Thank you, and good afternoon. With me today are Marianne De Backer, Chief Executive Officer; Dr. Phil Pang, Chief Medical Officer; and Sung Lee, Chief Financial Officer. Before we begin, I would like to remind everyone that some of the statements we are making today are forward-looking statements under the securities laws. These forward-looking statements involve substantial risks and uncertainties that could cause our clinical development programs, future results, performance or achievements to differ significantly from those expressed or implied by such forward-looking statements. These risks and uncertainties and risks associated with our business are described in the company's reports filed with the Securities and Exchange Commission, including Form 10-K, 10-Q and 8-K. I will now turn the call over to our CEO, Marianne De Backer.

Thank you, Sasha. Good afternoon, and welcome. I'm Marianne De Backer, CEO of Vir, and I am pleased to welcome you all here today. Since the last time we spoke, Vir has made some impressive progress on driving our scientific platforms, our pipeline and our clinical trials forward. All this positive momentum is encouraging as we seek to serve all the patients who are waiting, especially those with unmet medical needs in multiple infectious disease areas and beyond. Let me first call your attention to the updates we are most looking forward to at AASLD The Liver Meeting in Boston later this month. Our Phase 2 data readouts from two of our most advanced programs chronic hepatitis B and chronic hepatitis delta. As a reminder, this includes initial data from Part B of the MARCH trial where we are looking at combinations of our monoclonal antibody, VIR-3434 and our siRNA VIR-2218 for 24 and 48 weeks with and without peg interferon alfa. We also look forward to sharing initial data from our ongoing SOLSTICE trial, which is evaluating whether our antibody VIR-3434 alone, our siRNA VIR-2218 alone, or the combination of these can be a viable chronic therapy for patients who are co-infected with hepatitis delta virus. Thanks to the approximately $50 million in new BARDA funding, we have had positive momentum on the development of VIR-7229, our investigational next generation COVID-19 monoclonal antibody with a distinct combination of potency, breadth, and viral inhibition capability. This funding includes $40 million in Project NextGen non-diluted funding, which will support the development of VIR-7229 through Phase 1. We expect the Phase 1 trial to initiate in 2024, and we'll be exploring a partnership for the development of this antibody post Phase 1. The BARDA funding also supports alternative monoclonal antibody delivery technologies, such as RNA delivered monoclonal antibodies, which have the potential to revolutionize the field of antibody therapeutics with the ultimate benefit of enabling greater patient access and ease. This funding is another testament to Vir’s world class antibody platform and our ability to discover rare, broad and highly potent monoclonal antibodies with the hope of generating powerful new medicines. Switching gears to one of our newest clinical programs. In September, the first participant was dosed in a Phase 1 trial evaluating VIR-1388, an investigational novel T-cell vaccine for the prevention of HIV. This trial is especially meaningful, because it brings us and our supporters, which includes the Bill & Melinda Gates Foundation, the National Institute of Allergy and Infectious Diseases and the HIV Vaccine Trials Network one step closer in our shared pursuit of developing an HIV vaccine. We are hopeful that our unique approach will help close the longstanding public health gap in HIV prevention and we will look forward to sharing initial data from this trial in the second half of 2024. Finally, I want to give you a glimpse into some of the transformative strategic decisions Vir has made to drive future growth and increase patient impact. As you know, our founding mission was a world without infectious disease and we are now embarking on a broader vision, powering the immune system to transform lives. We have always seen ourselves as an immunology company first and are now ready to expand into new areas of growth by applying our deep immunology expertise beyond infectious disease with the first applications in autoimmune diseases and immuno-oncology. This is made possible by our platform that has already created monoclonal antibodies with enhanced selectivity and potency using AI-based protein engineering. We have existing in-house immuno-oncology experience, and we are already advancing enhanced antibodies for tumor immunotherapy with augmented selectivity and potency under the leadership of Dr. Alan Korman, Senior Vice President of Immune Targeting here at Vir. Prior to joining Vir, Alan led the discovery of three approved drugs for oncology. We are also embarking on a novel agnostic way to identify T-cell receptors specific for tumor antigens, an effort led by our National Academy of Sciences Immunologist, Dr. Antonio Lanzavecchia. We look forward to keeping you updated on this in 2024. We believe all of this is within reach thanks to our strong balance sheet, which allows us to take our chronic hepatitis B and chronic hepatitis delta programs through development inflection points, as well as invest in our core antibody platform and evaluate complementary external opportunities. Meanwhile, we will continue to be judicious in our spending and investment to ensure that we maximize the deployment of the $1.7 billion in cash and investments. Finally, I want to highlight that next week we will be welcoming our new Chief Scientific Officer, Dr. Jennifer Towne. Jennifer brings more than two decades of R&D experience and a proven track record of successfully developing breakthrough medicines and bringing multiple investigational new drug applications for innovative therapeutics forward. This includes bringing 16 drug candidates from preclinical research to IND and early clinical development. Her scientific and external innovation leadership experience combined with her deep immunology expertise will be critical to delivering on our strategy to go beyond infectious disease. I want to thank Phil Pang for expanding his responsibilities as Interim Head of Research. Phil will continue to lead clinical research, development and medical affairs as Chief Medical Officer to bring our late stage portfolio to fruition, which is our top priority at Vir. With that, I'll now turn the call over to Phil to provide an update on the progress we are making in our preclinical and clinical programs.

