Good evening, everybody. My name is Selena Kineley and I'm the Associate Director of New Mexico Epscore. We want to welcome you to our kickoff event, the keynote address delivered by Betty Korber from Los Alamos National Laboratory. I'm so pleased to be able to be with you tonight, although we would have preferred to be in person, we're really so happy to have everybody on with us this evening for this fantastic talk. I'd like to mention that this is the eighth year of our New Mexico Research Symposium, and we convene this every year in collaboration with the New Mexico Academy of Science. And our goal is to showcase the incredible research that's happening across our state at all of our colleges and universities, and as well as our national laboratories. Let me just tell you just briefly about the things that are happening this week. In general, we'd all be together in one room, and it would take place over the course of one day. But we've spread this out across five days now that we have a virtual symposium. You've joined us here tonight for the keynote address. Tomorrow morning at nine o'clock the virtual poster session will go live, and you'll have an opportunity to view the posters from a number of students in a wide variety of disciplines. And as well they will be judged by professional researchers and engineers in New Mexico, and there'll be an opportunity to vote for your favorite poster because we'll be giving a people's choice of award. I want to invite you back on Thursday for the Smart Grid Seminar, which will feature the research of the Smart Grid, the New Mexico Smart Grid Center, a project of New Mexico EPSCORE, and we have four graduate students presenting talks during that time. And then finally, on Friday at three o'clock will be our awards ceremony, and we will be showcasing some fantastic work of teachers as well as researchers in New Mexico, and also announcing the winners of the poster competition. Please, if you'd like to register for any of these events, you can find that on our website, and we have a cut lead down there at the bottom because our URL is really long, but we welcome you to go and you can go ahead and register for individual events right there from our website. As I mentioned before, we are proud to present this in collaboration with the New Mexico Academy of Science, and it's my great pleasure to introduce our next speaker tonight, who is Dr. Anton Sumali. He's the Vice President of the New Mexico Academy of Science. He's been working for Sandia National Laboratories in Albuquerque since 2002. And prior to that, Dr. Sumali was on the engineering faculty of Purdue University in West Lafayette, Indiana. Anton, I'm going to turn it over to you. Thank you, Dr. Connealy. Thank you everybody for your presence. Anton, turn on your camera so we can see you. Okay, sorry. Thank you, Dr. Connealy. Thank you everybody for listening tonight. The New Mexico Academy of Science has been collaborating with AppScore for the last eight years, especially in running this symposium. And the most important part of my presentation tonight is just simply NMAS, New Mexico Academy of Science, NMAS.org. That's where you go to find more information about us. Again, it's NMAS.org. Next slide. We advocate and resource and serve as resource for science and science education throughout our state. NMAS is open to any person interested in science or science education in New Mexico. We have five programs that I will introduce soon. Next slide. Our goal is to foster scientific research and scientific cooperation, increase public awareness, and promote science education throughout New Mexico. Next. Now, what are the advantages of joining us? Well, we serve as a conduit to give you a voice to science professionals, university professors, graduate students, science teachers, and practically everybody interested in science throughout our state. We advise, we consult with the state and local government and school boards, and we support science education at all levels. So if you want to have your voice heard, please join us. Next. We have five programs that I will talk to a little bit. The first one is the Junior Academy of Science. Next. This is an example of our new Mexico Junior Academy of Science competition. This is an example of research projects that high school students do for a few months before they present. There are six regions where high school students compete presenting their work in posters and paper competitions and presentations, and two of the each regions champions compete at the state level. Next slide. So the competition again is both written and oral. The deadline and the rules can be found again through NMAS.org and look for a junior Academy of Science. Next slide. The second program I would like to highlight is the outstanding science teacher award. And these are for high school and middle school science teachers. Again, more information on NMAS.org. And the next one is a combination is October 1, but you can prepare from now. If you have a favorite science teacher that shows extraordinary effort above and beyond their call to promote science in the state. Next. We run with the collaboration with EBSCORE. We run the annual meeting symposium that you're attending now. Distinguished keynote speakers for tonight. We have a really good one as as usual. Professor Dr. Betty Korber has done a lot of research on COVID-19 mutation and vaccination. That's the keynote speaker for this year. Hundreds of people like you are participating in this annual meeting. Those are all science professionals, university professors, grad students, and secondary students. So we collaborate again with EBSCORE. We have done that for eight years and we will continue doing that in the coming years. The meetings are always in November. It's open to the public. Next. Now, the third program I would like to highlight is the NMAS Journal of Science. And this is related to the New Mexico Journal, Junior Academy of Science paper competition that I highlighted first, because the regional champions are automatically invited to submit a paper to the journal. As our other invitees and anybody who would like to present their research results in a peer-reviewed journal, you are welcome to submit your work. Again, find information from NMAS.org. Next. Here are examples of journal covers that we have published throughout the decades. We have been in existence since 1906, by the way. That's before the state became a state. For Mexico became a state. The next program I would like to highlight is the National Youth Science Camp. This is a national committee that gather two winners from each state to attend an all expenses paid camp in West Virginia. And New Mexico Academy of Science does the selection for sending the two state champions to this camp. Next. Please join us again through NMAS.org. Regular membership is only $25 student membership $15 institutional membership like schools and libraries $25. There was also live membership for $400. Next. So, finally, and again, visit NMAS.org and you can find all the information I gave you tonight. With that, I turn the floor back to Dr. Connelly. Thank you so much Dr. Somali. I'd like to invite Ximing Liu to the program to introduce our keynote speaker for tonight. On behalf of New Mexico Academy of Science is the current president. I would like to welcome each of you to the 2020 research symposium. Please collaborate with the New Mexico App School and American Chemical Society for this conference to promote scientific research in science education in our state. Our keynote speaker is Dr. Eddie Colbert from the Los Anamos National Library. We are thinking about a topic that we are constantly thinking about the email system, vaccines, and the vaccine strategies for AIDS and COVID-19. The Betty Colbert research focus on viral evolution, human email response to infection, and the vaccine design. This focus on coronavirus response to the global pandemic. Some highlights of her research include vaccine designs to help with viral diversity, characterizing the evolution of a virus and the email pressure during infection, and developing sequence-based signature analysis methods. For her excellent research, she has received many awards and honors, such as the E.O. Lawrence Award, Department of Energy's highest scientific honor in 2004. The Secretary of the Department of Energy Award for her work on the Ebola Task Force in 2017. She got the Freeman Innovation Prize in 2018. R&D 100 Scientist of the Year in 2018. And the Patel Inventor of the Year in 2019. Please join me in welcoming Dr. Betty Hopper. Thank you so much for that introduction. Can you all hear me okay? Yes. Yes, all right. Let me see if I can get my slideshow started. All right, so I'm really honored to be here with you tonight and to share some science I love. This is going to be kind of a review talk, I guess, most of it, about how the immune system works and then how vaccines mimic that. This is a very natural defense mechanism to protect us from disease and I'm hoping that you'll walk away with appreciation for the incredible work your body is doing every day in terms of your immune response to the environment and with a notion of how vaccines are working. And I'm going to try to give you an update on COVID-19 vaccines and also AIDS vaccine progress. So what do you mean for in this talking in an open with about 15-20 minutes of just the immune response basics and how that works, then how that translates to vaccines. And then I'm going to give you a brief history of vaccines focusing on smallpox, and then the progress towards HIV and COVID. And then some of a, a couple slides about the scientific evidence of why we should be masking up now and why we know we should be masking up and why we know what's useful. So first, so first is non-self. That's, that's an idea that immunologists often talk about. So the way our immune system works is we have to recognize when something is dangerous inside of our bodies and we have to be able to eliminate it. And I'm going to open this with the idea of immunological tolerance. And this gentleman over here, Ray Owen was a mentor of mine, and he was a brilliant immunologist at Caltech. And not only was he a brilliant immunologist, he was a brilliant human being because he was one of the feminists who got women into the student body at Caltech. So he really forced that to happen back when, when I was a student myself, a graduate student that had just happened due to Ray's efforts. And essentially the idea of what is self at a molecular level is learned by the immune system during very, very early development. So your immune system learns not to react to the molecules and proteins that are you, your immune system is blind to you, essentially, so it doesn't hurt you unless you have an autoimmune disease. And when you do have an autoimmune disease, your tolerance fails, and you do start to attack your own body. And you've often heard of these diseases, lupus, rheumatoid arthritis, multiple sclerosis and type one diabetes are all situations where you actually have your own immune response acting against your body.  