Good morning to some and good afternoon to the rest of you. We are excited to be back here already again, this time to present our exciting results of the human challenge trial of our RSV project. To do that, I have here our President & CEO, Paul Chaplin, and Executive Vice President, CFO, Henrik Juuel, that will walk through a number of slides to discuss our trial results. Afterwards, of course, Q&A, where you have the opportunity to ask all the questions you may have. Before we walk through the presentation, I just want to read the following statement. This presentation includes forward-looking statements that involve risks, uncertainties, and other factors, many of which are outside our control, that could cause actual results to differ materially from results discussed. Forward-looking statements include statements regarding our short-term objectives and opportunities, financial expectations for the full year, as well as statements concerning our plans, objectives, goals, future events, performance, and information that is not historical in nature. All such forward-looking statements are qualified by these cautionary statements. We undertake no obligation to publicly update forward-looking statements to reflect subsequent events or circumstances after the date made, except as required by law. By this, I will hand over the presentation to Paul. Yes. Thank you, Rolf, and welcome everyone to this call. It's my great pleasure in the next few slides that I will walk you through the fantastic results that we reported today in terms of the high efficacy that we've observed with our RSV vaccine candidate in the human challenge study. However, just to set the scene, if you turn to slide three, I want to talk a little bit about RSV, the disease itself, and why today's news is so exciting, remind you about our differentiated vaccine approach and where we currently are in terms of the data we've generated to date. RSV is a virus that causes a disease very similar to flu or influenza, and many people talk about RSV being very similar to flu in terms of hospitalizations due to severe lower respiratory tract infections and deaths as flu. However, there are a number of publications coming out which are actually demonstrating that the morbidity and mortality of RSV is actually more severe. If you look at the hospitalization stay in the number of days patients stay in the hospital, it is significantly higher for RSV compared to flu. If you look at the rates of respiratory complications, such as pneumonia, it is significantly higher for RSV compared to flu. Other pre-existing conditions such as COPD and asthma are significantly more exacerbated than flu, leading to, as I said, longer hospital stays. The situation doesn't just last there. When you look at the mortality rates post-hospitalization, so one year post-hospitalization for either RSV or flu, the death rate for those patients who have been hospitalized for RSV is significantly higher compared to flu. RSV can have a devastating impact, causing hospitalization that has a significant effect on the morbidity and mortality of patients. It remains a very significant unmet medical need and is one of the highest burdens on the healthcare system. RSV can cause anything from mild symptoms, from typical of a cold, which is often referred to as upper respiratory tract infections. Here, publications talk about antibody responses against RSV being extremely important in protecting against these upper respiratory tract infections. However, as I've just indicated, it can actually cause more severe disease, often referred to as lower respiratory tract infections. Here, T cells have been shown in numerous publications to play an important role in clearing that infection. When we began to design our RSV vaccine candidates, we quickly realized we were going to be differentiated compared to the competitors who were all focusing on one antigen of RSV, which is F, which is surface protein. We quickly realized that with our vaccine platform, that was insufficient, and we end up now with a vaccine encoding 5 different proteins, targeting both antibodies to prevent the upper respiratory tract infections, but also a broad T cell response to hopefully prevent from severe disease. In terms of the clinic, that's exactly what we've seen. We've now completed and already published both phase I, phase II studies, where we've shown that our candidate, MVA-BN RSV, induces broad antibody responses, T cell responses against all five encoded antigens. In terms of mucosal immunity, which is the first part of the attack of the body's defenses to an RSV infection. Of course, regarding safety, we've shown typically with our MVA platform, a well-tolerated, good safety profile, even in the targeted population, which are the elderly. If you go to the next slide four. We embarked on a human challenge study because we wanted to determine whether these fantastic and differentiated immune data that we've already reported could translate into an efficacy in terms of an experimental challenge. On this slide, we're showing you the study design. We had two groups, essentially, of 30 volunteers. One group was given a single booster of our RSV vaccine candidate. The other was given a placebo. They were challenged artificially with an attenuated RSV strain and followed up for 12 days. The primary endpoint of the study was to hopefully show a significant difference in terms of the viral load in the blood, in the vaccinated group compared to placebo. Numerous