Thank you, Marianne. As Marianne mentioned, we are looking forward to sharing at ASLD data from our Phase 2 MARCH chronic hepatitis B trial and our Phase 2 SOLSTICE chronic hepatitis delta trial. First, I want to talk about chronic hepatitis B and our goal, which is to achieve a functional cure defined as lifelong control of the virus after a finite duration of treatment, a goal that would be welcomed by the 300 million people living with chronic hepatitis B. The only treatment available to achieve a functional cure is arduous and results in a functional cure only 3% to 7% of the time. We are aiming to set the bar much higher with a goal of achieving a 30% or better functional cure rate. Our hypothesis is that you cannot achieve a functional cure with only an antiviral or only with an immunomodulator, but you really need both mechanisms of action, which is exactly what we are evaluating in our multiple ongoing clinical trials. Our vaccine antibody VIR-3434 and our siRNA VIR-2218 can potentially act as both immunomodulators and antivirals. VIR-3434 has three mechanisms of action. First, it is a neutralizing antibody preventing viral entry of HBV and HDV virions. Second, via enhanced optimization, it removes viral particles and subviral particles from the bloodstream. Third, it has a modified Fc domain, which allows it to act as a potential direct immune activator, capable in vitro of stimulating dendritic cells to mature and create T-cells against HBV or HDV. This is otherwise known as a vaccinal effect. VIR-2218 can act as an antiviral by knocking down HBV RNA transcripts. VIR-2218 can also act as a potential immunomodulator because we believe the HBV protein hepatitis B surface antigen is an immune suppressor and by knocking it down, we can unleash the brake on the immune system. So VIR-2218 is designed to act by analogy like a checkpoint inhibitor. We have demonstrated that when VIR-2218 plus peg interferon alfa is given for 48 weeks, about 30% of participants achieved hepatitis B surface antigen loss at the end of treatment and about 16% had sustained hepatitis B surface antigen loss 24 weeks after the end of treatment. Although the number of participants treated to date is relatively small, this is the first demonstration that siRNAs can have a potential impact on functional cure rates. In that same study, Vir identified that we may be able to predict who will have an off-treatment response based on their endogenous anti-HBS antibody levels at the end of treatment. Vir was also the first to demonstrate the additive impact of combining an siRNA and a monoclonal antibody, specifically VIR-2218 with VIR-3434. This combination resulted in the largest declines in hepatitis B surface antigen ever observed after just 12 weeks of combination therapy. In Part B of the MARCH study, we are evaluating VIR-2218 plus VIR-3434 with and without peg interferon alfa for 24 and 48 weeks. To remind you, after 24 weeks of VIR-2218 plus peg interferon alfa without VIR-3434, we saw that 6% of patients achieved hepatitis B surface antigen loss at the end of treatment. Thus, for AASLD, the fundamental questions are around the role of our vaccine antibody VIR-3434. First, if we add VIR-3434 to VIR-2218 plus peg interferon alfa, will we see an end of treatment response greater than 6%? Second, if we replace peg interferon alfa with VIR-3434, will we see an end of treatment response better than 6%? Third, if we give VIR-3434 for 24 weeks or more, will we see any signs of immunomodulatory activity suggestive of a vaccinal effect? If so, that would strongly support the potential role of VIR-3434 in a functional curative regimen. Now let's shift gears to chronic hepatitis delta. About 100,000 people in the United States and potentially over 200,000 in the EU5 are currently estimated to have HBV/HDV co-infection. This is likely to be an underestimate, given the under diagnosis rates for chronic hepatitis delta. We believe having a highly efficacious, easy-to-use treatment for chronic hepatitis delta will drive the desire to be diagnosed. Delta is one of the most severe forms of viral hepatitis with four times greater risk of liver cancer and two times greater risk of death compared to hepatitis B. Notably, we don't yet have potent chronic viral suppressive therapy for delta. In recognition of this urgent unmet medical need, there are potentially accelerated paths to approval. Our antibody, VIR-3434 and our siRNA VIR-2218 can also inhibit the hepatitis delta lifecycle because hepatitis delta virus requires the hepatitis B surface antigen to be infectious. Notably, with the only currently available chronic treatment, 12% of patients achieve undetectable HDV RNA after a full 48 weeks of therapy with 45% of patients receiving some benefit. This regimen also requires lifelong daily subcutaneous injections. We have challenged ourselves to develop a chronic suppressive therapy that is better, not just in terms of efficacy but also in terms of convenience, safety and tolerability. I'm excited to see if we can get there. Data from the SOLSTICE trial will be shared as a late breaker oral presentation at AASLD. Specifically, we'll be evaluating the safety and antiviral efficacy of VIR-3434 alone, VIR-2218 alone and the combination of the two together in a small cohort of participants. Looking ahead to what we believe will enter the clinic next is VIR-7229, our next generation investigational COVID-19 monoclonal antibody, which is being funded in part by BARDA. This funding includes the parallel research and development of next generation RNAs, such as circular RNA or self-amplifying RNA that would actually encode this antibody, potentially allowing your own cells to make VIR-7229. This would be the ultimate combination of RNA and antibody technology. Instead of using RNA to encode a protein that your body then must develop an immune response against, this is about RNA encoding an antibody that directly defends you. Finally, a quick look back. As I know there remain questions about VIR-2482, our investigational prophylactic influenza A antibody. Our ongoing post hoc analyses have yielded the following two important insights. First, VIR-2482's ability to reduce cases of symptomatic flu improves to 57% for the 1200 milligram dose when the case definition includes fever, that is how symptomatic illness is defined. Second, this relative risk reduction increases further to 65% when excluding the cases of flu that occurred within a few days of dosing. Notably, our next generation antibody, VIR-2981, is not only more potent in vivo but covers both flu A and flu B. Furthermore, because it inhibits the neuraminidase enzyme, like all current flu antivirals, its mechanism of action has been clinically validated and is de-risked. The IND submission for VIR-2981 is anticipated in the second half of 2024. In addition to VIR-2981 and VIR-7229, we have two other preclinical candidates that we expect an IND filing for in the next 12 to 24 months. VIR-8190 is an investigational monoclonal antibody against respiratory syncytial virus and human metapneumovirus. You may have heard the news of the incredible demand surrounding the currently available monoclonal antibody for RSV. Imagine if you could have a single monoclonal antibody that not only covers RSV but also a second virus, human metapneumovirus that also causes significant morbidity and mortality in infants. We also have an investigational novel therapeutic vaccine candidate for the control of high-grade squamous epithelial precancerous lesions and HPV cancers called VIR-1949. Our talented researchers here at Vir have been very busy executing, and I'm excited to hand over the reins to Jennifer Towne as Chief Scientific Officer. She will no doubt further bolster our innovation mindset.

