other way false negatives can happen is of course when you get tested. If you get tested towards the end of symptoms, the virus might have fallen very low and you won’t detect it. Similarly if you get tested very early – and this is where the issue is with asymptomatic testing – if you get tested before symptoms, you might not find the virus because there isn’t enough to find and that’s a big thing that I’m trying to communicate at the moment with the use of testing for students to send them home for Christmas. We’re testing people who don’t have symptoms and the result only applies for the next 24 hours, you know, it’s your status at that time. But we do as much as we can to control the false negatives.
AR I think we have probably a final question coming up here and it’s from Amy Barber. Amy, are you here with us? Amy?
AB Yes, I’m here. Can you hear me?
AR Yes we can. Go ahead.
AB I’d just like to ask, why have there been such strong symptoms to this virus? Is it simply because it’s new to our immune systems? And has it been affecting populations globally differently at all?
AR So who would like to take that one. Why are we seeing such diversity – well, a strong effect but also such diversity in it? Do any of the three of you –
AM I think I’ll have that one. As an ex-virologist I’ll have a bash at the severity of the symptoms. I think we really don’t know, as I said, the period for intense research, proper virology research on this virus, will come once we’ve got on top of it I think. But, you know, what we do know is, as you mentioned, this is a brand new virus essentially to the human population which means there’s no background immunity. But also just the virus brings to a particular type of receptors and those are found on the vast majority of cells in the body. So what we see with every severe cases of Covid is actually it’s not a respiratory infection, it’s a multi-system infection, you know, we have brain bleeds, we have infections of major organs and so actually I think the idea that it’s a respiratory infection, clearly that’s how we get infected by breathing it in but actually if you get a really bad infection with SARS-CoV-2, what you get is infection of multiple organs and that’s just a result of the molecules on our cells that it binds to and the fact that they’re present in lots and lots of different cells.
AR Thank you, Alan. Nick?
NL There’s likely to be an underlying affect of human genetics and there have been some preliminary studies with associations with severe disease, you know, the interferon family of genes keeps coming up as a potential hit. I think over time there are studies going on to try and link the human genetics with severity and I won’t be surprised if there is a reasonably strong link to human genetics an outcome, but I think at the moment the jury’s still out on how important that is. The other factor that may be important is cross-immunity from other coronaviruses. SARS-CoV-2 is a novel virus but it shares a lot of similarities with other human endemic coronaviruses and it is possible that different levels of exposure to other coronaviruses have some modulating effect as well. So I think it will be a balance of those two things, I suspect.
AR Thank you very much. You know, I am going to squeeze in another question because we’ve just about got time for it. And it’s a question that was pre-submitted by Amy Williams. Unfortunately she’s not here on the call so I’m going to channel Amy Williams and ask you this question. She says, one huge concern I have for Birmingham’s response to Covid-19, including vaccination, is the city’s wonderful diversity. How can we ensure the response is effective across genetic, biological and cultural backgrounds? So how can we try to strip out some of the inequality that we’re already seeing in terms of the infection in our cities? I wonder if I could come to you, KK first with that particular question.
KKC Quite a lot of the inequalities – let’s stick to ethnic status – is not just about genetics, it’s actually about the circumstances of living that people from different ethnic groups or different lifetime experience and opportunities. I think there’s a lot of social disparities out there which I think in this post-pandemic world we must try to address properly. In this pandemic we have this ‘Black Lives Matter’ issue and we have seen these great disparities between different occupational groups. For example, during the first wave it was women who had the higher risk of infection, although more men died. So more women actually caught the virus; it’s because many of them did the essential jobs that kept society going and this kind of inequality is a variation I think. I’m pleased that Amy has raised this question and it’s absolutely crucial that as a university we must address this when the peace returns.
AR Thank you so much. Nick?
NL I think it’s a really important question and it’s something that’s on our minds. One really good opportunity we have now, and it’s the first time that we’ve had this chance, is because Alan’s got this testing lab on campus serving Birmingham postcodes and beyond, and because we have this link to genomic sequencing, we’re trying to push that in real time. So as soon as Alan gets a positive, we’ll try and genome sequence it within 24 hours. We’re going to use that information for the first time now to try and track clusters. So we’ve been doing this in the hospital quite effectively for a while looking at links between patients and understanding the role of hospital acquired infections, but we’re going to try and do this in the community now. So the idea is w will try and detect very, very quickly growing clusters of cases and then we’re going to, working with our local public health departments in Birmingham, we’re going to let them know that we have detected clusters that we think might be linked. What we’re really hoping and expecting is that that’s going to have an impact on public health teams’ ability to respond to growing outbreaks, whether those are workplace associated or often household or mixing associated in households and I think in Birmingham we’re going to really try and push this new model - we call it ‘real-time genomic surveillance’ – and for the first time try and do that at community scale. I think that is hopefully, you know, watch this space but hopefully over the winter that’s going to really pay off and pay dividends. And I hope that will help address the whole of the Birmingham and the West Midlands area and as you say, the rich diversity we have in this region.