And to achieve this, you have to be able to learn to not see yourself. And this, this guy I also want to talk about a little bit. Anthony Van Levenhoek. And he is the father of modern microbiology he was an amazing man who is really, really good at grinding lenses the best in the world when he lived in 1675 he had a microscope that he created, and he realized that there were tiny creatures in a drop of stagnant water. And no one had known this before. And he was an enthusiastic scientist. And I loved one of the quotes from him he nicks some plaque from his teeth with rainwater he looked at it and close up and he felt that it was pretty moving things in his tooth scum. And he wrote that all of the people living in our United Netherlands are not as many as living animals that I carry in my own mouth. Astonishing. And it's now we have a better sense of what that means. So when you look down at your own body this case of skin what's in it you're an ecosystem. As you and there's about. A vast number 3.8 times 10 to the 13 bacteria and other organisms living in you as well, which even out numbers your own cells and so this is all natural. And here's a here's a picture of the biogeography of an oral microbiome so we have within us these microbiomes and this is healthy. We have to have this we live with this every day. And our immune system has to be able to tolerate the healthy microbiota that occupy our bodies, but it has to be able to see and differentiate a pathogen when it gets into us. So you have this symbiotic alliance between your immune system and your microbiota. And this is, this allows a healthy immune response and this begins right at birth. So the minute you are woken up into this world. You begin to recognize the microbiota and actually Mother's milk helps with this process and helps with immune tolerance and also imparting immunity to the newborn infant. So people think about, you know, it's important to nurse because nutritional things but it's also important to nurse because it establishes this incredible immune response. So this ability to see what's different now, and what you need to be able to kill and wipe out is adaptive immunity so it's the part of your immune response it recognizes a specific pathogen and kills it. And then after it clears an infection from your body remembers it. So if you ever encounter that pathogen again, you can kill it when it comes when it when you're re encountering it. The way of virus works. Looks like I've lost a slide here but anyway, that's all right. The way of virus works is it actually occupies and enters our own cells and then uses that cell to reproduce and a virus requires a human cell or a cell for whatever organism is infecting to be able to reproduce So this is just an HIV example. HIV is this little virus and it has molecules on its surface that recognize a human target cell. And when they bind to that human target cell they enter it, and they load it with their genetic material and then they turn the cell into a viral production factory essentially. And so the cells no longer the healthy cell doing what its function is, it's just creating viruses and HIV is a chronic infection. And so when it gets into your cell it actually moves right into your DNA and starts reprogramming what the cell is doing. And you can also have these lately infected cells that persist for years. And so you don't actually ever clear this virus but rather you have this this long term latent infections, and these late infections can reawaken periodically and become active. And so that's what's going on with HIV and why you can have it for for 10 or 20 years before you actually get AIDS. So what is this adaptive immunity. It's partly T cells and T cells are called T cells because they originate in the thymus right here. And helper T cells direct the fine of the immune response. So they're kind of like the conductor of an orchestra they're the cells that some and all of the other cells and regulate them and cause them to produce antibodies that come in them to a point of infection. And it's these very cells that HIV infect so that's part of the dastardly nature of HIV is it actually infect cells that are really key and central to the whole immune response. And the gradual loss of these helper T cells is what causes AIDS.  The classic one is tuberculosis. So when you have HIV and tuberculosis finally your helper T cell response weakens to the point that the tuberculosis takes over. So that's the kind of way that HIV works. You also have another kind of T cell that also originates in the thymus called a killer T cell and these cells actually seek out and kill the spirally infected cells and cancer cells. And this is specifically molecular markers on the surface of their job is to is just to seek and destroy. And the way they do this is remember we had the virus getting into the cell and turning that cell into a viral production factory. And what happens, your cell chops up bits of the viral proteins and loads them into something called an HLA molecule. And this is an HLA it's our protein, and these HLA molecules carry a little tiny bits of the virus to the surface of a cell. And when they do that they trigger infected cells to self destruct. So here's an example of a T cell killer T cell coming along and recognizing the, the markers, this little bit of the virus carried in a human protein context on the surface of this cell. And when they see this and hit it, they send over signals called cytokines that causes the cell to self destruct. It's kind of a war zone going on us all the time. Our good CTL killer T cells are going through our bodies finding cells and causing this to happen. And I am going to try to play a movie of this because it's really fantastic to get to see this. But here's an example of an infected cell, the red one here. And this cytotoxic T cell comes up to its surface and it, it almost sort of touches the surface of the cells to see if it's recognizing that there's a virus in that cell and that's a cell that has to be targeted for depth. And when it finds its proper target. What it does is it loads it up with cytokines and it dumps them into the cell and causes the cell to self destruct so you can see the interaction.  I'm just going to progress a little bit through it. Here are the cytokines that are getting dumped now so it's made this bond and it's putting in the chemicals that cause the cell to self destruct. So anyway, I love this little film and I just wanted to share it with you. It was produced at Oxford and I appreciate this kind of lovely teaching tool that they made. So that's killer T cells at work. And one of the interesting things about those molecules that carry the tiny bits of virus out to the surface of the cell that the virus is infected is that we all have different sets of these they actually are unique to each person, the particular combination you have so you get them from your parents and mine are going to be different than yours. So if I say got the flu, I would see different bits of the flu virus than you would see. And what this does it makes it very hard for immunoscape to create the population level because we all see different parts of a virus. So that's one half of the immune system. The other half is this adaptive immunity that we're going to be considering is something called a B cell and a B cell makes antibodies and most working vaccines some of these antibodies. And that's going to be the heart of the COVID-19 vaccine we're going to talk about in a bit. And the reason they're called B cells is because they originate in the bone marrow. So neutralizing antibodies are special kind of antibody. And what they can do is they combine to a virus, and when they're bound to the virus, they block it from infecting the cell that it would normally infect. So neutralizing antibodies are special and they're able to prevent infection of cells antibodies can also bind to and mark viruses or virally infected cells for destruction. And just like those killer T cells were able to kill an infected cell antibodies can can recognize that there's viral proteins on a cell and cause an infected cell to be killed and laced and that's also a beautiful function of these antibodies. So antibodies have a nice trick that they can do. They can evolve during the course of an infection to bind better and better to their target. So what happens is in antibody will hit hit a virus when it first comes in and it'll see it pretty well, but the B cell that carries antibody will keep mutating and the antibodies will get selected for better and better and better binding to their target. So you get really very potent and efficient antibodies by the end of the infection. So here's just an example of a neutralizing antibody response. And here's the virus and this is an envelope protein from the virus and this envelope is what's able to bind to the CD4 molecule that identifies this as a CD4 T cell. Remember that's these beautiful cells that orchestrate the whole immune response. So this guy if he hits this and is able to bind to it, the virus is able to get into the cell and take it over. If you have a neutralizing antibody it blocks that interaction and it prevents it from happening. So immune memory. When you get infected with a dangerous bacteria or virus your body mounts an immune response to control the infection. After you clear the infection. Some of these memory cells are left behind and they stay on patrol. So if you're re exposed to the same pathogen, you don't have to go from the beginning and mount that whole immune response over your memory cells are there and they will make a quick and potent response that can either completely prevent reinfection or sometimes infection can happen but the disease is really modulated and less severe. So what vaccines do is instead of requiring that you be infected, they use you a harmless bit of protein from a virus or an in that inactivated or a dead virus. Some part of the virus or a virus that can't replicate. So can't get you sick, but your immune system can still see it, because these vaccines retain molecular features that are specific for the pathogen. So your immune system system can respond to that. And you can develop T and B cells like you would to a natural infection that recognize the pathogen, but you don't get sick or you only get very mildly sick.  