If you do not test, you will not know - a focus on COVID-19

Clare Taylor: 0:15

Welcome folks to ESWI Airborne. You're listening to the podcast of the European Scientific Working Group on Influenza, otherwise known as ESWI. Today's episode is part of a series on intervention strategies, bringing you the latest developments and insights from research on how respiratory virus infections can be detected and treated. In particular, COVID-19, the virus that caused one of the world's most deadly epidemics in recent years, is what we're talking about here today, and I am delighted to welcome our three expert speakers. First up we have Dr Xavier Lopez Labrador, Senior National Health System Investigator at Fisabio, Public Health and Associate Professor at the Medical School of the University of Valencia, Spain, and Xavier's main interests, his lab's main interests include hepatitis viruses, respiratory viruses, virus epidemiology and metagenomics. He is also an executive member of the European Society for Clinical Virology. Welcome, Xavier, to ESWI Airborne.

Dr Xavier Lopez Labrador : 1:23

Thank you, thank you for having me and a pleasure to be here with you today.

Clare Taylor: 1:27

Okay, awesome, up going to a northerly place now we're going to hear from Dr Pontus Nordenfelt, associate Professor at Lund University in Sweden. Pontus is a man on a mission. He is committed to a quantitative understanding of immunology, cell biology and microbiology, with a strong interest in antibody function. Welcome, Pontus.

Dr Pontus Nordenfelt: 1:53

Thank you so much Clare.

Clare Taylor: 1:55

And finally, a familiar voice for regular ESWI listeners ESWE board member, clinician, researcher and all-round superman of the lowlands, Marco Goeijnbier, is with us today. How are you doing, Marco?

Marco Goeijnbier: 2:07

Very well, always a pleasure, Clare

Clare Taylor: 2:09

Thank you so much. So, folks, let's dive right in. Where are we now with COVID-19? I've heard various different statements from major public health authorities. Is this endemic, with periodic epidemics? What do you agree? What's the state of play here?

Yeah, well, where are we? Well, in the case for the Netherlands, we did gain 70 million virologists over one pandemic. Some of them have to consider to retire now. But virus-wise it's very interesting and I agree that to some extent with your statement that COVID or SARS-CoV-2 being endemic now. It's one of the notorious severe acute respiratory infections, or SARI pathogens, and maybe we slowly see some seasonality occurring. But that's a bit under debate because you definitely see short upsurges now smaller outbreaks. But I'm not really sure what you think, Xavier.

I think we may be beginning to see an endemicity, but I'm not sure about it. So there is a year-round circulation and there are mainly two peaks, one in the wintertime and another in the summer. But in my opinion they can still change with the evolution of a new variant which is going to be escaping immunity. We still don't know. But also we are still waiting for the stabilisation of the other respiratory viruses circulation, in my opinion. So this season that we are in now may be the first one with flu going into full power again, and then we will have to see whether there is a room for SARS-CoV-2 in the wintertime or not. So that's still to be determined.

Absolutely agree there that it's very interesting how SARS-CoV-2 is behaving now, but it's also just as interesting to see the other respiratory pathogens coming back and returning into seasonality or not.

Clare Taylor: 4:04

And so that's an interesting concept whether there's actually room in the winter season for different viruses to get along, and in terms of what we have to think of, like what the risks are from SARS-CoV-2 infections now, are new variants and long COVID two of the biggest threats for people, or what would you say here?

Well, that's not really an easy one, Clare. New variants or mutations in general play a role in upsurges, outbreaks and seasonality. Covid is not that severe now at least in the hospital, as it was during the start of the pandemic, but still a very, very serious disease, specifically in those with underlying comorbidities and decreased immunity. So currently new variants might be a factor in the occurrence of new outbreak, but much more attention should be put also towards vaccination coverage, efficacy and so on, timing on vaccination, duration of protection or even co-administration with other respiratory pathogens. So it's really multifactorial here. Of course, long COVID is a really big issue. I think there was also a specific podcast on long COVID. We can talk for hours on long COVID. So of course everything plays an important role: New variants, long COVID but it's not . biggest one or the biggest threat in my opinion

I'm curious about your other here opinion about whether we will see a new sort of morbid variant that will cause severe morbidity, and or whether we just see lesser variants over the over, over the time, so to speak it's.