AR Alan?
AM Very, very quick. I think there’s also reasons to be really confident and hopeful that that social demographic mix that we have in Birmingham, we will reach it all. You look at some of our Directors of Public Health – Justin Varney, Lisa McNally – they’ve done phenomenal jobs at reaching what other parts of the country have been difficult to reach communities with regards to educating them about Covid and testing them and we’ve got wonderful Directors of Public Health in the region who I have absolute confidence this will not be an issue for us.
AR Thank you very much and with that I’m going to bring the Q&A to a close. We did have lots of questions, thank you very very much. I would like to invite each of you to just leave us with a closing remark. Thirty seconds if you can. This is your chance to sum up everything we’ve just talked about over the course of lunchtime in thirty seconds. KK?
KKC It was Armistice Day last week. In 1918 the Armistice was signed at 5.45 in the morning on that day but the ceasefires did not take effect until 11 o’clock. Between these several hours, over 2,500 people died so we’ve got vaccines coming on board now, on line now, so please in the meantime don’t die during this period. We must work together, work harder. Birmingham has been very much damaged in this Covid time; we have over 1,500 people dying from Covid so listen to the government advice - social distancing, wash your hands wear a mask.
AR Thank you. Nick?
NL Very similar thoughts. Firstly thank you for everyone who attended the webinar and asked such good questions, it’s been really fun. Yeah, I think biologically the virus hasn’t changed. We’re basically dealing with the same – despite the mutations we’re dealing with essentially the same virus that we learnt about for the first time in January. We don’t yet have a vaccine but vaccines are coming. We all want to have a nice Christmas with our families but you know, none of that changes the fundamentals of transmission, you know, there’s very high prevalence in the UK, very high in the West Midlands in fact. Wanting it to go away doesn’t make it go away. Everyone on this webinar should now understand enough about transmission and I’m sure you knew this already, that transmission is predominantly through close contact particularly in indoor spaces, in poorly ventilated spaces. As KK says, wear a mask. We can’t rely on government advice to keep you safe entirely. Use your own intuition, your own understanding of the virus and as KK said, we’ve got to get through winter. I think a vaccine will be coming but yeah, try and avoid it; it’s a sacrifice but I think it’s one well worth paying.
AR Alan, a final word from you?
AM They’ve stolen all the good points. I guess what I would say is, you know, everyone’s yearning for a ‘can we go back to normal?’ and I think coronavirus is here to stay. The impact it’s currently having isn’t here to say but coronavirus is here for a while. I guess what I would encourage people to think about is do we want to go back to the old ‘normal’ or actually what could a new better normal look like? There’s lots of things that can change on the back of the pandemic. Pandemics have changed the course of human history, you know, the Black Death, the 1918 Flu – they changed the courses of human history. This might be our chance to change things for the better. There’s a hell of a lot of other things need change in the world beyond coronavirus and this might be a chance to just piggy-back and do things better.
AR Thank you for ending on that optimistic note, Alan. And thank you everyone for attending today’s Bringing Birmingham to You event on mapping the virus. We had nearly a hundred questions coming in so thank you so much for all of those. We tried to cover as much ground as possible with those questions and I hope you feel that some of yours have been answered. I’m sure you’ll all be virtually joining with me to thank our fantastic panel – Prof K K Cheng, Prof Alan McNally and Prof Nick Loman – for being here today, but also for all the work they’re doing to help protect us and our families. We had one particularly wonderful comment that came in when we were talking about social media from Barbara Fogherty and I’m just going to read that out. ‘Please don’t be depressed’ - this is for the panel – ‘please don’t be depressed by the change in social media narrative; the silent majority are fascinated by the science and very grateful for the amazingly huge strides made in all areas of detection, modelling and prevention’. And of course I can remind you all that all three of our scientists here today are very active on social media as well, so please do follow them, particularly on Twitter, and they’ll keep you updated. As we continue this series online we’re keen to hear from you about areas of research that you’re interested, that you think should be a focus for future webinars, so please do share your suggestions with my colleagues in the alumni office. And finally thank you to them for staging the event today, for all the support behind the scenes that you haven’t seen but we’ve been very grateful for. And absolutely finally, we’d love your feedback. When I disappear, when we all disappear from your screens, you’ll still be able to use the chat function and there’s a very short feedback survey there and that will help us to plan future events. I do hope you’ve enjoyed this one and found it worthwhile. Thank you again everybody. Until next time, stay safe, keep well.
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