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Recently published research suggests a strong causitive link between infection with Epstein-Barr virus and development of multiple sclerosis (MS). Two decades worth of data analyzed by 

 showed that participants who were infected with EBV had a 32-fold risk of developing MS. Further research from Steinman et al published in 

 has demonstrated a possible causative mechanism. 

, in partnership with the Consortium of Multiple Sclerosis Centers (CMSC), previously organized an 

 to discuss Ascherio et al's findings. As we look to better understand the implications of these findings, 

 spoke with Alberto Ascherio, MD, DrPH, and Lawrence Steinman, MD, to try to answer some of the most pressing questions that the healthcare provider and patient communities have in regards to treatment, prevention, and overall public health. Watch the discussion below:

® Peers & Perspectives discussion on the relationship between Epstein-Barr Virus and multiple sclerosis. I'm Matt Hoffman, managing editor of 

®, and I'm joined here today by Lawrence Steinman, MD, a professor of neurology at Stanford University, and Alberto Ascherio, MD, DrPH, a professor of epidemiology and medicine at Harvard Medical School. Thank you both for joining me today.

Dr. Ascherio, much of the conversation obviously starts with your recent research. A lot of the buzz started there, so I guess it makes sense to start with you. So very briefly, just to summarize, for those who are perhaps unfamiliar or haven't had an opportunity to read the paper, could you just summarize what you and your colleagues found?

 Yes, we studied the relationship between infection with the Epstein-Barr virus and risk of developing multiple sclerosis in a large population of over 10 million young men and women in active duty in the US military. And we found that those who were not infected with Epstein Barr virus, they don't get MS, and the risk of getting MS is virtually zero until they get infected with the Epstein-Barr virus. After infection, the risk jumps up 30-fold, and that cannot be explained by any other known factor. So, the conclusion—we can get more into the details of the study—but the conclusion is pretty compelling that the Epstein-Barr virus is the leading cause of multiple sclerosis.

 Absolutely. And then so, obviously, that leads to a lot of questions in the clinical community. And the paper is causing quite a buzz, but I think the next big question there is really is why? We have this causative relationship that we're seeing, and we have almost two decades—correct me if I'm wrong—of literature that have kind of culminated to this point and this understanding. But obviously, as many people are aware, and as you're both well aware, a very large swath of population, more than 90%, is infected with Epstein-Barr virus at some point in their lives. But not all of us, and even most of us do not eventually develop MS. Only a minority do so. Dr. Steinman, I don't know if perhaps you would be the best person to kick it to here, but from a pathological perspective, what's going on? What do we know about why that is?

 Well, I think it's, first of all, a magnificent discovery, a combination of decades of work that my colleague has done using a precious resource: a military database. And it just shows the value of these public health tools that can lead to better health. But one of the leading questions is, and you raised it, most of us, more than 90% of us have been infected with EBV. And we live our lives when we don't have MS. So, what additionally might be going on that takes a person who is infected, and somehow culminates in this disease called multiple sclerosis?

I have been working at Stanford with some gifted colleagues—Tobias Lanz, MD; William Robinson, MD, PhD; Peggy Ho, PhD, MS—we've been working for decades. And part of the answer—and only part can be explained, perhaps—by a concept called molecular mimicry. You get infected, but a few additional switches have to be thrown, or, I use more dramatic term, a few extra fuses have to be lit, before you get the explosion that we call MS. So just in the simplest terms, there's something in one of the molecular components of EBV, called transcription factor called EBNA1, or Epstein-Barr nuclear antigen 1, and it resembles a piece of protein that's found on the white matter. If you somehow have an immune response against a small region of that EBNA1, your body may mistakenly attack a piece of your myelin. And there are all sorts of subtleties in how similar one piece of the viral machinery resembles one piece of our white matter. A few changes have to occur before even that mimic becomes the harsh beginning of what we call MS.

It's a detailed story that's still being worked out. And of course, knowing this, and knowing the amazing correlation between EBV and MS, it raises all sorts of great possibilities of treating the disease, or even eradicating it someday in the future.

 Absolutely. From a public health perspective, Dr. Ascherio, what could that potentially mean? Just thinking of the possibilities, obviously, therapeutics are kind of the first thought that pops in my head, but potentially could this mean that we could this we could develop something as simple as a vaccine against EBV that could then prevent the development of MS?

Yes, I think if we had a vaccine that prevents EBV infection that confers what we call sterile immunity, I think almost certainly that would prevent MS. The large majority, if not all, cases of MS.