secondary endpoints. We were going to be looking at the clinical symptoms, and also the immunogenicity of the vaccine, and obviously, safety. If we go to the next slide, I'm very pleased to announce, as we did this morning, that we were able to meet the primary endpoint. There was a significant reduction in the viral load in the blood in those subjects who had been vaccinated with our vaccine candidate compared to the control, and you can see that on the graph on the right-hand side. The measurement that we do is a so-called area under the curve analysis, and this was significantly different between the vaccine group to the placebo, and you can see with a P-value of 0.017. The primary endpoint of the study has been met, and this is obviously a clear indication that our vaccine is highly efficacious in suppressing the viral replication following an experimental challenge. In terms of safety, no serious adverse events or vaccine-related serious adverse events were reported, and the safety profile is identical to the ones that we've already seen and published in the phase I and phase II studies. In terms of the immune responses, again, exactly what we've already published. We induced good neutralizing antibodies that were not significantly boosted post-challenge, indicating to us at least, that the immune responses are sufficient to induce the efficacy that we're now seeing against the experimental challenge with RSV. If you go to the next slide, as the viral load slide was a bit small on the previous slide, we've blown it up. Ladies and gentlemen, one moment, please. Continue to stand by while I reconnect the speaker. Sorry for that. We apparently were disconnected, so I'll just start again on slide six. We took two measurements, twice a day for 12 days post-challenge, and you can see there's a significant reduction or suppression of the viral replication in the vaccine group. If we look at the median value of the vaccine group, this is actually 0, which means that the vast majority of the vaccinated subjects had no viral load whatsoever. If we look at the mean value, that's 94 in the vaccine group versus 430 in the placebo group. A highly significant suppression of viral load in the blood. As I said, that fulfills the primary endpoint of the study. If you go to the next slide seven. As I said, 1 of the secondary objectives was also to look at the symptoms. Each volunteer recorded a number of symptoms each day, twice a day, for 12 days post-challenge. You can see these are significantly suppressed in the vaccine group compared to the placebo. Not only are we suppressing viral replication in the blood, this is translating to the reduction or elimination of any typical symptoms that you would see from a mild RSV infection. What does this really all mean in terms of the vaccine efficacy and what could we expect, hopefully, from a phase III study? If you go to the next slide, this is a little busy and I'll walk you through it, but these are basically the three categories that everyone who has done challenge has really looked at. If we start with the first level of efficacy, which we call asymptomatic or symptomatic, this is to determine as a number of volunteers who had at least two positive PCRs for viral load. You can see that in the vaccine group, that was seven out of 30. In the placebo, that was 15 out of 31, and that translates to an efficacy of 51.8%. In the paper that was published using Ad26 as a vaccine candidate, the same efficacy was reported as 37.7%. The next level of efficacy is mildly symptomatic. This is again defined as two positive PCRs for viral load and at least one symptom of any grade. You can see we only have three in the vaccine group versus 13 in placebo, which translates to an efficacy of 76.2%. Again, in the paper published for Ad26, this is reported as 45.8%. If we then go to the most conservative level of efficacy, which is referred to as moderately symptomatic, again, two positive PCRs of viral load and at least one Grade 2 symptom. We only had two subjects in the vaccine group versus 10 in the placebo, and this translates to an efficacy of 79.3%. Again, in the quoted paper for Ad26, this is reported as 61.9%. Now for Pfizer, again, we are assuming their 100% efficacy that they reported in their Q2 also refers to this same level of moderately symptomatic. While we had two subjects in the vaccine group, Pfizer presumably had zero, and leading to 100% efficacy. Again, with a group size of 30, I'm not sure that's meaningful. If we go to the next slide, there is another way of measuring viral load. The first measurement, and all the other measurements we've been talking about, is using PCR, essentially. Another measurement which was included in the study was to actually recover virus through growth on tissue culture. This is the efficacy I'm showing, which is slightly less sensitive than the PCR method. Again, if we look at asymptomatic or mildly symptomatic or moderately symptomatic, we now have an efficacy of 77.9%, 82.8% or 88.5%. You can see at the more conservative level, we only have one subject vaccinated that failed to be fully protected at this more stringent criteria. As I said, presumably Pfizer had zero. Again, is that meaningful, one subject, two subjects, or zero subjects in a group size of 30? My opinion is not really. If we go to slide 10, just to sum up what I've walked you through. We have a highly differentiated vaccine encoding five different antigens of RSV. We've shown that this vaccine candidate stimulates