Good afternoon, everyone. Thank you for joining Jefferies Healthcare Conference 2025 edition. I'm very happy to have Marianne Backer with us, CEO of Vir Biotechnology. Thank you. Thank you, Juliette. Hello and good afternoon, everyone. Thank you, Jefferies, for the opportunity to provide the latest update on Vir Biotechnology and the rapid progress we are making across our pipeline. I will be making forward-looking statements. For more details, please review our website regarding notices, legal disclaimers, and regulatory filings. At Vir Biotechnology, we are committed to using the power of the human immune system to transform patient lives. Twice already, we have done that. Once during the COVID pandemic with Sotrovimab, an antibody that we isolated out of patients affected with the virus and further perfected into a therapeutic. A second time, actually, for Ebola with Ansuvimab or mAb114. Now we are again at a pivotal moment with promising data across multiple programs in our pipeline where we can really do this once again. At the core of our research is a fundamental connection between cancer and viruses. Obviously, both cancer and viruses represent formidable threats. While the human immune system is quite amazing and naturally equipped to fight these threats, both cancer cells and also viruses have developed ways to invade the immune defenses, leading obviously to serious disease. Our approach is to develop therapies that really empower the immune system and the immune system's ability to also overcome these evasion strategies. We are doing that by leveraging our deep understanding of immunology, and we are also developing innovative solutions. Now, what are those innovative solutions? First of all, we have a long history, almost 10 years now, of discovering antibodies and developing them into powerful therapeutics. We do that these days with the help of AI and our platform DAISY. Further, since last year, we licensed in a patented platform to mask T-cell engagers or other proteins such as cytokines. It is really versatile. That allows us to develop cancer therapies that target specifically the tumor while leaving healthy cells intact. This approach offers us a competitive advantage and a unique position not only now in the field of infectious disease, but also in the field of cancer immunotherapy. Now, let's have a look at our pipeline. We are set up very well to deliver value in 2026 and beyond, as you can see here. On the left-hand side in oncology, we are focusing on solid tumors, and we are using our dual-mask T-cell platform that I just talked about. We have a PSMA-CD3 T-cell engager in phase 1, VIR-5500, which we are evaluating in both early and in late-line prostate cancer. We have a HER2 CD3 T-cell engager, VIR-5818, also in phase 1, which we are exploring in a basket trial across multiple indications. We have an EGFR CD3 T-cell engager program, VIR-5525, which we dosed the first patient just in July of this year. Again, phase 1, and that program has the potential, and we are evaluating in non-small cell lung cancer, in head and neck squamous cell carcinoma, in colorectal cancer, and other EGFR-expressing tumors. On the right-hand side, in infectious disease, we have our hepatitis delta program, which is in phase 3 registrational trials with the goal of delivering a chronic suppressive therapy for patients that could really set a new standard of care. That regimen consists of an antibody that was discovered within the labs of Vir and further optimized, and we combine it with a different modality in a siRNA. Underpinning all these programs is a focused capital deployment strategy. We have about $811 million in cash and investments at the end of the third quarter, and that provides us a cash runway into mid-2027. This financial position also allows us to take a number of our programs through very critical value inflection points. Now, let's dive first into our oncology portfolio. There we are really leveraging the ProX10 platform that I will talk about a little bit here. You all know T-cell engagers. It's a modality that holds tremendous promise, and there are already 10 T-cell engagers on the market available to treat patients. They have this promising potential, but they have really been held back often due to toxicity and frequent off-tumor activation, activation in healthy cells, and cytokine release syndrome. What we are offering as a solution is to mask the T-cell engager to ensure that it really only gets activated in the tumor. That is what you see here. The power of our platform, ProX10, really lies in this universal masking approach. What you can see here in this visual in the middle is really the T-cell engager, the tumor binding domain, which can be PSMA binding, HER2 binding, EGFR binding, is depicted in light blue, and the CD3 T-cell binding domain is depicted in the dark blue. Normally, if this T-cell engager enters the tumor and is unmasked, it can bind the tumor on one side, bind the T-cell on the other side, the T-cells get activated and can kill the tumor cells. Now, again, what you want to avoid is the toxicity that is often seen with unmasked