Thank you, Phil. We're pleased to share our financial results for the third quarter of 2023. Total revenues were $2.6 million compared to $374.6 million for the same period a year ago. The primary reason for the decline is lower collaboration revenues from Sotrovimab compared to a year ago. We continue to expect collaboration revenues to be at minimal levels and potentially make a negative contribution to our top line due to the ongoing required investments to support the marketing authorization of Sotrovimab, which our partner GSK leads the efforts in. Turning to operating expenses. R&D expenses in the third quarter of 2023 were $148.3 million compared to $114.2 million in the same period in 2022. In the third quarter of 2023, we have recorded an expense of $21.9 million for the cancellation of Phase 3 manufacturing activities for VIR-2482, our investigational flu monoclonal antibody. With this expense recorded, costs related to VIR-2482 are now largely behind us. Other drivers of year-over-year growth were the investments in our ongoing Phase 2 studies in hepatitis B and hepatitis delta. SG&A expenses in the third quarter of 2023 were $41.1 million compared to $43.2 million for the same period in 2022. The decline was primarily driven by lower consulting expenses and stock-based compensation. For the third quarter of 2023, we reported a consolidated net loss of $163.4 million compared to a net income of $175.3 million for the same period in 2022. Turning to the balance sheet. We ended the third quarter of 2023 with cash and investments of $1.74 billion compared to $1.9 billion at the end of the second quarter of 2023. During the third quarter, we made a payment of $67 million to our collaborator GSK for excess Sotrovimab supply and manufacturing capacity, which were originally recorded as a liability in 2022. With this recent payment, the liabilities to GSK are effectively paid off. Excluding the payment to GSK, our cash utilization during the third quarter was approximately $94 million. In closing, I would like to add that we are taking measures to optimize our cost structure and capital allocation. You can expect us to continue to be strong stewards of capital and have a disciplined approach to capital allocation and expense management.