But you're left with immune memory that can recognize the real pathogen if you ever encountered. So let me walk you through that slide.  You may not get disease with COVID. So this is a little COVID virus. You may not even realize that you're infected, but your body knows and your body is mounting a really fantastic immune response that clears the virus.  But if you make it through, you have an immune response to your cover, you feel better in the virus clears, but your body is left with immune memory cells, T cells and B cells that recognize this virus and that are waiting. So now you've got you're a protected person and if you become exposed to the virus again, you might not be infected at all or you might have a mild infection, much more likely to have a mild infection that clears quickly because you have this potent immune response lurking and awaiting to defend you. So what does a vaccine do? Well, here's our COVID virus again. It takes just a part of this COVID virus. And what everybody's targeting right now is the spike protein, which is this yellow protein on the surface. So rather than a whole virus, which will get you sick, you just get the spike protein in, you put that in the vaccine, you vaccinate, and you make the immune response, you get the antibodies, you get immune memory cells. And if you get exposed to the virus, you're either protected from infection or have a mild infection. That's the dream. That's what we're all hoping for. And that's how many, many other vaccines have worked historically. So let's go to the first vaccine. And this marvelous story, which I think is humanities, perhaps our single greatest triumph, we talk about going to the moon, to me, eliminating smallpox from this planet is just an extraordinary feat. And it took a global coming together and everyone in the world working together to make this happen. And it was a long time it happening. And we now have completely eradicated smallpox no longer on this planet, but it caused between 300 and 500 million deaths in the last century. It's a very ancient disease. It's been with us for at least 12,000 years. Those who survived smallpox were often scarred and were sometimes blinded. And the very last case of smallpox on this planet was diagnosed October 26 1977 thanks to vaccines. Now this whole process began with something called variolation. So in China in 1549, there was the first publication of this method to prevent severe smallpox smallpox. And the idea was that you pattern a smallpox scab and you blew it into the nose of a healthy individual. And this is really risky. So, if you were very elated like this. There's a 2% mortality rate, but there was a 30% mortality rate with a natural infection. So smallpox was coming through your community or your area of the world. You have this kind of a choice you can make if you're living in China and people knew how to do this. This practice was so successful and the disease was so horrific that it began to be spread through China. And then to Persia, Turkey and Africa, and then to Europe. So Lady Mary Montague was an English ambassador's wife and Constantinople, and she saw the success of this method and she brought the method home to England in 1721. And she had smallpox herself and went through it and she had her children variolated. One thing that people often don't know about our history was that George Washington was an early Vaxxer, and he virulated the Continental Army, and we probably would not have won the war if he hadn't. So in 1776 the Continental Congress prohibited virulation, because it was so risky that 2% death rate was still, you know, happening with a smallpox epidemic raging in Boston. Washington was wise and the only sun and troops that were already immune because they had smallpox and survived it. But then 10,000 of his troops invaded Quebec, and half were ill, and the new troops were really quick to second. And this I thought was an interesting quote from John Adams, our misfortunes in Canada are enough to melt a heart of stone. The smallpox is 10 times more terrible than the Britons the Canadians and the Indians together. This was a time that Washington made the decision to virulate the Continental Army, 40,000 American troops. This was a huge risk, it had been illegal he did it anyway, and it paid off infection rates in the army dropped from 15% to 1%. And we won the war, and this was certainly a factor. So that that that wasn't a real vaccine in a sense because it was so dangerous. Edward Jenner noticed something else he noticed that milkmates were immune to smallpox, and he hypothesized that this is maybe because they've been exposed to cowpox and gotten a mild infection that protected them. So in 1796 here's blossom the cow blossom got smallpox. Her dairy mate Sarah Nelms visited Dr Jenner and she had a mild case of this cowpox. So Jenner got some pus from her hand. And on May 17, he rubbed it into scratches that he made in the arms of James Phipps, his gardener's boy. And then he started virulating young James trying to give him smallpox the real thing he tried and tried. The kid never got smallpox. So he never was able to successfully infect them. James is protected. And they realize that this much more mild disease could protect you from this much more dreadful disease. And so we, this was really the first vaccine. So we have this slide it's from the old paper in 2007, but what it shows you are many of the vaccines that you guys have gotten in your life, or perhaps before you if it's smallpox. This shows you the peak annual cases, peak annual deaths. In 2006 cases in 2004 cases after so these are vaccines that were licensed before 1980. So this is what vaccines did in terms of deaths and cases for all of these lethal diseases, or could diseases that could be lethal. And certainly that caused a great deal of suffering and and pain during the sickness. This is, I think this is just a most beautiful set of numbers science magazine in 2015, tried to show this in another way. So this is how many cases there were of all of these different diseases in all of these different years as you move from 1945 to 2015 the end of this, when this end of this chart. And the red circle is when the vaccine was first introduced. And you can see the circles get smaller and smaller every year because the vaccines are working. So this goes away have a tie to say chicken pox rubella measles. Just this fantastic thing of the diseases really diminishing every year and these are dreadful diseases polio with almost eliminated polio at this point. And that's because it's so interesting that now people are afraid of this vaccine and it's coming back so we have completely eliminated measles from our country, and now it's beginning to come back and it occasionally can kill children. It's also coming back in Europe for these same reasons. So we had eradicated it. We've got work to do. Let's move us towards a coven 19 vaccine. When coven first became understood that it was that it was spreading in China, and the Chinese sequenced it made it available. People acted very quickly to start many different kinds of vaccine ideas so currently 52 vaccines are in clinical trials. I'm sorry. 36 are in pre-clinical trials. Yes, I said that correctly. And there's probably more like 200 that are being explored right now. This is just the list that the New York Times has and I took this out yesterday. So there's lots of levels of trials. And phase one is just making sure it's safe. You get the right dose to get a good immune response. Phase two, they expand that out. So this may be 100. This may be a thousand. And this may be phase three, 30,000. Here they're starting to look for efficacy. Does the vaccine really work? And we've already got 11 vaccines in this stage, which is really phenomenal. I've never seen anything move like this in my career. So here again is the coronavirus. You saw this guy earlier in the pictures. Infects human cells via spikes. So here's a spike protein, and it binds to receptor called ACE2. And almost all of the most forefront vaccines are based on the idea that you can elicit antibodies with the vaccine. They'll bind to the spike and the spike won't be able to get into our respiratory cells. So that's the principle that people are working on. And here are six that are being tested in the United States. And I just wanted to give you a sense of the different kinds of vaccines. In these six phase three trials, they're enrolling between 30,000 and 60,000 volunteers. And this is one idea. You don't use the whole virus. You just use spike and you just use the protein with something called an adjuvant, which helps stimulate the immune response. Then there's an idea where instead of including the spike protein is purified, you take an mRNA from the inside of the virus, which is its genetic material that encodes for this spike protein. And you put it in a lipid nanoparticle. So that's just a little tiny, tiny droplet of that. This can get taken up by the cell and then the RNA starts to get expressed and make spike proteins. So a couple of them are in RNAs and the