T-cell engagers or even with single-masked T-cell engagers. Our masks here, which you can see, are quite unique in that they are comprised of these long polypeptide chains that form an envelope around the T-cell engager. They fold around it, and they shield it from activity. The masks contain protease-cleavable linkers such that they only get cleaved by proteases in the tumor microenvironment. The result is a very targeted release of the masks and then activation again of the TCE specifically in the tumor. This universal dual-masking technology functions a little bit like a Trojan horse, if you will, and is key to addressing the toxicity challenges that are often faced by both, again, unmasked as well as single-masked T-cell engagers. We expect this approach to offer a lot of differentiation. First of all, therapeutic index. We really have the opportunity to maximize the therapeutic index because our masking strategy allows for higher dosing and potentially improved efficacy while maintaining safety. Second, lowering of toxicity because, again, the masking is really when the masked T-cell engager is mobilized in your bloodstream, nothing is supposed to happen. Really, only when it enters the tumor microenvironment, the mask is being cleaved off, and there it exerts its effect. It is really protecting healthy tissue. Third, what the masks also do is they actually provide a longer half-life to any molecule that they mask. In the case of our PSMA CD3 T-cell engager, for example, it extends the half-life from somewhere between 8 and 10 days. What that allows us to do is to pursue longer duration of dosing. We are exploring both weekly and Q3 weekly dosing. Of course, that is especially important in the early lines of therapy. Now, fourth, these masks, so X10 masks, have already been used in a drug that is on the market, Welltuvio. That gives us a lot of confidence around the safety of the masking. Finally, the platform is really a plug and play. Every clinical asset that you see in our pipeline has the same mask, the same protease-cleavable linkers. It is not the case that with every new program, we have to redesign the mask or redesign the linkers. It is a plug and play platform. We are now using it also in our preclinical programs. We have seven preclinical programs that really deploy the same masking. Let's now start looking at some of our clinical stage programs. I will start with our PSMA-CD3 T-cell engager for prostate cancer. Dose escalation for, maybe I'll just go back a moment, dose escalation for this program is ongoing in both weekly and every Q3 week dosing as a monotherapy in really very heavily pretreated patients. These are patients that have exhausted all lines of therapy. That's something important to keep in mind as you will be looking at the efficacy. We are also now exploring, since this year, the combination of VIR-5500 with an ARPI and enzalutamide in first-line MCRPC patients. Let me show you just one case study. This is a study that we also shared earlier this year. It's a 73-year-old man with advanced metastatic prostate cancer who had already tried nearly every standard treatment. As you can see here, some of them, several taxanes, enzalutamide, and so on, yet very extensive disease. With over 20 bone metastases and a very high PSA level at close to 1,000. Despite all these prior therapies, his cancer progressed. He joined our phase 1 trial and received step-up doses of 200, 300, and 400 micrograms per kilo. He tolerated the treatment very well. He did not need any steroids, also no IL-6 pretreatment. He had minimal toxicity and saw quite impressive results, very rapid and significant PSA declines with more than 90% and with sustained declines over multiple months. Here you can see on the imaging studies on the left-hand side top panel that, and this is a whole body MRI, you see significant anti-tumor activity with essentially liquefaction of the tumor after treatment. This is, again, already after week nine of treatment. On the bottom panel of the imaging, you can see the corresponding PSMA PET, which is fully in line with what we were seeing on the PSA side on, again, the MRI and PSMA PET. His pain symptoms also improved significantly, matching really what we were seeing in his scans and in his blood work. I think this is a great case that highlights not only the deep biochemical and clinical responses that VIR-5500 can have in, again, a patient with a very high burden disease, very high burden prostate cancer, but also the promising safety profile of VIR-5500. Again, unlike with some other TCEs, he did not experience any major toxicities, and the ProX10 masking technology was really offering what we had expected for the drug to work primarily at the tumor site and minimizing off-target effects in healthy tissues. This also helped us get support for higher dosing, and we have been continuing to dose escalate in this trial. We just announced recently at our earnings that we will be sharing a very comprehensive data set on VIR-5500 in the next quarter. Yeah, let me just briefly show you some of the efficacy that we have shown earlier. This was data from earlier