It's a bit of a gamble, right, because everything we predicted so far we were often wrong or the scientific community was often wrong. COVID kept surprising us, but we did see, after the pandemic, that suddenly, for instance, mycoplasma pneumoniae or RSV was much more lethal, much more severe. Xavier mentioned that this might be the very first heavy flu season, but last flu season 2023, 2024 in the Netherlands, there was also a moment where every ICU capacity was taken due to severe influenza. More recently we did see some very, very severe COVID cases in Western Europe, but then again, my basic specialism is critical care, so I'm really at the end of the story. So maybe I'm not the best person to ask. Maybe Xavier has a better answer than me.

Well, I don't have a real answer yet because I mean we don't know what's going to happen this season with the flu. But we have the feeling that it's slightly the late season, so it's not really on the normal spot yet, but we haven't seen a lot of SARS-CoV-2 cases in the last months. I mean, we are only looking for hospital admissions, so people with severe disease which require admission, and there's been kind of a decline of SARS-CoV-2 cases and then RSV and flu are taking over. So how this is going to end in the winter we don't know. But we're very curious that this is going to be a difference. So we don't know yet. I wouldn't bet for being seasonal next year, so 2025, yet I would wait maybe for another season.

Clare Taylor: 7:23

Okay, we'll have to meet back here in a year's time and see who was right. Maybe we'll take bets at the end of this episode, but what I am hearing from you is that it continued, although we feel maybe in the media and so on, the kind of warning has receded that there's still a risk of serious illness and hospitalisation, so vaccination remains very important. Are the vaccines changing to deal with new variants, and do you think this will become as standardised as the annual flu shot?

Oh well, I think it's becoming clear that the boosters are helpful, and it probably will be very clear this season with what is happening, Because now in Europe we have a dominant variant which was starting to dominate after summer, which is most closely related to the last vaccine booster. So the strain use for the 2024 booster is an updated vaccine and that is giving more neutralising capacity to this new recombinant variant which is now dominating in the wintertime. And, on the contrary, it's been shown as well that people with the outdated 2023 booster have not such a good neutralisation. So SIDA from patients with a 2023 booster are not neutralising enough as SIDA from patients with the 2024 booster update, which that means, probably, that we will need to continue monitoring. And then this data supports the current recommendation of updating the COVID vaccine booster to provide, especially to provide protection against severe outcomes. And then I see that.

But isn't that also a big problem there, Xavier. You're talking about boosters, so the often extra vaccines, boosters, every half year, every year, and then also we have the, the yearly flu vaccine, and then we have the introduction of the RSV vaccine. Isn't that the biggest problem, that people are getting a little bit tired of vaccines?

Oh yeah , that's another important question what's going to happen when we get the RSV vaccine in place and then also so the introduction of a second booster, because France has approved to give a booster in the spring for a particularly sensitive population with the highest risk for severe So how is it going to be vaccine hesitancy when we have this in place? And actually we have also to take into account that the best month for vaccination is not necessarily overlapping for the three big players RSV, flu and SARS-CoV-2. So we don't know, we don't have the solution yet. How can we manage with this triple vaccination in risk groups? And are we going to need a spring vaccination and then late autumn vaccination, so two vaccination rounds? We don't know, and we don't know how SARS-CoV-2 is going to fit in that window period. Are we going to give, as last season here in Spain, both flu and SARS-CoV-2 vaccinations at the same time, knowing that it's not maybe the best for SARS-CoV-2. One potential option is that well, it's given by the, because RSV vaccines will be probably not given every year, but there is a trend of thinking that that we will need, like, two vaccination campaigns. I don't know if you agree with that.

Well I I do agree to it looking at the efficacy, but on the other uh, there's only so many times people want to get a shot per year. I think we have to decrease So I think most efforts should be put in in combination, but I don't know Pontus wants to add there.

yeah I know, I agree, and I was thinking about the new vaccination platforms essentially whether . there's a way to MRNA mrna vaccines, for instance, eat more easier to to break the timing as well that we were previously part of this cycle with influenza. I don't know. I think there needs to be innovation in that regard as well.

Clare Taylor: 12:10

a really interesting mix of human and administrative and scientific problems coming together. But, Pantas, Pontus if we can stay with you for a moment, and really I'm kind of curious if you can help us unpack your scientific research, because, as I understand it, you use a range of techniques to study host-pathogen interactions, so you look at what is actually happening at the cell level. Is that right when there's an infection? And can you tell us more about your work? This is antibody discovery and antibody function and what it means.