wonderful results from Pfizer. I'm going to go over them in just a second that came out this morning. It was such a lovely thing to be able to give you guys this talk today because today is a very hopeful day. I don't know how things are going to unfold completely, but we've got really encouraging news on this vaccine, which is an RNA vaccine. And then another strategy, which is showing a lot of promise, is you have something called an adenovirus. So in an adenovirus, the DNA is the genetic material. And you put in a spike gene, and you let this adenovirus, which is weakened cold virus carry that in and get expressed. So I'm going to give you a little bit more background about. Let me see, I'll show you two of these vaccines, how they work. And I just heard a talk from the people who created these vaccines last Thursday. So I'm going to summarize some of the points they made. This one was this adenovirus COVID spike gene vaccine was really pushed forward by Dan Baruch at Harvard, and he uses a vector. So a little virus like this is called a vector, where it's pretty much a harmless virus, but you put the gene that you want expressed into its genome and it carries it in. It can be used to carry in lots of different kinds of viruses. So Dan and I have worked together on HIV vaccines, but he's also worked on Zika Ebola RSV. He knows that adenoviruses themselves are safe and very immunogenic in people. They've been tested a lot already. There's pediatric experiments with this vector using different viruses. And it's effective down to six months of age. So the current Charles Arton kids, but this is really promising that we'll be able to maybe quickly move a COVID vaccine down into lower age groups because we have this past experience with this way of carrying the spike gene in. So the team at J&J and Janssen who he's working with know that mass production strategies are already worked out. Several hundred million are projected and could produce up to a billion doses in 2021. So this vaccine works out. They're primed and ready to make more of it. And one of the really lovely things about this vaccine is the potential for a single shot to work. They're going to be working in monkeys, which is usually the test system. And this is an amazing timeline. They were already here for these vaccines. The ones I've been telling you about in the last slide. So in January 10th, the sequence was released. And within days, Dan's lab at Harvard had ordered the genes to be gone work on this, this system. And they partner with J&J and Vid MC. And they created the vaccine in the lab. They did a mouse study. They did a monkey study. They did a human safety study, one of those phase one early studies. And then they moved on to human efficacy already by September 2020. And this is an astonishing timeline. And what I can tell you is the human beings who worked together to create this thing have been working 60 to 80 hour work week since in February to make this happen for the rest of us. I'm just going to show you one picture. So this is what you do in a monkey study. And here, every line represents a different monkey and this is in the lungs and this is a nasal swaths and there are six monkeys represented here. So there are six lines, but it only looks like one. And this is how much virus there is in the lungs. So if you don't give the vaccine, there's lots of virus in the lungs. And this is days following the time of infection here. And if you look in the nose, which would be important say for being contagious, maybe not so much for sickness. There's again, if you don't give a vaccine, lots and lots of virus. And here there's one monkey that had a little tiny blip of virus in the nose. A single shot was able to confer this protection on a single shot would be wonderful for mass immunization programs in the world because you wouldn't have to call people back in. It would only take one shot of the vaccine so it would go farther. In the study they were able to determine that neutralizing antibodies those ones that block infection with the strongest correlative protection and a 60,000 person trial is currently in your way in North and South America and South Africa. I was also going to tell you a little bit about the Moderna COVID-19 vaccine, which is one of these books, I'm sorry, mRNA vaccines carried in that little lipid particle. It's also got wonderful properties. It also showed that neutralizing antibodies were comparable between many different age groups among older people. They're excited to have 30,000 people enrolled that are good mix of age, race, gender, and other risk factors and this is all important because there might be subtle factors that would impact say, say one race versus another. So you want to make sure it's working for everybody and that there aren't any hazards associated. They're March, by March 14 already they had a phase one started by May 29 phase two started by July 27 phase three, and their enrollment is now completed and so they're going to be moving along very quickly with news for us. Like I showed you a figure from dance paper and the group that group is Jane Jay and Jensen. This is this is again, no, no virus in the lungs hardly at all in these infected monkeys. So if you don't give the vaccine lots of virus in the lungs if you do give the vaccine very very little. There's eight animals in each of these points, and the nasal nasal slots very very little in the nose of these these monkeys wouldn't be very contagious by breathing. So it helps both the vaccine from getting getting infected and sick and having infections in the lungs, but it also helps the people that the vaccine would be exposed to. So this is the beautiful news that came this morning and I just lifted this straight from the press release. So, in their first interim analysis so this is beginning and much more needs to be done, but they shared this and this is just really array of hope. The vaccine was a remarkable 90% effective in preventing COVID-19 and precipitate in participants. So, so this was a rare very helpful for all of us for the world. They used to do schedule see you had to get vaccinated or they got vaccinated twice. They had 94 confirmed cases in their group out of 43,000 participants, and they have this diverse multicultural background. And I just want to take the moment for us all to thank with our hearts the people who volunteer for these trials, the many many people who are taking a risk for everyone else because we don't know yet with the vaccines when it's an unknown in humans how it's going to work out. And so they've taken this on for the rest of us. So thank you to all of them, many many different groups of people age groups. There are no serious safety concerns so far. I hope this continues. They're going to be submitting an emergency use authorization within a few weeks to the FDA. They're going to wait for a little bit longer time to get their safety milestones in place, hoping this will be their week of November. And the clinical trials going to contend continue to get a few more cases in these groups so they can also study other endpoints like the impact of the vaccine on disease severity, how sick you get if you do get infected and the virus breaks through the vaccine, and also how well the vaccine works if you give the vaccine to a person who's already been infected. You know, there's different things that might happen there but one thing that might happen is it might really boost your initial response to the first infection and make it even stronger protection. And they also have great protections for how much they could make if all of this goes well so this was just wonderful news we got today, and things are well on their way, and it's exciting. And so, why could this all go so fast that this unprecedented speed partly it's because the technological framework was ready. People knew how to do these mRNA deliveries these antivirus deliveries that the technology has really advanced and so there's all these ways to port the spike protein into people that were safe and that were well understood. You know, in January of this year when we knew we had to get going on this. I can't say how hard my colleagues and and my group at Los Alamos City has worked trying to push COVID vaccine research along everyone is so committed to this. The virus evolves relatively slowly and this is a huge factor. This gives a single target a chance at working and I'm going to compare this with HIV in just a moment. What will the vaccine studies have to look into safety, making sure there aren't adverse events and as you guys are probably seen in the news if there is when they stop the trial and figure it out before they let the trial proceed. Make sure there's not major side effects. They want to make sure the vaccine elicited mean response doesn't somehow enhance disease or maybe as the vaccine response wanes and it becomes less potent and strong over time. Make sure that there's no bad effects due to the immune response to the vaccine and people who got it. So this will have to be followed. The efficacy will have to be really studied can the vaccine prevent infection. What's the level of benefit so that's the beginnings we're beginning to see that out of the Pfizer study and it's 90% so far. So good. Does the vaccine reduce disease severity? How best to deliver the vaccine? So we're just learning this now. Is one shot enough? Maybe it is for the adenovirus. How durable is the vaccine response? Does it last six months? Does it last a year? What are the correlates of protection? Is it neutralizing antibodies or are other parts of the immune response really important? Will it work well against contemporary emerging variants? And this is what we are trying to work on at Los Alamos. Can it augment protection in people who are previously infected? Does it work well in young people, particularly well in young people and old people?  