Concerning treatment, there is a bit more uncertainty there because they strongly depend on the mechanism by which the Epstein-Barr virus causes MS. That, you know, I think that would be interesting point of conversation in future research. Is the virus driving the disease process? In which case, if we target the virus, we could stop the disease process? Or is the virus triggering a mechanism that can survive even without the virus? And I think that that is the really big question out there for the 2.8 million people with multiple sclerosis.

 Absolutely. I'm curious. For the pair of you and for your colleagues, what are the other remaining questions? What are the things that we need to figure out in terms of determining this potential cascade of events from infection to the onset of MS, or the disease process that we call MS. What, what do we need to do to figure out what is happening in the interim period there?

 Well, I think there's a lot to learn. I think one of the really remarkable, amazing parts of Dr. Ascherio’s research has been to not only say it's EBV, but that the details of the paper point to that particular region of the—I call it the molecular machinery of the virus—that EBNA1. We were really struck by one of the tables in the paper, at the very top of the list, was the region that contain the part of the molecule that we were looking at. The probability value was something that started out with 4 zeros in front of it, and it was right at the top of the list. Fortunately, there most of the major hits were in that area because it does raise an important question: if the capsid molecules were definitively involved, and they don't seem to be, that would make the type of vaccine that people are thinking of quite problematic because if you had a susceptibility, that vaccine could unleash something that's unwanted. So, the good news is, that is not the case.

I'm thinking of my older sister who got polio 3 years before the Salk vaccine. Could we someday make MS something that no longer is seen, and young neurologists will only read about it in the textbooks in the future, in the same way that polio has been largely eradicated in the world? That's the big hope. But there's a lot of good fortune so far as the story emerges, and not some stunning roadblock. So far, so good. As we heard, the vaccine is the best hope. But there are some other elegant strategies that include antivirals and some other techniques.

One of the things that happens in MS that's so unusual is that the immune system wanders, for some reason, into the central nervous system. And the cells that are infected take up residence inside the central nervous system and they seem to like it very much. They get in, they don't seem to be able to get out very well, and we have antibodies produced within the brain itself. That's an unusual situation. For over 50 years, neurologists have used that observation to help define a diagnosis, even before we had good imaging. A person would have what are called clonal—here's a fancier term, oligoclonal—immunoglobulin inside their spinal fluid. And there are a few other diseases where that happens, but not many, and MS is the most notable. So there's some amazing pathophysiology and the whole story.

Thank you, Larry, thank you for pointing out the convergence between the epitope that is leading the new response in our study. Your work on cross reactivity with glial antigens, I think that that is really exciting. I just want to stress what you say, the importance of EBNA1. Even before the study, we found that among individuals who are infected with Epstein Barr virus, there is a very strong gradient between the response to the anti-EBNA1 and the risk of developing MS. So, you see the higher the anti-EBNA level, the higher the risk of a MS, and this suggests that, your recent finding, Larry, on this cross reactivity, molecular mimicry with the glial camp, could be critical to disease development. So we're looking forward to look more in depth to these aspects of the disease causation.

One of the really bright lights about the whole thing is that even before all this activity, we've been in contact, acquaintances of us have visited Dr. Ascherio in his office—he's been most welcoming. And now on a research front, we're just discussing some very interesting collaborations between the two coasts, and it's going to lead to something worldwide. So that's very reassuring that you're speaking to the public and, and MS patients.

To me, one of the other big issues, as a person interested in neuroimmunology is, if EBV and an immune response, somewhat unwanted, to one of its parts of the machinery happens to trigger MS, does the disease continue because of that response? One of the very interesting things that everyone is aware of, is that with some of the other common herpes viruses and other viruses, the cells that make antibodies to them are also inside the spinal fluid cells that are making antibodies to measles, to rubella, to another herpes virus that causes chickenpox and later in life, zoster. Do they have any role in the continuation of the disease? Or in the development of the attacks? The so-called relapses? Maybe yes, maybe no. And if yes, then it makes certain strategies more favorable and other strategies, less favorable.

What we would like to have is a so-called magic bullet—and a vaccine would be the best way to do it. That raises another question. Should the vaccine be given early in childhood? Or should we wait till people get to high school and college? Those are really important questions. Will this be yet another vaccine that our children get when they go to the pediatrician? They get a lot, and we've really done a very good job of eradicating diseases that 100 years ago would kill people, or, like my sister, caused a significant disability throughout the rest of her very nice life that's ongoing. These are things that we don't have answers for, but I think everyone is working very hard to try to get those answers.

I think that poliomyelitis is a good analogy that I often bring forward. Also, to highlight how a common virus causing a rare disease is more the rule than the exception. Now the polio virus used to infect usually all the children in the United States, but only 1 in 400, developed the polio disease. We never figured it out why that 1 in 400 did and the others didn’t, but we eradicated the disease. So, in that sense, the relationship between Epstein-Barr virus and MS could be seen in the same way.