I just want to start by saying that my lab has previously focused on antibacterial antibodies. That was our primary research area, but then the pandemic hit and we, as everyone else that could tried to figure out can we help in any way? So we looked at the platform that we had developed, because we were working with group A, streptococci, which is a human specific pathogen, and there were problems getting antibodies and still is towards this pathogen. I want to explore that. And so we had building a platform that was human centric, where we took blood from humans in this case patients that had been recently infected and then from that blood take out the B cells, which are the antibody-producing cells, and then from those genes we could then express monoclonal antibodies, and the rationale being that if we can have antibodies that have been made in humans against human pathogens, we might have a better shot at finding the good ones, so to speak. So I mean, that's the background where we are in terms of discovery. But then how do you find a good versus a bad or non-functional antibody? So that's why we spent many years setting up many different experimental setups to measure these monoclonal antibodies very carefully.

How do you measure that Pontus? Because, for instance, I was on call this night I have a severe soft tissue infection patient in the critical care due to group a streptococcus and eventually we just decide to give immunoglobulins. Then we give every, every antibody that's there, so so we give IVIG.

That is actually interesting. That was our starting point, because in IVIG, you don't really know what antibodies you give. So we wanted to develop a few specific ones that we knew were good, that we could supplement IVIG with, for instance, that could hopefully improve this. So what we focused on in terms of bacteria was phagocytosis, so we tried to measure that process really, really carefully and and it is much more complicated than it sounds. So, in fact, it's essentially measuring how many of our white blood cells eat the bacteria or eat viruses, but it's quite tricky to get very accurate measurements that you can compare over time and actually tease out small differences between a good and a bad antibody. And then we measure complement activation. We measure ability for antibodies to agglutinate, so it's to aggregate bacterial viruses and many other aspects we measure in detail. So, using that, I mean this was a long background, but that's where we started. This was in March 2020, pandemic just hit Sweden. We managed to get our hands on seven patients who were critically ill. We got blood from them and then could purify B cells and generate a number of antibodies. And so, since we were not a virus lab from the beginning and we knew that everyone else was focusing on in virology, typically neutralising antibodies we thought, okay, we won't help out much by doing what everyone else is doing. So we focused on what we were better at, phagocytosis or other functions that are not linked to neutralisation specifically. So we found and tested quite early on that if we took an antibody that's bound to spike protein of SARS-CoV-2, but in a place where it didn't neutralise, some of these antibodies could actually protect just as well in an animal model as a neutralising antibody, just by being really good at phagocytosis. And we've been continuing along those lines, exploring those aspects. How can we improve these other functions to essentially trigger the immune system to become better at fighting the infection instead of blocking the infection from happening from the start.

Clare Taylor: 17:05

And Pontus you have published on this. Do you have a reference for us?

Yes, so we have a perhaps easier to take that. We published a review article in Trends in Immunology in 2024. So is Armani Izadi, the first author, and then I was the last author. Here we summarised our thoughts on this, and also we're, of course, not alone in the field. It's an enormous field, the source of the research. Many other labs are also exploring these areas.

Clare Taylor: 17:38

Of course, how long a journey is it between where you are with it now and there's actually people in in Marco's clinical setting being treated?

I mean, this was actually in terms of using monoclonal antibodies. That was before the vaccines, actually, but then they focused on the neutralising aspects. If we want to go around the route of our so-called non-neutralised antibodies, it doesn't necessarily need to be that long away. It depends on the need and the clinic, I would say, because what they would offer these antibodies. So the problem with the neutralising ones is that they are focusing on an area, a very small target area, the epitope that the antibody is binding to, which is heavily mutated and under a strong evolutionary pressure. The neutralising antibodies tend to lose function over time quite quickly, whereas if you target other areas that are evolutionary conserved, that are completely necessary for the virus to function, then those antibodies might be able to bind longer, and also across multiple viruses as well, even to other beta coronaviruses. So we call these broadly protective antibodies. So there I think it could be of interest, because if you can make antibodies like that, they can be kept at the clinic for years and be useful for many different scenarios. So that, I think, is a very interesting thought and might be interesting also to pharmaceutical companies to explore in the future, because they won't lose function as quickly as a neutralising antibody. But antibodies are expensive.

And Pontus, as an antibody specialist there, I would love to hear your opinion. So after the pandemic in the Netherlands we saw a huge increase of group A streptococcus invasive infections in the past two years, I think 300-400%. Could you postulate anything? Is that about the loss of antibody due to social distancing?