I want to make sure it's working in everybody. And how about people with other risk factors? So all these things need to still be understood. When they are identified, something to think about. There are 7.8 billion of us on this planet and county. And we're in this together. Manufacturing has got it scale up and it's going to take some time. And this is really a global problem. So if we were able to get things down in our country but it wasn't going down in other countries, this virus moves and moves readily and moves easily. So we've really got to attack this pandemic together because of the way it moves so quickly. Epidemiologists in public health departments, including those in New Mexico, are developing plans to effectively and equitably deploy working vaccines as they become available. And they're trying hard to think how the best and the epidemic, who to give it to frontline workers, will definitely be prioritized so the doctors and nurses who are making such sacrifices to take care of all of us. Populations at highest risk were severe disease like elderly people or people with diabetes, and they want to make fair distribution to diverse communities and make sure everybody gets fair access to the vaccine. And they're thinking about how best to do that right now. So when the vaccines do become available they can be provided to our communities in New Mexico and elsewhere in a fair and very reasoned way to harness the most power to prevent the epidemic from continuing to spread. So the things that my lab is going to try to do to help, we don't design these vaccines, but we are trying to monitor the emergence of vaccine resistance because this virus evolves really slowly but it does evolve. So we want to make sure that if there isn't a new variant out that it's swiftly identified and can be countered. People are going to have to continuously work to optimize and improve vaccines and therapies. And another thing my lab is interested in trying to work with is preparing for future coronavirus epidemics that could present against the diverse coronaviruses that are saying that populations that might enter the human population next year or the year after so we want to be, we want to be prepared for the future. So this is from the CDC and New Mexico is not doing so well right now and in the United States, we're in a very bad situation. So we've had 234,000 deaths as of November 6 and many many cases. So this is the last cases in the last seven days per 100,000 people and New Mexico is unfortunately looking like we're in the midst of an epidemic. The headlines this morning were that we've topped now 10 million cases. So just in a couple of days since I prepared this talk over the weekend, we passed this border and global cases 50 million so the US is not doing very well here, and the world is not doing very well here. I love this song by flogging Molly, it's been the worst day since yesterday, and here is a map of what's happening since yesterday so this is New Mexico's new cases reported since the previous day. And you can see what's happening here's November 6. There's been 1284 new cases in one day. And this is, you know, we're in the midst of really a crisis right now and what we have to do is pull together. And what we can do, what we can all do for ourselves for our families and for our communities is to wear masks, and it's kind of hypothetical now we have really solid evidence that this can help at a level that will help the epidemic be contained, or at least more limited. It's, it's not going to be perfect but try to limit the numbers while we're waiting for the vaccine and we're waiting for a time of year that's more favorable than the winter which is a rough time. So if you live in a place where most people wear masks, you are far less likely to know people who have COVID symptoms, even in states with really high population density so that with this. This is, is it something that came out last week in the Washington Post a graphic that they supplied based on very good hard data of states in the United States, and these are people who wear masks, most of the time, and they're out in the public, and they tend to know many few people with COVID symptoms. So I think this is really compelling evidence that Max are beneficial but I like this evidence even more. There's a very recent study that came out of Kansas, and it kind of had a nice control aspect to it so the state of Kansas does not have a mask mandate, but counties within Kansas the blue ones here do so 20 counties had a mask mandate and 80 counties didn't have a mask mandate. And this is sort of showing you the average in these pop, the average per 100,000 people in these different counties summed up. And what wound up happening is within 14 days of the mask mandate the blue guys are the counties that did have a mask mandate. The rising infection rate leveled off, and it never got worse was the counties that didn't have a mask mandate just has kept rising and kept rising and this is highly significant and it really decreases the chance of transmission to have the mask and I thought this was very nice because the counties were well controlled. Our governor has been doing a fantastic job of leading our state I think. He said a great quote on October 27 expressing a very real concern if new Mexicans do not stay home and do not limit their interactions with others to slow the spread of COVID-19. Our hospitals will be under overrun. You get in a car wreck, there will be no place to go. If you deliver baby there may not be a bed in the hospital for you. It continues at this current velocity with no roll over. No coming down. It is hard to describe how catastrophic that is. Please stay home. Wear your mask if you go out. We all have to do everything we can to slow the spread of this terrible virus. And really, this is for all of this and when you do this you're doing this for everyone in every one in your community and your family. This is really for all of us. So this is what we've got to do while we're waiting for the technological solutions to get to us. One of the things that's been really, really remarkable in this pandemic has been the global response and sequencing and there's this thing called GIZ aid which is based in Germany and it used to handle all the flu sequences in the world and now it's handling all the COVID-19 sequences in the world and people are pouring them into this database. So throughout the globe, there are vast numbers now let's see 180,000 sequences and with those sequences come the date they were sampled of this virus where they were sampled if the person had disease or didn't have diseases often included. So we have this incredible portrait of the evolution of COVID all over the world, thanks to this database and thanks to the generosity of the scientists who are who are making their sequences available to everybody else in the community to try to understand them together. It's just really phenomenal. There is a real bias in the sequencing effort. And this is because the UK is this dark blue here and this is the number of sequences, number of these SARS-CoV-2 sequences that are available and 150,000 here. And if you don't have a sense of scale, this is really, really remarkable to have this many genomes available, but really a lot of them have come from the UK. So the UK has done this huge effort to get the sequences out that many, many other places are contributing to. So you have to look at this global database sort of knowing, oh yeah there's a lot from the UK. There's a lot from the US. There's a lot from Australia. There are sequences from all over the world. And you can have a real change in the number of sequences in a given week. For example, Denmark, you guys may be reading in the press about the mink farms in Denmark that are passing between minks and humans. And so Denmark last weekend, this I, my friend will Fisher made this graphic last Thursday, you can see Denmark's right at the bottom here this really thin pink line not too many sequences. But now it's the fourth in the world, because there was a huge effort in Denmark to understand the spread of the virus that was in the minks and in the people. They submitted 8000 sequences over the weekend. And now you can see this big shift so every once in a while you'll get a big shift. So this data has biases and imbalances but it is an amazing resource. And one of the things that my group has been doing is just trying to understand, are there emergence of new strains that are an issue that we should be aware of. And we started writing the tools to explore this in February and early March. And we realized there's this one particular here's the spike protein that we've been talking about. And this is one particular amino acid, which is just one little bit of the protein. It's a position 614 that it changed. And you can see that really when this were all orange so there's this global epidemic of the original form, the D 614 form. So this amino acid goes from D to G. And you can see it's becoming much more frequent in the world. So this is the frequency of the two forms relatively speaking over time and by the end of May, there's almost none of the original but we could see very early on that this thing was really changing fast. And so we were concerned about it and we found out by working with colleagues at Dick University and Sheffield University in England, that this form that we were nervous about being more transmissible because it was really taking over the original form. In fact, was associated with higher viral loads in the upper airway so there was higher levels of virus in people. And if you cloned these spikes with the both forms and you compared them in a laboratory bench, we could see that they were also more infectious in these pseudoviruses. So we published this in in cell in in August. And since then we've it's been shown to be more transmissible in animal models. And this is one of the tools that we have at the database that was developed by my colleague Warner. And these are the team at the database that's made this happen, but you can sort of see the transition between the two viruses every time so these are just little 10 day intervals. This is prior to March 1 and the orange is the original form. The blue is the new form and the size of the circle indicates how many sequences came from these countries. And this is all data that came through just a through this amazing global effort, but already by March 11 to 20. This