very strong broad antibody and T cell responses, including mucosal immunity in the elderly population. Today, we've announced extremely exciting results that has translated into a highly efficacious protection in a human challenge model. The next steps moving forward is to reopen the discussions with the regulators on our phase III design. We had a design that was agreed with the FDA, the world has changed post-COVID, we need to open up those discussions again. As we've always said, we need to attract a commercial partner. In the last two weeks, we've had a major de-risking event that we announced last week in terms of securing the funding for our ABNCoV2 program on the back of reporting some exceptional data for that vaccine candidate. This week we have de-risked the phase III with the announcement of the highly promising and exceptional data from the human challenge. It's less about the risks of phase III today for RSV, more about the time to market. With that, I will open up for Q&A. Operator, handing back to you. Ladies and gentlemen, I apologize for this technical difficulty. The Q&A has started. If you wish to register for question, you can press star one on your telephone keypad. Once again, that's star one for your registration of Q&A. Once again, I apologize for this technical difficulty. The Q&A has started, and we have one person that wants to ask a question. It comes from the line of Michael Novod. Please go ahead with your question, announce your company's name. All right. Thanks a lot. Yeah, it's Michael Novod from Nordea in Copenhagen. A few questions. First of all, you are referring to the clinical trial design, and things have changed post-COVID. Would you still believe that it would take a two-season clinical trial in phase III? Would that be a requirement or would that be suitable, when you sort of discuss with the regulators? Secondly, we've seen that the J&J has previously announced they had a breakthrough therapy designation for their RSV vaccine. You seem to have data that's clearly better. I know there's challenges in comparing across trials, but clearly better data. Is that also something you're seeking, i.e., a BTD on your vaccine? Lastly, regarding partnering, given the likelihood of probably a larger trial is needed, given low infection rates for RSV in society, is that something that sort of accelerates your pursuit of a partnership on MVA-BN RSV? Thanks a lot. Yeah. Thanks, Michael. The first question related to the two-season requirement for RSV. I think in part, to be honest with you, the original design that we had for two seasons, we did for two reasons. One was to demonstrate the requirement for seasonality of in terms of a booster, but there was also a requirement to potentially de-risk the study by having that futility analysis after season one. To be honest, as we sit here today, I think that requirement has now gone out the window as we have de-risked the phase III. I think, as I said at the end, I think now it's all about time to market. We're looking at designs that get us the fastest approval possible. I think we're looking at one seed study, very similar to most of the competition. The other question was the breakthrough designation. I think with the data that we've just reported, I think everything is very much on the table in terms of what we will pursue regulatory-wise. The last one was partnerships. We've said all along that we need a commercial partner, and the reason why partnering discussions have stalled is because whenever you're doing something that's going to generate pivotal data, everyone wants to see that data. Now that data is reported, it's out, we will resume those partnering discussions. I'm sure there's going to be a lot of interest. Couldn't have really asked for better data than what we already have. As I said, I think we've de-risked a lot of the things, and I think partnership discussions will now resume, and we do need a partner on board to commercialize the vaccine. All right. Very clear. Thanks a lot, and congratulations. Thanks. We have another question, and it comes to the line of Jesper Ilsøe. from Carnegie. Please go ahead with your question. Thanks so much. It's Jesper from Carnegie. A question for you, Paul Chaplin. Given that you say it's less about phase III risk, but more about time to market now, given the data you've shown. How do you actually see your, say, key selling points versus competition? Besides you having an F protein target instead of just the S protein. Assuming, for example, that Pfizer actually shows quite good efficacy, and assuming that GSK as well have a good vaccine, they are basically ahead of yours. What key selling points do you have to actually gain a decent market share in this market? Thank you. Thanks. Well, the endpoint of all phase III studies will be the reduction of hospitalization, which is obviously reducing severe disease. As I said at the beginning of my presentation, there's a lot of publications kind of demonstrating that T-cells play an extremely important role in preventing those lower respiratory tract infections. I'm not saying antibody doesn't play a role at all, but T-cells are crucial, and that is a big differentiating factor for our vaccine in that we are not only trying to stimulate antibodies, but we're also trying to stimulate broad T-cell responses. Time will tell whether that differentiating factor leads to a better efficacy. We have to keep in mind that with the human challenge, that data we've just reported, it's the