this year. Again, this was still very early in dosing, but as you can see in these results, every single patient, 100% of the cohort who had a starting dose of 120 micrograms per kilogram or higher experienced a measurable PSA decline, 58% PSA 50, and then 1 out of 12 or 8% PSA 90. These are obviously, these were very promising early response signals, and again, considering the very heavily pretreated nature of these patients and still at very low doses. Now, let's look at the other side of the coin here, safety. Again, this is data from earlier this year, and here you can see that we saw a very well-tolerated profile overall. We observed no dose-limiting toxicities, and what was immediately striking is the very low incidence of CRS with only a small percentage of patients experiencing grade one or two events at those dose levels. This is, again, without the use of prophylactic steroids or any anti-IL-6 medications. Again, early but efficacious doses. Also, very briefly, these were early data on durability. Again, data was early, but this chart demonstrates that we could show some early signs of durability in some of the patients that were dosed at these low levels. Again, overall, very encouraging package for VIR-5500. The fact that we saw these responses with such a favorable safety profile suggested that we had significant headroom to dose escalate. That is exactly what we have been doing since January. As I mentioned, we plan to share a quite comprehensive data update in the next quarter for our monotherapy cohort. Let's briefly switch to our HER2 program. This is our HER2 CD3 T-cell engager for 5818, which we studied in phase 1, really in a basket trial, a lot of different tumor types. I just wanted to show you one patient case because it was such a very visible example of the transformative potential that the asset had. This is a compelling case. It was shared earlier this year. This is a patient which presented with very, as you can see, extensive ulcerated chest wall lesions that had invaded her skin also and the back, a stark illustration actually of the treatment-resistant nature of her tumor and her disease and someone very unlikely to respond to any existing therapies. This patient had exhausted nine prior lines of therapy, including in HER2, and nothing worked. What you can see here is the response of VIR-5818. It was immediately visible, as you can see in the top middle panel, very quickly within days. You can see, again, the image in the middle at the top. You can see the drug in action, redirecting the patient's own immune system to attack and control her disease. By cycle four in the bottom right, you can see that there's an impressive clearing of disease. This, again, was without any dose-limiting toxicities, no grade 3 CRS or any significantly elevated IL-6. In the meantime, as you can see here in the middle for our HER2 program, we have shown also compelling data in metastatic colorectal cancer patients. I won't have time to go into it here, but again, early signs that this could work across a number of indications. For the HER2 program, we have finished our monotherapy dosing, and we are now still dosing in combination with pembrolizumab, so that dose escalation is still ongoing. Finally, I want to briefly mention our EGFR program, our EGFR CD3 masked T-cell engager. For that program, we dosed the first patient in July, so it is still very recent. Phase 1 study enrollment is progressing as expected. Here also, we are evaluating both monotherapy and in combination with pembrolizumab. We believe this program has the potential to address a significant unmet need in patients that have a multiple of solid tumor types where the current EGFR targeted therapies are having important limitations, sometimes also really to do with toxicity. Finally, here in the very bottom of the slide, I want to just mention very briefly again the plug and play nature of the platform, the ProX10 masking platform. It allows us to very rapidly progress to other targets. As I mentioned, we have now seven preclinical programs that we are exploring. The clinical experience that we have from our clinical programs, our current programs, is really helping us a lot in informing what targets to pursue preclinically. We are obviously not ourselves going to take forward seven preclinical programs, but we have a lot of interest in partnering. There will be a mix of programs that we can take forward ourselves and others that will be partnered. Okay, let's switch gears now to our infectious disease portfolio and most importantly, our hepatitis delta program, where we have shown some very promising data recently. Maybe very briefly about the disease. Hepatitis delta is an orphan disease. It's a small RNA virus that only can infect patients that already are infected with hepatitis B. It's the most severe form of viral hepatitis if patients have that dual infection. As you can see, it very dramatically increases the risk of cirrhosis, of liver cancer, and liver transplantation, and eventually mortality. The statistics are certainly sobering. Over 50% of the patients living with Delta face liver-related