is what the sampling looked like and you could see places that had really well established original epidemics that were raging locally. Once this blue form got introduced, it really started taking over and this happened virtually everywhere in the world so it was the repetition of this pattern that caught our eye in in late March and early April. By early April, the transition to the new form had happened much more radically and by mid July there's really virtually none of this left. What's important is that this is the format that we want to be working with, and we wanted to understand why it was moving so fast. So other studies that we began in April as soon as we notice this effect, we're to try to figure out why and this is a graphic made by my colleague Aaron, and he uses the supercomputers at Los Alamos to model the way the protein moves and sugars in space and how it's dynamic proteins don't just sit there. And what he discovered was that it tends to be in this one up confirmation where one of the arms of the spike goes up. When that happens this is exposed and it can get better access to ace to that molecule it uses to invade human cells, and it also exposes really good neutralizing antibody sites. So my colleagues, David, David Montefiore and Drew Weissman were able to show that it's the new form is actually more sensitive to neutralizing antibodies not less. So the blue form, it gets a more potent response to neutralizing antibodies than the old form. So it's not like this is this new form is more resistant is actually more sensitive to the circulating strains but it was really important to work that out. And why we know that's because it favors this open confirmation that both lets it bind to its receptor better, but also exposes its antibody sites. So Atlanta what we're doing is just supporting the vaccine effort by continuously tracking mutations as they arise and are detected and gives a, and advising our scientific colleagues who we've been working with for years on HIV who are now taking on co good as well. The scientists who are going to be testing the vaccines and the antibodies that we might be using is therapy. What are the panel of SARS co two viruses that they need to test to make sure that the virus is going to be working against most of the circulating strains in the world, and that the vaccine will stay effective so that we're trying our best to help them to contribute. And there are now several new spike mutations that are beginning to increase, increasing frequency globally and we're following those and working with our colleagues to test what that might mean in terms of the phenotype. And there are some rare mutations, but they're near that ace to binding site so there's maybe specially biologically important so this is the kind of thing we have our eye on. And I'm going to turn to HIV just quickly. This is this is sort of to give you a sense of scale. There are 38 million people living with HIV in 2019. And 25 million people are currently getting treatment, and 1.7 million people were newly infected with HIV last year, and roughly 700,000 people died from AIDS related illnesses and this is down from 2 million a year. Because of all of these people getting treatment which is fabulous but we still don't have a vaccine for HIV. As the HIV epidemic began, though, there have been 600 to 100 million people who've been infected, and between 25 and 50 million people have died from AIDS related causes. COVID in one year, we've had 3.3 million cases. Over the prior week and 4946 million cases in 2020 this is the number of November 6 data. This is changing every day and 1.2 million deaths. So in one year, you know we've had more deaths of COVID than we have with HIV. And what do these numbers mean and you think about a million deaths it's hard to realize that each one of these is somebody's friend or child or lover or mother. Because these are hard deaths. So the scale of this 1.2 million deaths in this year and we're not even done with it yet. About 15 million people died in World War One, between 1785 million people died in World War Two so you know the deaths due to HIV are comparable to this. The scale of 1918 affected about 500 million people and killed about 50 million people and usually in a typical full year between 12,000 and 50,000 died so you can see the scale of this problem and and why we're so focused. Why can we get a COVID vaccine in one year and we're not going to get a COVID vaccine in one year and we're not going to get a COVID vaccine in one year. Beautiful minds all over the world than trying to get an HIV vaccine, you know, since 1986. Well, it's because COVID's holding still and not evolving very fast, whereas HIV is evolving incredibly fast. And if you compare to HIV proteins you line them up up to 40% of the amino acids can differ between these two envelope proteins. So, even within a single person over time you can have 10% amino acid variation. I'm showing up in a single person and HIV doesn't just evolve by a base change the way we think of evolution happening but it also we combined that it has insertions and deletions and it radically modifies sugars on its surface. So all the red bits are really, really variable bits of the virus and the blue bits are the more conserved bits. But this is what this the map of the envelope protein in terms of diversity. And these are our neutralizing antibody sites that are cross reactive and they're these neutralizing antibodies that target these sites are able to hit different HIV strains. But there's always some little bit of diversity that can impact their binding. So this is what we're up against. And I made your graphic to show you what I look at all day on the computer screen this is actually an alignment of COVID protein. And it's right near the ACE2 binding region. And if I have a blue dot, it means that it matches the Wuhan strain and it hasn't mutated and it's exactly the same as the Wuhan strain. So this is the bit, every single row of dots here is a different virus and now as you've just seen there's about 170,000 of them number increasing every day available and gives eight and every column is a different column of amino acids in that protein alignment. And when you see a little spec like this, it means the amino acid has changed so it does change a little bit. And every once in a while you get transmission of the change. It's happening a little bit, but mostly when you look at the COVID alignment it looks like this very very little is going on, except for that 614 site, which changed in spike it went from all one thing to another thing. There are a couple of other sites that are coming up a bit but for the most part, it's really conserved so these vaccines that I was just telling you about are all based on that Wuhan strain that original strain and sequence that came out of China sequence became available in January when the virus started making vaccines, but it will probably work against this wild, wild collection of viruses from all over the world because there's so little variation, and antibodies do tolerate a little bit of variation. This is now what the online that looks like in the CD for binding sites it's it's the counterpart for that. It's where the envelope hits the cell and again every row is a different sequence. So when you get a color change here is a different amino acid from the HIV reference strain called HXB2, and the immune response sees about 10 amino acids at a time, maybe. So you've got all this variation and you're going to have this is a really good antibody targeting region, you can see how variable it is. What virus do you put in to make an immune response that can see all of these amino acid variants in the protein that becomes really difficult problem, and how you get antibodies to a vaccine that can tolerate this variation and make all of this virus responses is is really at the heart of a lot of vaccine research. So here's a phylogenetic tree of HIV. And what we do is, we've come up with a scheme called mosaics, where I take all of the diverse viruses from around the world that we have with HIV. And I use a computer to create fake envelope proteins that look and feel like envelope proteins but their combinations of these that in combination will give the best maximal coverage of this entire global set. So if I'm working with a vaccinologist and he says all I can put in our three different arms. I'll set the algorithm to say okay design for me the three best envelopes to cover this great diversity. They don't have to be natural but they have to look and feel and fold like a natural protein. So that's, that's basically what the constraints are, and I design these things in my colleague, Dan Baruch, who's worked so hard on the COVID vaccine and also Bart Haynes at Duke University has tested these vaccines and I'm going to quickly walk you through the tests. Here's the macaque that Dan's been looking at them in. And this is number of challenges so you vaccinate the animal, he's been vaccinated out here, and then you start in trying to infect him with HIV. And this is the animal that didn't get these are the set of animals, I'm sorry they did not get the vaccine they got a placebo. And this is the set of animals that got two different ways of presenting the mosaic envelopes that they told you about. It took a lot more hits a lot more exposures to infect these animals on 246 all of the animals were infected by three exposures most of them the first time they're exposed with no vaccine to this delay as a benefit. And, and Dan could show that our mosaics was able to give us kind of benefit, even to heterologous viruses as early as 2013. So this was good. And I know that when the animals finally didn't affect it after you kept exposing them and kept exposing them, they survived if they had the vaccine, and they died, if they did not they died of AIDS if they didn't have the vaccine. And this was because the vaccinated animals were better able to control their, their level of irony when they first got infected and later on. So this was really encouraging. And knowing this, they went forward with Johnson and Johnson, and Jensen, this vaccine subsidiary of this company, and