Thank you, Sung. We will now start the Q&A section. Please limit questions to two per person so that we are able to get to all of our covering analysts. Operator, please open up the lines.

I have two questions. One is a big picture question for Marianne. So you mentioned that you wanted to expand strategic focus on autoimmune diseases and immuno-oncology. Could you share with us your key rationale for selecting the lead indications? And my second question is more for Phil regarding the AASLD update. And if I hear you correctly, you mentioned that you're looking for in general for HBV over 30% functional cure. So for this particular MARCH part B data, given we know that this is still on treatment completed treatment. So what will be the initial bar you'll be looking for so that we can maintain say after six months of treatment that could be above 30%?

Our goal at Vir is to evolve into a comprehensive commercial organization focused on developing products that meet significant patient needs. Since our inception, we have identified ourselves as an immunology company, concentrating on enhancing the immune system's ability to combat diseases. Initially, our efforts were primarily directed toward infectious diseases. However, we have established a strong B-cell antibody platform and a T-cell platform that we plan to leverage for broader applications. These technologies can also be applied to restore immune balance to combat cancer and treat autoimmune disorders. We are not starting from the ground up; we have an experienced team led by Alan Korman, who has a proven record in immuno-oncology with the discovery of major drugs like YERVOY and OPDIVO. Additionally, we are collaborating with renowned immunologist Antonio Lanzavecchia, who is developing innovative methods to identify T-cell receptors targeting specific tumor antigens. Our objective is to utilize our extensive knowledge and technology, including AI and machine learning, to enhance immune interactions and address not only infectious diseases but also other areas of significant unmet patient needs. Regarding the AASLD updates, we began by exploring the effectiveness of combining an antiviral with an immunomodulator in chronic hepatitis B patients. Initially, we examined whether adding siRNA to interferon alfa could improve the low functional cure rates. So far, we have achieved a 16% sustained antigen loss with this combination, which is the highest reported in this area. We are also investigating the potential of using our antibody 3434 in place of interferon alfa or in conjunction with it. In Part A of the MARCH trial, we found that the combination of siRNA and our antibody produced additive effects, resulting in a 2.7 log decline in S antigen without safety concerns. This encourages us to look forward to our Part B results, where we will explore the same combination with and without peg interferon for longer treatment durations. I would like to invite Phil to provide further insights on what we can expect at AASLD.