Unfortunately, one of the challenges we have is that there is a long lag time between infection with Epstein-Barr virus and the onset of MS. That reminds me of the situation between human papilloma virus, for example, and cervical cancer. Still, today, we don't really have clear evidence that the vaccine is preventing cervical cancer. We're starting to see that the vaccine reduces the risk of infection and reduces the risk of cervical dysplasia. But it will take many years before you can actually prove that the vaccine prevented the cancer. In MS, it will be the same situation. We could have, tomorrow, a vaccine against the Epstein-Barr virus, but it will take many years before we can actually demonstrate and see the decline in the risk of MS.

I think we will also face a similar challenge for treatment, that is more your field, Larry. So how are we going to do that? It seems so difficult to do trials given the efficacy of the anti-CD20 drugs in multiple sclerosis—how are we going to test whether new drugs targeting the virus could be more effective?

Well, that's very true. The most common form of multiple sclerosis is what we call relapsing-remitting—there are attacks, and then you go into remission. And there are about 15 approved drugs in the United States to treat that disease and a particular group of those drugs that we call anti CD20s. They work on the B cells that are infected by the EBV. It's very, very effective in the relapsing-remitting form, and it has some benefit in the progressive form. If one has to design a trial, they may have to deal with the reality that we can't do a placebo-controlled trial in the industrialized world. The workaround in a lot of these trials is to go to parts of the world that can't afford 1 of these 15 drugs, and you do the trial there and you get a nice answer. Besides the ethics of doing it that way, there's the reality that the parts of the world where we do those trials are becoming wealthier and may be able to pay for the drugs and their populations will demand it. So, I think it's really challenging.

The other thing too, is this disease comes on most commonly in young adulthood. It affects women about twice as frequently, maybe three times as frequently, as men. In the comparison with polio—with regularity, during the summer months the polio virus that lived in the intestines was transmitted more readily. It's not transmitted through the air, it is transmitted through a different route, the so-called fecal-oral route. So, kids would go to camp in the summer, or they would go to the swimming pool in the in the town, and 1 out of 400 or 500 would be unlucky, and there was a big seasonality to it. We weren't as aware of the transmission then. There were other really fortuitous developments. A professor—whose son was in my class at medical school—working with another professor a few 100 yards away from the School of Public Health learned how to grow polio in a plastic dish, and that made all the difference in getting to an exceptionally effective virus. But the good news was, the trials were easy to run, and they could be run on a massive scale. As I understand it, there was pretty general agreement this could really change the lives of families so that they didn't have to worry about their kids getting polio in the in the summer. And the vaccine trials went on magnificently. The only thing I remember is lining up in school, and we knew as boys that if the shot hurt that we shouldn't cry because the girls would see us, and the girls wanted to show that they were stronger than us anyway. That was the issue—it wasn't whether we should get the vaccine or not. The world has changed. Unfortunately, this won't be so simple.

 And so that kind of brings me to a question for the two of you. Obviously, you know, the development of something like a vaccine to prevent MS would be a magic bullet, Holy Grail type of development, but again, not something that's going to happen overnight. With Dr. Ascherio, you brought up an interesting point with the relationship with polio how we didn't fully elucidate the sort of cascade of events and why, despite high exposure rate, the development of polio was only what it was. I'm curious—is it sort of a similar situation here? Do we need to model how this cascade of events happens, and what's going on? Or would that be the next logical step to develop something like what we have for cervical cancer to reduce the risk of MS and then eventually see how that plays out? Does that sound like something that, feasibly, would be the next step forward or a next step forward? Or would it make more sense perhaps to help increase diagnosis or impact diagnosis in some way to help understand this cascade of events that's happening?

I think we know, and Larry hinted to it, that the vaccine could—depending on the mechanism by which the Epstein-Barr virus causes the disease—also have a theoretical adverse effect. If the immune response against the viral capsid, for example, cross reacts with brain antigens, a vaccine wouldn't necessarily be a good thing. I think it's important to understand the mechanism in parallel with searching for a vaccine. We want to make sure that the vaccine will elicit an immune response that is not going to be cross-reactive or triggering our immune process that we're trying to prevent. We may be able to eradicate the disease with the right vaccine, but it's important, in parallel, to fully understand the mechanism that underlines the relation between Epstein-Barr virus and multiple sclerosis.