they did an evaluation where they matched monkeys and they did a phase one to trial in humans. The idea was they would try a bunch of different ways of delivering these mosaics they tried six different ways and 72 different monkeys. And they would say which one of these worked best for protection. And then, at the same time, they put these measurements into people to make sure they were safe. And they decided that they would use if they were able to get a very strong preventative effect in the monkeys, and they were able to elicit comparable immune responses in humans and they were safe and in phase one to trial that they would go on and test these for efficacy. So they were able to get very good protection in monkeys and this, this was the particular delivery that worked best. So this again is monkeys that didn't get the vaccine and trying to infect them you try over and over. Most of the monkeys are infected. The percentage of monkeys infected is what's on this axis. The percentage of monkeys infected the first time they're exposed, but with the animals that got this particular regimen for the vaccine. After many, many exposures, they're still after six exposures still lots of monkeys that remain uninfected, and they're doing much better than the animals that weren't vaccinated. So this was the one to go with. The correlates of protection are not neutralizing antibodies in this case remember I showed you how neutralizing antibody works and blocks infection of a cell. And that's what we're going for with these spike, these spike vaccines that are being tested right now for coven. In this case, for this particular kind of a vaccine, the correlate of protection, the part of the immune response that best correlated with giving this protective effect turned out to be T cells or Eliza which is just general antibody responses there are no neutralizing antibody responses. So this vaccine is calling up different aspects of the immune response to confer this protection and monkeys. So they showed that they could get these aspects of the immune response in humans using the same vaccine. And now this trial is called a Makoto and it will be finished in 2021. This is a much smaller trial than we've been thinking about with COVID because it's called a phase to be will be able to hopefully to tell if there's some efficacy. There's 2600 women in this trial, and this is to just give you a sense when a vaccine trial goes through this kind of thing. It's a huge number of people of great heart who work with all of the amazing volunteers to test the vaccine and see if it's effective. We're also doing a second trial in North and South America that's a phase three trial, but these results will be coming along later so we're hopeful. This vaccine does have a benefit in monkeys. It does have an opportunity to reach out against these diverse forms, but it may not work we don't know we'll just have to see what unfolds in 2021. There's a little bit of a pause on this vaccine study because of COVID, but these amazing people have been keeping it going through the COVID epidemic. And these are just, I've been giving you acknowledgments throughout the talk, but these are in particular people who have worked with me, and who inspire me in my work every single day Charles Darwin, and my dogs who keep me thinking and going. But these are my friends and colleagues who have worked on these vaccines with with me to get in the code to where it's at now, and to help us think about how to do these mosaic designs to try to contend with diversity. So, that's it and I would be happy to take questions if you've got some questions for me. Yeah, hi. Go for everybody. Okay. Thank you very much, Dr corporate for such a wonderful presentation and very up to date information. So we are so glad you have the information you want released from today. So, so happy. Now, we can let our audience ask you any questions. Oh man, we have quite a few of them. So thank you so much in advance. The first question that we have is what is happening to our microbiome during this pandemic when we are trying to avoid all exposure to new bacteria viruses etc. It's a very good question but I don't have a clue about the answer, but I really do like the question. And because I'm so engaged in the vaccine side I'm not and I'm not actually even trying to read that literature but I guess there is a literature on on the topic. I'm sorry I'm not going to be able to help you with information there though. All right. Next question then. If, if antibodies make one have less severe reaction, a second time, why do some have a more severe reaction, more severe second reaction, or have those cases not improved. There's really, I don't think we have a good sense about second with COVID with about second infections yet so we know they can happen. And also that the antibodies tend to decay pretty quickly after you've been infected the first time. We don't know a lot about what drives some people to get sick and some people to stay well or not even feel symptoms. So we know that age is a strong correlate we know being male is a correlate. We know diabetes is a correlate but we don't really really understand why we actually know that high antibody levels as a correlate but that just could be a consequence of having a lot of virus when you get very sick. So there's just so much that still remains to be understood. And we're just beginning to get you know cases they're definitely cases of people who have gotten reinfected. And we think that actually they may have gotten, they tend to be less severe overall as my sense of the literature. So we're hoping one of the things that will unfold as these massive vaccine studies are revealed over the next months. And what we'll know a lot more in 2021 is if you give the vaccine to a person who was infected, you may be really boosting their immune response and making them do much better on reinfection. And another thing that happens when you get COVID is your immune system is compromised you're not in an ideal setting for making a response. The advantage to a vaccine is that you're giving it when the person is healthy and they can really maximize their immune response make a really good strong immune response. So it might be that the vaccine can even do better. In some cases, or in many cases we just don't know. This is going to all have to unfold where we're working, we're walking into a fog and trying to sort it out and clear it out with data as we go. I don't know, I just, I'm so amazed by the global effort that has made us get to this point this fast. It's just, it's almost inconceivable how hard and how fast people have worked to get us here, but we many questions are still unanswered so what we do know is that the vaccines that are going forward to phase three have gotten through those phase one really doing really well. And now we know that one of them in the earliest preliminary analysis looks like it's very effective. We know they're very effective in monkeys and we haven't seen that harmful effects in monkeys. So that's where we're at, but, but there's so much left to unfold and that's one of the questions that will unfold over the next half year or so. Thank you for that answer. Okay, we're just going to rapid fire and we have so many people asking you questions. I hope I'm going to be able to answer a few of them, we'll see how it goes. The next one is will fires COVID to vaccines protect against other coronaviruses as well. That's a really good question. So, so one of the things that people are trying to do is to characterize the antibodies that come out of natural infection. So convalescent syrup, they take the antibodies out of a person who's healed and gotten over corona, or they take vaccines here and they isolate the antibodies. Once they've got that I said, then anybody called they can really begin to look at it. And one of the first things they do is they look at panels of other coronaviruses so where where we've gotten coronaviruses from we've had three bad epidemics with in humans because of coronaviruses. The first SARS epidemic, which thank God was contained the murders virus which comes to us via camels and continues at very low levels that is very lethal, quite a frightening virus. And then, there are many, many diverse viruses in bats and you might have heard about pangolin this this charming little animal that has also gets infected by coronaviruses and the virus that moved into us this time SARS-CoV-2 has as its closest relatives mostly a bat virus but has a bit of pangolin in it to these viruses recombine some level. But when you start looking out in the world of coronaviruses they're very diverse. And so, people like Ralph Barrett at North Carolina have a panel of different viruses that they can test antibodies against. And what, what he's trying to do with his colleagues in this kind of testing the diversity of responses find antibodies that are able to really cross react and we don't know when the next coronavirus spill over into humans is going to happen. It's happened three times in 20 years it could it could happen again next year. You know, so the notion is we don't know what the next one is but we know they're really diverse. So, one of the things people are trying to do right now is see which of these antibodies might be really cross reactive and able to work against other coronaviruses. And then you can maybe make a cocktail of antibodies that could be ready. If another one slips into the human population. This is something I'm trying to do a little bit I'm working on a T cell vaccine that could be pan coronavirus and work with many different, not the whole of coronaviruses, it's too diverse, but maybe the beta virus which the two stars and the most viruses are in that family. So people are beginning to think about that now, and they can actually test the antibodies against these different viruses, and see which ones are able to cross react so they can, they can physically check that experiment and do it, and is being done now. So that that's ongoing kind of a future looking effort as we're working on this pandemic to think ahead so we don't get stuck again. Outstanding. We have, I'm wondering if NM and math would like to jump in while we still have time. And if that Betty you would be able to stay on for a few extra minutes to answer all of these questions. Yeah, yes. Okay. We'd like to, we'd like to enter invite Jiming and Jane to turn on your camera and make our presentation and then we'll come back to answering questions.  