Thank you, Marianne. And thank you, Gena for the question. So maybe I'll put a couple of statements in context first, which is that predicting off-treatment rates from on-treatment response rates is still very much in its infancy. As you know from our previous presentation at EASL, we were the first to demonstrate that if you had an endogenous anti-HBS response, you were more likely to have an off-treatment response. And that was one of the first times there was any hint of a predictor of off-treatment response from on treatment response. So I can just say generally that, of course, in answers to your question, if one is looking for a greater than 30% off-treatment response, then the on-treatment response should be at their or higher, and that would be the clinical bar to progress a regimen forward, and that's true for all the regimens that we're looking at. But to be specific at AASLD, I think what's really important to think about is that with Marianne's statement, we've proven that 2218 can have a role in a functional cure. The next question is, can 3434 have a role in a functional cure? And that's why in my prepared remarks, I've talked about the fact that when you have 2218 plus interferon for 24 weeks, you see only 6% of patients having an end of treatment response. And the first question we need to answer is if we add 3434 or replace peg interferon, will we move beyond that? And therefore, really honing in on the role of 3434 that it can have either in achieving an end of treatment response and then hopefully later on an off-treatment response. So the answer to your question is that predicting an off-treatment response from an on-treatment response is still in its infancy. You would need at least a 30% rate. And what we're focused on for AASLD is will 3434 get us closer to that answer?

I would like to follow up on Gena's question about the expansion into autoimmune and immuno-oncology. Marianne, could you outline how you plan to approach the metrics you’ll share with investors regarding capital allocation and how they can monitor your progress in these two areas? Additionally, concerning RSV, I understand it's still in the early stages, but considering the commercial success that Pfizer and Sanofi are experiencing with their products, could you describe your vision for the clinical development of 8190 over the next few years? Thank you.

Maybe we'll start with the RSV question. Phil, do you want to give a bit more color on where we stand with the program?

So with our 8190 antibody, which is both covering both RSV and human metapneumovirus, the answer is that we believe we can bring in IND forward in the next 12 to 24 months. And the path is relatively straightforward and has really been blazed by others where in the infant population, what you're trying to demonstrate is prevention of lower respiratory tract infections or lower respiratory tract infections medically attended. And we believe that there's a relatively straightforward path to do so after you obtain Phase 1 PK data. Beyond that, as you know, this is a partnered program with GSK and we are working closely with our collaborator to determine the fastest and most robust path forward. So that's what I can say about the 8190 at this time.

And then, Paul, on your first question, I first want to clarify that the efforts we are doing in these new areas are at the discovery stage and maybe also ask Sung to provide a bit more background on how we are allocating capital here at Vir.

So, Paul, in terms of the metrics, as Marianne said, the efforts in autoimmune and oncology would be discovery and that's not an expensive part or doesn't require a large investment at Vir. The capital allocation here will still largely be directed to our mid-stage programs in hepatitis B and hepatitis delta. Those will be ongoing for the foreseeable future and the majority of our capital allocation will be directed there. Now, I just want to add that in the past year-to-date, our capital allocation has been heavily directed towards a couple of items. Obviously the Phase 2 flu study and the related Phase 3 manufacturing activities. Also, the liability we have to GSK related to Sotrovimab supply and manufacturing. As you probably saw from the press release, we did take a write-down for those manufacturing activities. So those costs, the flu costs are behind us now and the liabilities of GSK are effectively paid down. So again, the capital going forward will largely be directed to the clinical stage programs.

So I would just add in addition to capital allocation to predominantly our clinical stage programs, of course, we continue to explore if there are external innovation opportunities that could help us accelerate our programs or complement what we are doing here at Vir.

It's Billy on for Eric. Couple ones from us. First, just following up from that last question. So with the external opportunity, do you see this as something maybe for more the new immuno-oncology side or the historical virology side of the business? And then I'll pull up my one after.

Eric, we could not understand you very well…

Can you hear me now?

Could you try again?

So the question was just following on from the previous question about you stated some complementary external opportunities you were looking at potentially and whether these would be more in the immuno-oncology space or in the historical space of virology?