Yes, I think you're right that is the major hypothesis here that we saw an enormous decrease in group A strep infections during the pandemic. It essentially vanished and we expected it to come back, but we didn't really expect to come back this hard. So it appears that we probably benefit from having constant exposure to group A strep because most of us are in contact with it quite routinely and most of us have a good immune response to group A strep. So we can handle it and probably train our immune system to keep handling it.

So I'm linking this with the current outbreak of metapneumoviruses in China, right, that also it may be because of a declined posture during the last year and the years with the pandemic.

That's an interesting one, because hMPV was the only one of the other viruses RSV and flu in the Netherlands that kept relatively stable during the pandemic, so RSV and influenza completely vanished, while hMPV was continuously still there at lower rates.

I have a question for Pontus, a very quick one. Are you linking the non-neutralising antibodies correlation with the T cell response? Because for other infections we see that neutralising antibodies actually are not absolutely necessary or detectable in protected individuals, right? So what do you think about the T cell responses linked to these non-neutralising, broadly protective antibodies? Is there any correlation?

I think most likely that you need a good T cell response actually to generate the antibodies, to get the T helper response, at least for viruses. It's a completely different story I think for bacteria it's much more complicated, but for viruses, yeah, t cells are probably very important here. But I haven't studied and I'm not an expert on the T cell response, I wouldn't want to go further than saying that they're important.

Clare Taylor: 22:12

Pontus, is your work important for diagnostics? I mean, do you learn more from this about an individual's immune response?

Yes, thank you for that. I think we are learning and this is something which is kind of interesting that when we developed these different methods to measure antibody function, we focused on these monoclonal antibodies they're the only one but then we applied that also to serum samples and also IVIG that Marco mentioned, where you have a much more complicated system. We have many antibodies binding to the same target in different ways, and I think that is something that diagnostics is right now not covering particularly well. You get information about if you have an antibody response at all. If you have antibodies that are binding, but you don't get information about what they're doing. You have to correct me if I'm wrong, but I haven't gotten that indication from the clinic that you're understanding or measuring how the antibodies are, just that you have the antibodies. So what I'm thinking and hoping for the long term is that these that we and others have been building over the years is that, if you can make them simple enough, you can take serum from patients, run them through and actually get a quick answer to whether a patient has a good immune response to certain pathogens. That could then give information whether they are at risk for certain types of infections, and I'm thinking particularly about immunocompromised individuals that maybe have lower or especially lower, where you still have some immune response, but are they vulnerable to certain pathogens, for instance. But we're pretty far from that yet.

Clare Taylor: 24:02

Okay, well, no harm to look into the crystal ball from where we are now and stay with diagnostics, especially because we have Xavier with us and you really know a lot about this. I think you led the charge during the pandemic right with the emergency diagnostics lab and scaled extremely rapidly. What was this like?

To make a long story short, I mean it was challenging kind of this topic at the time, but very rewarding at the end of the day. Because we have an active surveillance platform where the Fisabio is actually the research and reference part for the regional public health laboratory. But the regional public health laboratory deals mostly with environmental, food and water microbiology. But we were from 2012 to 2013, we have a platform for active surveillance of respiratory viruses in hospitals. So we have a network of 5 to 10 hospitals that we sample during the flu season. That's what we were doing and we already had from then, so 10 years on a panel of 20 something respiratory viruses being tested regularly. So we had the platform in place and we were asked by two sides because we also belong to a global network, the Global Influenza Hospital Network. And then WHO asked the network to do retrospective testing for when COVID was starting to circulate and at that time so we have a curfew and all the people in the lab were sent home and I was alone by myself setting up the PCR and then testing, well, I tested something like 3,500, so 3,500 samples by myself, just to see when it started to circulate, and that was something like 16 hours per day. And then, at the same time, putting in place the in-house PCR assay for SARS-CoV-2 to transfer it to the regional public health laboratory. And we did it and it was stressful. And then in April we already started the emergency lab with 200 samples per day capacity. This is a small lab, it's not hospital-based, it's a regional public health lab. And then by the end of April we were just going through 1,000 samples per day on two shifts with a robotised platform. What I found fundamental was the capacity of the government to let you buy whatever you wanted even in a public institution and for this, the state of emergency was fundamental because that allowed the administratives to buy whatever you wanted. So we were timely, able to get four robotic platforms and get that capacity in 30 days, which allowed us to test nursing homes, basically, and help hospitals who had lack of supplies, because we choose for alternative methods which were not in vitro IVD proof at the time. But that was what we did. So we tried not to overlap with the regions and supplies that were needed at the hospitals and actually we had a break of supply from the two major robotic platforms that we already had, which were commercial. So we went to an open platform and several suppliers, and that was the thing. So it was a stressful but very rewarding at the end of the day.