mortality just within 10 years of diagnosis. The progression to cirrhosis, as I mentioned, is very, very rapid, taking an average of only five years. Moreover, these patients face three times the risk of liver cancer compared to patients that just are infected with hepatitis B alone. These figures sort of underscore the need for an effective treatment, but unfortunately, in the U.S., there is no treatment available for patients at this time. The right-hand side shows you a little bit about how many patients we expect there to be. We expect about 60,000 actively viremic Delta patients in the U.S. and a little bit less than double that in Europe. Again, no treatment available for patients in the United States. There is one treatment available for patients in Europe, and that is bulevirtide. This shows you on the left-hand side our most recent data. What we showed at the liver meeting AASLD just a week and a half ago from our phase II SOLSTICE trial is that when Delta patients are treated for 48 weeks with our dual regimen of an antibody and an siRNA, 66% of the patients, you can no longer amplify the virus from their blood. We call it target not detected, so you can really no longer detect the Delta RNA in the patient's blood. That's very impressive efficacy. While we have not done really comparative trials, on the left-hand side of the panel, in the gray there, you can see the only drug that is on the market for Delta today in Europe is bulevirtide. In the MIR trials, they saw about 12% target not detected after the same period of treatment. What is also really important to point out is that our regimen is a once-a-month dosing, while bulevirtide is a daily injection. Patients have to daily inject themselves for the rest of their lives because both ours and the competition's are chronic therapies. Very briefly about the differentiation. First, we are seeing, as I mentioned, very deep Delta antiviral responses with 66% of the patients achieving target not detected already after 48 weeks. Second, it is a monthly dosing. From a compliance perspective and an adherence perspective, really important. Third, our combination of the antibody and a siRNA allows the HBs antigen levels to be dropped almost four logs. That is really important because the Delta virus is basically almost like a defective virus, and it uses the hepatitis B virus S antigen to really be able to replicate. Bringing that down four logs is really very important. Fourth, we are seeing very good efficacy, not just in non-cirrhotic, but also in cirrhotic patients. The reason why that is important is because patients that show up at the doctor's office already often have some level of cirrhosis. It is important that your regimen is working in these patients. Then fifth, and of course, very important, we have shown a very favorable safety profile in our phase two SOLSTICE trial. We believe that all that taken together demonstrates that our combination regimen has the potential to set a new standard of care in Delta treatment. Our SOLSTICE phase two trial data, if you're interested, were also published in the New England Journal of Medicine, and we have provided a link on our website. Very briefly now about our registrational trial design. As you can see there at the top, based on the strength of our data, we were awarded FDA breakthrough designation, FDA fast track designation, EMA PRIME designation, and EMA orphan drug designation. All those designations are in hand and will, of course, be helpful as we accelerate this program as much as possible. We have three parts of the registrational trial. Eclipse 1 and Eclipse 2 combined really are the pivotal studies supporting the marketing application, both for the U.S. and Europe. Just last month, we announced that our Eclipse 1 trial is already fully enrolled. That is two months ahead of schedule. Our Eclipse 2 trial is on track, and so is our Eclipse 3 trial. Enrollment is actually going really, really well. We feel very good about delivering top-line data by the first quarter of 2027. A lot of clinical programs are ongoing, and all of that is underpinned by a strong financial position, as I mentioned at the beginning. We have a projected cash runway until mid-2027. We have strict financial discipline. We have also been strongly prioritizing our portfolio. This gives us the resources to advance our key programs to critical value inflection points. We are also actively pursuing strategic partnerships, as mentioned before. We are exploring a partnership for our hepatitis delta program outside of the United States. Also for our T-cell engager programs, especially for clinical programs, we are seeing a lot of interest and are exploring partnerships. This is, again, a quick snapshot of our pipeline, but let me just quickly go to the catalysts. A very important catalyst is our VIR-5500 program with data in the next quarter. As mentioned, our delta program is going to have top-line data in the first quarter of 2027. We believe that by executing on these priorities, we can create significant value for shareholders while transforming patients' lives. Thank you for your attention.