So as mentioned, we are looking at external innovation really from the perspective of how can we accelerate what we are already doing. I really do believe that we have world class expertise in our platforms and we want to, of course, stay at the forefront in our field. And so we are looking at anything that could help us stay there, potentially including both infectious diseases or beyond.

So 24 weeks after treatment, it's somewhat varied, but you can still expect that they will remain on NUCs. Typically, what occurs is that once they show they have lost surface antigen for at least six months off-treatment, their NUC would be halted, and then they would be monitored for a period to ensure that they do not relapse. However, it's important to note that NUCs primarily suppress HBV DNA, and thus surface antigen loss, which is a protein, would not typically be influenced by the nucleoside reverse transcriptase inhibitor. While it's not a perfect correlation, we are looking forward to and preparing for the post-treatment data of our drugs while still using the nucleoside reverse transcriptase inhibitor.

First, I am wondering if you can discuss the bar for regulatory approval in HDV or hepatitis delta. And what you would need to see in SOLSTICE to give confidence that this program is on track? And then secondly, what would be the next steps for the delta program, specifically would you possibly be able to move directly into a Phase 3 program after SOLSTICE readout based on all of the data that’s been generated across HBV and HDV?

So I mean, as you know, the goal of therapy in delta is chronic trial suppression progression as well as reduction of liver inflammation that's also how the bar is set on the regulatory side. Phil, do you want to add any more color to what we want to see in SOLSTICE?

So exactly as Marianne said, the regulatory bar is two log decline in HDV RNA and the normalization of ALT, that was one of the bars that was set early on to allow for an incentivized drug development. And I think that that's one of the bars one to look at. But I think another part to look at is undetectability in HDV RNA, that is another marker that is closely associated with clinical benefit. So we are looking at both of those bars. I do want to remind you that for AASLD we are going to be having a small cohort of patients treated for a relatively short period of time. And I think that we will have to just wait to see what that data looks like to be able to know what the next steps are going to be. But as I have mentioned in my prepared remarks, the regulatory pathway can be accelerated if warranted given the unmet need in this space.

This is Nik Gasic on for Roanna. Thanks for taking our questions. Maybe first, could you remind us, I guess, what the status is of the next-generation 2981 antibody against flu A and B? I guess, could you talk a little bit about how this antibody is differentiated from 2482 aside from the flu B targeting aspect as well? And then secondly, could you discuss some of the learnings which you might apply from your experience developing 2482 in flu A to the development of 2981 in flu A and B? Thanks.

So I'll start and then ask Phil to provide a bit more depth. So first of all, as you rightly pointed out, one of the major differences between 2482 and 2981 our next-generation flu antibody is the fact that it covers both flu A and flu B. It's also a different mechanism of action. It's a neuraminidase inhibitor and that is a mechanism of action that has been proven to work before. We have also seen in vitro that the antibody is more potent than 2482. So there's a lot of differentiating components here for our next-generation antibody that we feel are very relevant and interesting. And as it relates to our learnings from 2482, as Phil pointed out in his prepared remarks, there's some learnings that we already have based on initial data analysis. I mean, obviously we have seen that for the clinical trials, it does make a difference whether you include fever in your primary endpoint. It also is really important how much time elapses between someone being dosed and someone being infected. So these are of course very important learnings for us. And we are of course continuing to analyze the data and grasp as many learnings as we can for our next steps. And maybe, Phil, you can talk a little bit more about all the data analysis that is ongoing and that we are planning to learn more about by beginning of next year?

So Nick, one of the key questions that always arises, particularly in the field of infectious disease, is how the results from our laboratory studies translate into clinical settings. In addition to the insights that Marianne highlighted, we need to understand how to adjust the dosage based on our in vivo findings to ensure clinical effectiveness. Being the first company to conduct a prophylactic outpatient flu trial provides us with important data that will help us relate pharmacokinetics to pharmacodynamics. This understanding is crucial for determining the necessary dosage and concentration needed to translate laboratory results to clinical applications. This process will significantly benefit our 2981 development, and alongside Marianne's points about clinical endpoints and timing, our goal is to bridge the gap and utilize 2482 to inform 2981. We are already planning a series of studies to minimize that gap as much as possible.