I just want to comment, I think, this mindset that we all had during the pandemic of just getting things done and getting rid of unnecessary bureaucracy. It was so fantastic to see, and we were hoping I think a lot of us that after the pandemic we should have learned that. Okay, now we know how we should do it, but I have the feeling that everything is just regressing back to the normal.

Almost need another pandemic right.

Clare Taylor: 28:50

No, steady now, Marco.

No, but I absolutely agree with Pontus there.

Well, maybe because we have a kind of a post-traumatic disorder now, but I hope we have an imprinting of what pandemics meant to us. So getting rid of the superfluous administrative requirements for a public institution for us was fundamental.

Clare Taylor: 29:15

And Xavier, have you seen work on diagnostics? Have you seen their techniques continue to evolve since the emergency was over, let's say, or do you feel it's stalled?

Well during the first year, what we saw we did the gradual availability of a manufactured, developed test. But we, for the first year I think, we did mostly in-house testing, but then, steadily, we had even national capacity for producing most of the tests, which is so. We had even national capacity for producing most of the tests So what I saw for the whole last three years, four years general updating of all the microbiology labs in the hospital and in public health, extensive upgrade to robotic platforms, high throughput platforms, which were limited mostly for research at the time, and then also the expansion of test availability for different and diverse manufacturers, just to avoid what happened, the bottlenecks and if you were sticking to one or two platforms you could get, I mean without supplies. And then most diagnostic labs in Spain now are 24-7, serving capacity. And also well there was an steadily increase on the use of syndromic testing panels. And that I don't know for the clinical side and I will ask maybe Marco so, if he thinks it's this sustainable, because there was a reimbursement, either the government or someone has to reimburse that. Or maybe we have to move some machines for respiratory disease for testing the big three first, so RSV, flu and SARS-CoV-2, and then perform syndromic testing if the clinician requires it. How do you think about that?

So syndromic testing would be that you test for specific symptoms, a specific panel. So, for instance, somebody that comes in with respiratory complaints you sit in the respiratory panel and which pathogens are in the respiratory panel. I think that's an interesting discussion. If this is sustainable, Xavier, I think we could record a completely different podcast there and talk for at least an hour. So I'm a big fan of test as much as you can and get your panel as big as you can. And that's because in the hospital I work I have the luxury position that we actually have a respiratory panel at the door at the emergency department with 13 . T. hat made that we discovered the mycoplasm upsurge after COVID very early, the hMPV upsurge that's now shown in China. We saw an increase in hMPV last year in May, June and July before the summer. If you do not test, you will not know, and I think somebody who is in intensive care department without a diagnosis that's always a bad thing.

I totally agree. Yeah, that's ideal. But I think we are with a stretching budgets too, because of the year-round surveillance, and this year we are facing that one proposition of oh you test the big test, the big three first, and then we will see what happens. Because we've been doing this for 15 years, testing for 21 viruses and then considering some bacteria as well, but now it's so these budgeting questions.

Taking budget in mind, then I'm the wrong person to ask, you can ask my wife. I'm horrible with money, though.

Right, right, me too. Yeah, I'm not a good person on budgeting.

Clare Taylor: 32:52

Very frank discussion, I have to say in this episode. Before we wrap up, I just do want to touch on long COVID, because we had a previous episode of ESWI Airborne, I think, broadcast mid 2023 and it was really astonishing the kind of variety of ways in which long COVID affected people, really disrupting lives and livelihoods and so on, and I just wanted to check in, any of you can come in on this, but it's probably for Marco, I think you were on this episode. Have we advanced at all the scientific understanding and how it could be treated since we last spoke about this?