Yes. Thank you, Betty Colbert on such a wonderful presentation. So as our appreciation. And on behalf of New Mexico Academy of Science as a current president, I would like to present a distinguished speaker award to you. Thank you so much. Thank you. Thank you so much. Yeah, this block here home address. Fabulous, I really appreciate that I appreciate the chance to talk to you into everybody who's zoomed in to be with us tonight. See we have more than 100 participants. More than 100. I think so 112 are noticed. Thank you for your presentation the moment they go. Well, thank you. Thank you all for being here. So that's lovely to hear. I wish I could be with you in person. Yes, in the future, we will. Thank you. Thank you. Brittany. All right. And going back to the question. There's so many. I could maybe answer some via email over the next day or two, if that's possible, I don't know if we don't have time. I'm sure that'd be possible. Um, for sure, we should have your information if you've registered for this webinar and we can pass your questions along to Dr. Cobra, if, if that's what you prefer. Definitely going for a bit, but if there are some left to me and I'd be happy to do that. I think, okay, we will just do a few more then. Don said I had COVID-19 in March and have donated convalescent plasma four times 15 bags of 250 milliliters. Should I worry about diluting my own antibodies by over donating. No, you should not you've got that that's a wonderful thing to have done and know that's not a that's not a concern I don't think but that's just a magnificent thing so thank you. I have some more technical questions that I'll probably pass along to via email, but we'll go with more general ones. There's about two or three more. What will what we've learned in addressing the COVID-19 assist in addressing other present viruses. Yes, I, it will certainly. And that's true for every vaccine effort. I, you know, one of the, it, it's been one of the hardest things in my life to work for 30 years on an HIV vaccine, and to not have one and to not know if we will have one next year we might and I would have been, it'll be lovely if we do. We have learned so much through that HIV process. So, you learn things about ways of presenting viruses you that are generalizable. So the what the viruses that we're going with with COVID so swiftly that were the delivery methods that were available. You know, in February to get this thing moving. All of those have been tried in HIV, or in at least in the monkey systems and, you know, and with other viruses and so we have things about their safety record we have things about potential adverse events we know what to look for. We know about dosing we know about a lot about adjuvants. And so every time we start conducting a lot of trials, and internationally, the international scientific community, we learn, and all of that can be applied in the future to other efforts and new pathogens as they as they come into the human population, or animal population you have vaccinating veterinary vaccinations are also very important things. So you, yeah, we will learn a lot, and hopefully we'll also get an effective vaccine. One of the things that we may have to learn from flu is that flu does, you know, change every year, but so at the population level it evolves pretty slowly also in the human population. But it shifts away from the year before is virus globally, and scientists monitor that and then have to, you know, create a new vaccine that's going to deal with the new variant that's out there. We may have to do that with COVID also, but we have experience with that with flu. We've learned so much so we'll be able to apply that experience to COVID so this, you know, this this vaccines that we've been hearing about may help us beautifully in 2021 So the virus may shift a little by 2022 and we know how to look for that because of other vaccines so so these things all are in kind of in feed knowledge feedback loops and yeah there's a lot to be learned from this for beyond COVID I think. All right three more questions and then we'll let you go to sleep. We are successful in finding a COVID-19 vaccine is it possible that we will be able to find a vaccine for all coronaviruses and eliminate the common cold. Oh, that's a great question I um There are other ways of getting colds besides COVID so that's one one route to colds but there are other viruses that can cause colds like adenovirus is the ones that Dan has made a non replicating virus adenovirus but that virus can cause something like the common cold. And I think that it's not going to be one, you're going to have to make a specific vaccine for every, every pathogen that gets into the humans, and we've got a few corona viruses that do cause colds like the question is addressing. And we can maybe learn methods and we can maybe get some cross reactivity. We can learn strategies where we could put in the spike from those, those viruses. There's a lot of money and resources, obviously, to try to get a corona virus vaccine for SARS code to. So maybe that can blaze the trail for other vaccines in the future and I think that's quite, quite plausible. But, you know, investing this level to get this kind of vaccine out is going to is going to create a knowledge base that maybe will translate to help with other, other viruses. Awesome and this next question I'm sure is on a lot of people's minds. It's two parter. It says why are people getting COVID-19 more than once. And what are some things we can do to build our immune system. Well, those are good questions. Well, I think they're getting it more than once, likely because their antibody response is waned. And it starts up, you know, really high levels right after you're infected and kind of goes down. And that could be part of it and we don't even really fully understand the pace of that yet. So there's papers in the literature that say it wanes pretty quickly. There's other papers say that it lasts for, you know, much better. So I think we're still learning that and starting that out through people like the lovely person who, who so generously has donated his convalescent Sierra that's the kind of thing that provides that sort of information. That's one reason. Another reason is, it's possible they might have a very rare escape variant or something like that. That's, that's able to infect or get past the antibodies. That's also the kind of thing we're going to have to keep an eye on internationally and see if it's happening much we don't know yet. But there isn't very much variations like but there's a little.  And that maybe sometimes allowing this to happen. All right, last and final question, and just a reminder to everyone if your question wasn't asked out loud, we will pass them along to dr copper after the webinar. But the last question we have for you this evening is, can we expect the emerging coronavirus sex vaccines to be effective in people with compromised immune system. Well, that's a great question to and it might be more difficult so they're, they're using the in these really large studies. They're using a whole lot of different kinds of volunteers right so people who are maybe a greater risk or have some kind of compromised immune systems so I think the answers to that will unfold as these these trials unfold and that data becomes available. But there's also another avenue that people are pursuing very hard and that's called a therapeutic and so rather than give a vaccine what you do is you get antibodies and you get them say out of a convalescence serum, you can clone an antibody, you can see if it's good potent neutralizing antibody. If it is, you can make a bunch of that clone and you can use it as a therapeutic. So, my colleague Erica Oman Sapphire is leading the assessment of these antibodies for the project work speed, which is a national project to make things move fast. The idea there is you would take a little cocktail it's called that maybe two or three of these antibodies, and you would give them as a therapeutic agent. So the prisons and have to mount their own response they're able to be given these antibodies which could help and if they get infected you can give them, if you can give them quickly. You've got a chance at really, you know, cutting the virus off before it can cause disease so that would maybe also be a possibility for someone who would need additional boost beyond just what they could get from their immune system and a vaccine. And also for people who don't get the vaccine, but who become exposed and infected that might be a way to help treat those people. So you're using the immune system, but you're using it differently than a vaccine you're giving them the antibodies rather than having them make themselves. Thank you so much Dr. Korber for your incredible generosity and your fantastic talk that I think was in was very informative but also gave us a lot of hope about the the plans for the vaccine and how science here in New Mexico is really working toward finding a cure and the and the vaccine is pretty, pretty exciting. So I just want to remind folks who whose questions weren't answered. Brittany is a whiz and she'll make sure that she matches up the question and the person and the email to Dr. Korber so that you'll she'll be able to follow up with you after the, after the fact so one of the sad comments about doing this in a virtual spaces that we can't really applaud you but we can all give you virtual applause that so please join me in thanking Dr. Korber for your time and expertise and your work on all this so thank you so much we really appreciate you tonight thank you. Thank you for this chance I really appreciate you. Thank you. We wish everybody a great night and invite you to join us for the rest of the research symposium.  Thank you all have a good night and see you around. Good night.