Considering the design of future trials, would you think about using the WHO and CDC endpoints as the primary endpoints for upcoming flu trials? How should we approach this since both endpoints involve fever?

I think we may be a bit more advanced than that. We recognize that fever, or temperature, is important. There is a slight difference in temperature definitions between the CDC and the WHO, with 37.8 versus 38.0 degrees Celsius. We are considering that, along with other symptoms well covered by 2482 in post-hoc analysis. We will compile all that information to make our decision. Fever will certainly be part of our considerations moving forward.

We have one on the SOLSTICE trial with data at AASLD. Approximately how many patients worth of data should we expect, and are each treatment group pretty balanced? And what efficacy measures do you expect to report in addition to the primary endpoint?

I will just say that obviously this will be the very first time that we show really very initial data also from our SOLSTICE trial. So as Phil mentioned in his prepared remarks, this is still with a small number of participants in each of the arms. But we will see some initial data on, of course, 2218 alone, 3434 alone, and then the combination. Anything to add there, Phil?

No, I don't think. And maybe I'll just clarify a couple of things that essentially we are going to be looking at, as Marianne pointed out, the monotherapy and the combination therapy. And the way in which the study is designed is we enrolled a very small number of patients in those monotherapy arms. And then if they showed signs of antiviral activity or didn't show signs of antiviral activity, they would or would not roll into a combination treatment arm to be able to really understand how the two drugs work together or don't work together. So that's going to be the design of the trial and we look forward to sharing data at AASLD.

How important is getting HDV to undetectable levels granted that the regulatory bar is a two log decline?

So I think that the answer to your question is certainly getting to undetectable is a higher bar than a two log decline. I think that there is good clinical data suggesting that undetectable correlates well with clinical outcomes. And I think that as I mentioned before with the current therapy it's about 12%. So I would say that that 12% of course happens after a full 48 weeks of therapy. And the question is, can we meet or do better than that given the fact that we have been following our patients for a much shorter period of time. So I think we'll just have to wait and see what AASLD has to say and let the science speak.

Just a quick one on the HIV program, Phase 1 readout. What type of data do you plan to announce from that the second half of next year? And what will give you confidence or what would you need to see to proceed with the next steps in that program?

Phil, do you want to take that one?

As you mentioned, Joey, this is a Phase 1 study focused on immunogenicity in healthy volunteers. The primary objectives are safety and immunogenicity. We aim to determine whether the HIV insert is immunogenic and to measure the CD4 and CD8 T-cell responses. Additionally, we want to identify the types of T-cells generated, specifically looking for effector memory T-cells, which are unique in that they reside in the mucosa and can act quickly without needing to multiply. We also plan to investigate the HLA restrictions of these T-cells, including whether they may be restricted by MHC-E, which could indicate a distinctive immune response that the virus might find challenging to evade. We expect to report initial data from these immunologic assessments next year.

And then maybe just to add that, you know, the HCMV-based vaccine or what we call the T-cell platform, I mean, learning those initial data for HIV will also really be helpful in guiding us for our next investigational T-cell vaccine that is focused on the HBV.

Thank you, operator. And thank you all again for your time and attention today. To close, I just want to leave you with these couple of takeaways. First, we continue to make progress on our clinical programs, and you can expect new data from our ongoing Phase 2 chronic hepatitis B and chronic hepatitis delta clinical trials, to be presented on November 13th. Second, we are expanding our strategic focus beyond infectious disease first to offer immune diseases and immuno-oncology. We are also pioneering the discovery of RNA delivered monoclonal antibodies, thanks to the help and new funding from BARDA. And lastly, the $1.7 billion in cash and investments that we have available to support the advancement of our hepatitis B and delta clinical trials and our core antibody platform, yet, additionally, it enables us to evaluate complementary external opportunities that strengthen our existing platforms and pipeline. So thank you again, all of you for joining us today. We really appreciate your time and your interest in Vir. Operator, you may end the call.

Thank you all for joining. This does conclude today's meeting. You may now disconnect.