And then there's some other approaches that are more dramatic and more targeted. The question comes up very often, “Well, I had infectious mononucleosis—and that's caused by EBV—am I going to get MS?” And the reassuring answer is it’s very unlikely that you will. We do know—and a lot of it comes from Dr. Ascherio’s research—certain genetic factors and certain environmental factors actually increase your risk even more. We have certain genes that have a fancy name—I won't spell it spell it out. They're called 

, and they have to do with how our immune system chooses what part of a virus that it attacks. You can attack the front end, the back end, or the middle end, and HLA is very much involved in that. So certain people are at higher risk. Then, certain things in the environment can make a big difference too. If you have a low level of vitamin D, it's not good. If you're a smoker, it's not good. And there are some simpler measures that could also make a big dent in the rate of MS.

To get to the heart of the issue, number one on the list would be a vaccine. Number two on the list is an antiviral. But when do you give the antiviral? Do you give it when somebody has infectious mono? Do you give it to everyone at the health clinic at Harvard or Stanford or in the high school when they got infectious mono? That type of trial that might be done—they're not easy to run. And would it even help infectious mono? Many kids who get it have to miss months of school, they got so tired and fatigued. That's one of the major presentations of having mono. And of course, just to riff on to another topic, in MS patients, massive fatigue is actually a real problem, and then there's other syndromes, we call them—we don't officially give them the designation of a disease—such as chronic fatigue syndrome. Are these manifestations of EBV? Should we be a lot more understanding of people who get it? Maybe they would benefit from an antiviral. There's a lot of opportunity. But the opportunities, aside from a vaccine campaign, become difficult choices for companies and health institutions who want to go down those paths. Fortunately, people have learned from COVID-19 that there's a health benefit and a business benefit to doing something that is beneficial in these diseases. And I'm thinking about how well the Pfizers and Modernas and some of the companies making monoclonals have done during COVID. They may have the financial incentive and the financial treasure chest to get some of this hard work paid for.

This remind me there are two topics that I think would be interesting to briefly talk about. One is the therapeutic vaccine possibility. A vaccine can not only prevent infection but can modify the immune response to infection. So, I think that will be a dream come true if we could have a vaccine that modified the basic therapeutic effect on MS.

The other is the question of progressive MS. You know, there are 2.8 million people with MS out there, and we mentioned the anti-CD20s, which are very effective in the relapsing-remitting phase, but a bit less effective in preventing disability and disease progression. Is there any possibility that the Epstein-Barr virus is still playing a role in these late stages? I don't know. What do you think of that, Larry? That will be a fantastic thing if we could really stop the disease in those individuals.

My guess is yes, it does. Those cells are there throughout the disease. One of the things is a discovery in that area in the molecule called EBNA1, we identified a specific molecular mimic, called glialCAM. But right next door to that Tomas Olsson, MD, and his collaborators at the Karolinska Institutet in Sweden discovered another molecular mimic. And right next to that, anther group in Oklahoma discovered another molecular mimic. How that happened, I don't know, and the field doesn't know. It's very fortuitous to see a stretch with all of these. The molecule that Olsson and coworkers discovered in Sweden is a chloride channel, a pore in the membrane for chloride, part of sodium chloride in table salt. The part we discovered also has to do with the chloride channel. That's very interesting. It may be that at different stages of the disease, their immune responses to different parts of EBNA1.

But what also keeps staring me in the face is there are three viruses that I mentioned that are also very prominent and an antibody fingerprint is very prominent in the spinal fluid: measles, rubella, and another herpes virus, the one that causes chickenpox and zoster. Do they take over later in the disease? Those are questions that can be addressed, and we'll find out. But certainly, one of the possibilities is that the initial driver continues to be a driver throughout the course of disease. Those are the sort of granular issues that have to be answered and can be answered—will be answered—by a lot of ongoing experiments as we get a blueprint.

But I think people will be impatient. “Can't we get started with the trials?” And it raises some other intriguing issues. If 90% plus of us—it's actually higher—have these lifelong infections, and the EBV goes into what's called latency, is it doing any good? Maybe. We've had a lot of discussions, as many states now are deciding that we're tired, we don't want to wear masks anymore. And the mantra these days, is we have to learn to live with viruses. Well, one exemplification of living with viruses is EBV. Most of us live quite okay with that infection. But the big issue is the unknown.

I think another very big message to the public is: science is hard. It takes a long time. There are many great ideas that don't succeed when you test them. But the only way we can get to something miraculous like a polio vaccine is through the kind of research that people like Tom Weller and John Enders did getting close to 75-100 years ago. It's tough. And the public must, in my opinion, show far more respect to people on the front lines doing research, and the people taking care of people have unfortunate viral infections. That seems to be lost. Early in the pandemic, in New York, when healthcare workers would leave the hospitals, the fire department came, people were cheering. Now, do you see what's happened? How did we fall so far, so fast? There were some other major events in recent human history called World War II, when the war went on for years and people didn't stop because they said they were tired of the war. They would have liked to have done it, but it was a war. We have to realize that these viral invasions are also a form of war. It may be easier to get to a vaccine or an effective antiviral than it is going to be to change the way we humans have started behaving.