Yeah, so it wasn't that long ago, so I think there isn't one clear answer there. Clare, Long COVID is a huge heterogenic syndrome. Even the case definition is under debate, so that makes it a little bit difficult. I learned a lot from talks and papers from Professor Peter Openshaw and his group. They really dive into the different phenotypes of long COVID or the post-acute sequelae of coronavirus disease, and the different phenotypes have a different underlining pathophysiologic mechanism also needing different treatment approaches. For instance, if you have a phenotype that the hypothesis that there is a long lasting, persistent low levels of viremia attacking the virus might help, but if it's persisting inflammation, hyper-inflammatory state, immunosuppression or immune modulation might be the key to cure. But currently there are some big international collaborations ongoing also looking into drugs that are already available and their role and that might even be the answer with metformin or colchicine or other drugs that are already widely available have some immune suppressive effects, but not that much because if you over-suppress you, of course you get your opportunistic infections. We might need the answers from there, but I'm pretty sure the other two might have something to add here.

Clare Taylor: 34:55

Okay, yes, let's have the last word from each of you on therapeutics and what's promising and what's in the pipeline. If you can get that crystal ball out, but let's say a near to medium term crystal ball, if they have such a thing, Xavier, what do you see coming up?

Well for vaccines. Maybe it'll be good to have an availability for mucosal vaccines, so like a live for flu, because that may be advancing on the way of reducing transmission, because we know that vaccines given to the mucosa are being demonstrated to raise more IgG levels, which is an antibody that can block the virus just in the place of infection. That'll be interesting to see how the phase two and three trials of these type of vaccines come forward. So another point worth a comment may be the availability of more protein-based vaccine brands and preparations, especially if thinking on the immune-compromised and the elderly and the high-risk population, because protein vaccines actually, especially if they are adjuvated with new adjuvants, they may help in increasing the immune response and the antibody titus for these individuals. So nowadays we only have one updated vaccine of that type and it will be interesting to have more of these in the future.

Clare Taylor: 36:37

Great. Thank you. Pontus?

Since I'm an antibody person, I'd like to talk about those. First of all, there were clinically available antibodies early on in the pandemic, but they lost their function due to the virus evolution. But I've seen that there's so many labs and companies working on new neutralising antibodies and they're trying to find those that would be targeting places where the virus can't evolve away from, and I expect that to come in the not so distant future, a few of those available that will help and if we're talking about neutralising antibodies, they will in particular be useful for prevention of prophylactic treatments and so forth. And also, what I'm perhaps even more interested in are the therapeutic ones that you could give in acute situations, and here the non-neutralising ones, have shown a bit more promise, at least in the academic paper so far different animal models and so forth. So there I think it's a bit longer term, because there are so much more you have to think about when you are triggering inflammation in a body, you don't want to do that, you know overdo it, because then you can risk doing more harm than good. So we have a lot to learn there, but I think that's a bit long term and that it also will be something that will happen in the antibacterial field as well, where there's a huge need in the future for such treatments. So if I want to say one thing, it's new types of antibodies that will come.

Clare Taylor: 38:25

Okay, coming soon. And Marco?

I really see a future for a vaccine against multiple pathogens and also taking away from the public talking about single pathogens and vaccination and trying to prove, for instance for RSV and for COVID and for flu, that it's important to get your vaccination. So we really need a transdisciplinary approach, but also psychology, social sciences, to actually see that somebody gets his respiratory shot and as little shots as possible with as broad possible prevention

Clare Taylor: 39:04

okay, that's great, and let's hope that this podcast today made its own small contribution towards that psychology. I'd like to say thanks to each of you Pantos, Xavier and, of course, Marco for being with us today and sharing insights from your research. That was a really interesting conversation. Now for our listeners. If you've enjoyed this discussion as much as I have, then stay tuned. Today's episode is one of a four part series on intervention strategies. In other episodes we'll be honing in on RSV, influenza, hMPV and if you don't know what that stands for, you'd better listen in and finally, a special episode covering all of these respiratory viruses together. So don't miss it and keep tuning in to get the latest on intervention strategies and research from experts in the ESWE network and beyond. And until next time, dear listeners, stay safe.

Aida Bakri : 40:08

ESWI Airborne is brought to you by ESWI, the European Scientific Working Group on Influenza and Other Acute Respiratory Viruses. These episodes would not be possible without the team's efforts and we would like to extend special thanks to our ESWI Secretariat, our technical and IT teams, our arts team and our host, Clare Taylor. The podcasts are recorded virtually and we thank our guests for their participation in this inspiring series. Talks are adapted to a global audience and are intended to be educational. For any specific medical questions you may have, these should be addressed to your local general practitioner. Many thanks to our sponsoring partners and thank you for listening.

If you do not test, you will not know - a focus on COVID-19

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