prevention of mild symptoms of upper respiratory tract infections where antibodies are thought to play a bigger role. There we are toe- to- toe with the competition. The whole discussion of pre-F, F alone, all that, I think that's now been proven not to be of any value. We have F, others have pre-F. We all have the same efficacy. The question will be that in the phase III, do we have a superior efficacy from severe disease? Time will tell, but that could definitely be a differentiating factor. Okay, perfect. Note here, how do you see your safety and other, say, differentiation points just as you know, administration, all these things you have in the COVID vaccine as well. How are the other differentiating factors with yours versus competition if there are any? Thank you. Well, I think the only one I can really comment on the Ad26 vaccine platform, obviously. Okay, your line is connected back again, sir. Thank you. Okay. Sorry, everyone. We were disconnected again. I was just answering the question about safety, and as I was saying, I'm not sure where we got cut off. Ad26 clearly, through the COVID vaccination, we know had some issues in terms, rare, I would say, in terms of inducing blood clots. We have not seen such effects with our MVA platform to date. That could be a differentiating factor. Time will tell. I think we're in the chasing pack here with everyone else. We need to start the phase III. It's all about time to market. We'll see who has the better vaccine when the efficacy and safety comes out through phase III. We remain very bullish and very upbeat about our chances. Would you like to proceed with the next question, sir? Yes, please. Okay. Our next question comes from the line of Michael Novod. It's a follow-up question. Please go ahead. Thanks a lot. I just had a single follow-up question. Talking about the tolerability and your vaccine, you previously had a strategy to go for the elderly. How are you sort of assessing this and maybe that's also going to be done sort of in collaboration with a partner around sort of taking into children and adolescents where you also have a significant disease burden in the U.S, for example. Just some comments on that, please. Yeah. Our strategy has always been to focus initially on the elderly, which is what we'll do. We will be exploring the pediatric indication. The timing of that remains unknown, but as I think you just indicated, that would be something that we'll discuss with, hopefully, a future partner. Okay. Thanks a lot. Our next question comes from Thomas Bowers from Danske. Please go ahead, sir. Yes. Thank you. I hope you can hear me. Just two questions remaining here from my side. If we just take any comments you have maybe on the production capacity. I'm just wondering now that you are sort of indicating time to market versus two season trial here. Just want to make sure that you are able to produce a large enough material for a last single season phase III, maybe to start in already 12 months time or maybe even sooner if you are, as you also think you have highlighted, potentially including the southern hemisphere, so maybe even six-eight months from now. Also with all the delay you had to do with J&J in mind to produce Ebola vaccine? My second question, just looking at competitors, I may have missed some of your answers before on the fusion, but just going to ask here anyway. it seems like big pharma consensus, you can say, has been focusing on pre-F as the best monovalent target. in your multivalent approach, you stick to the F protein plus all the G and M and M2 subtypes. With this data in hand, is it too early to make any new conclusions about pre-F? I guess my question is, do you have anything in the data already that support F protein part, or is this more a multivalent approach that sort of limits the viral load in your view? Yeah. Thanks, Thomas. The first question related to production, I can tell you we've already manufactured the phase III material. That we have no problem on. It's an interesting thing you bring up the pre-F versus F. Our strategy has always been to try and mimic the immune responses that RSV would induce, because we know if you've had an RSV infection, you're generally protected for at least a year. RSV doesn't have a pre-F or an F. It has an F, and it expresses both pre-F and the full F. We've shown from infected cells with our vaccine, this is exactly what we see. We see a mixture of pre-F and F. I think the human challenge model is all about, as I said, reducing mild symptoms, and the theory goes that that's more related to antibodies than T cells. If that is true, the data today says it doesn't really matter whether you have a pre-F or an F. I think that whole notion that the strategy of pre-F is superior, I think has just gone out the window. I think where we may still have an advantage is that with a broad antigen approach simulating a broad T cell response, as I said, if you talk about preventing severe disease, most people believe that's more to do with T cells than it is antibodies. If that is true, we may have probably the best vaccine candidate in the bunch. Great. Perfect. Thank you very much. Once again, ladies and gentlemen, if you wish to ask a question, you can press star one on your telephone keypad. We appear to have no further questions, sir, I hand the conference back to you. Okay. Thanks, everyone. Thanks for your time, for the questions. Sorry for the technical challenges, but hopefully the message got through. Thank you and have a great day.