 I think that brings us to an interesting point in terms of communicating this to the public, particularly in a time like we're talking about now, where the public is—whether through correct information or otherwise—keyed into a lot of science-related news. There's more access to information. through the internet and things like that, and I imagine that patients on the same side, especially as shared-decision making has become a prominent version of practice, are more involved in and a little more informed about what's going on with their disease.

From your perspective, how should this type of information and this relationship between EBV and MS be communicated to the public? What is the the advice you have for your colleagues when they're speaking either to the lay public or patients with MS about how this relationship operates and what we understand about it today to this point?

I have to confess—I'm not very good at that. I should be, I'm in public health! I have focused on spending that time with our research and our finding, to fully understand that. I really need help in that. Fortunately, I can collaborate with people in our communication department and others who are better at how to convey this to the public.

I share Alberto's struggle. Neither of us are our actors, thought it might be fun to have thought that we could have a career there, maybe. Besides attempting to communicate the realities of scientific research and the rare triumphs, we need help from offices of communication. But it would also help since people seem to have a lot more interest in people in entertainment and sports, that if we had one of these discussions with some famous star there asking some of the questions to us or reflecting.

Unfortunately, the entertainment side of expressing developments in science has—we're losing the battle to people who don't know science. They're not mainline scientists, they don't know that harsh day-to-day realities of going to work, and usually, having your experiments fail. People don't understand it. They go to watch the rockets take off in Florida, and there's a lot of wild cheering when the rocket launches. Most of the time, for we people in science, the rocket is on the pad, and it blows up. We have to make that clear, that it's not so easy, and when there is a triumph, this has to be recognized. When I'm in an airplane, I want the people in the cockpit to be experts. People don't apply that analogy to learning about medicine and medical science. Any old spokesman will be just fine for some people. I don't know how we let that happen to ourselves.

 It certainly does speak to the challenge of communication, and I think the sort of exponential growth of technology and access to information has kind of made that a complicated and convoluted conversation in terms of how to communicate those things effectively, and who should be doing it, and how to give the people who shouldn't be doing it the proper platform to do so.

I'm curious, though, in the meantime, obviously, again, there are a lot of questions and conversations that that this research—specifically in this relationship—have led us to and I know there are many more that I'm sure will pop up along the way as we continue to dive into this. But, in the immediacy, in these next couple of years, what's the first thing that the two of you would be focused on in terms of research? Imagine a world where you can get the funding you need immediately. There are no extra steps, no applications for grants, you have the funding. What would be the immediate thing you would seek to do in terms of the research, whether it's modeling how this infection sort of become develops into MS, or what the background environmental factors do to expedite that process?

For me, it is collaboration. In fact, you know, I've been discussing—just last week, we learned the possibility of joining forces to brainstorm together and see what the next step could be with many other people who are virologists and MS experts. Collaboration is the key word here for the next couple of years.

I would agree. There's that old saying that “It takes a village.” It takes a village of scientists with different skill sets—virologists, immunologists, and so on. It would be a surprise many people to learn that I'm reading textbooks and papers in virology because I have to get up to speed.

But you've also said something that's rather amusing. Imagine a world where you didn't have to write grants. Well, we started having discussions between Stanford and Alberto’s group at the Harvard School of Public Health, but we had to essentially take a week off because everyone was up to their eyeballs writing grants. Even as I talked about the life of the scientist, most of the experiments blow up on the launching pad. The other reality is to get to the launching pad, one has to go through an endless cycle of grant writing. I don't see any replacement for that because we just can't hand out money—it would only go to older people with track records, and that would be very bad for the development of science. It's a very imperfect system.

I think collaboration is key. There are a lot of easier experiments to do that just require time and effort continue to mine the data and the tables. In the paper that appeared in 

, each and every one of those big hits, statistically, deserves attention. They shouldn't escape our attention. Just because something is at the top of the list doesn't mean it's the most biologically meaningful, although I'd like to think so. But they're all telling us something, especially with the kind of statistical values. I can't say that enough, because if not for the amazing depths of the bank that Alberto was able to work with through the US military, these answers would have been much more difficult to come by. We don't have a national health care system in the US, so the closest potential ways of doing it would be through a health care system like Kaiser—a very big health care system, and very rich for epidemiology. But they can do studies on hundreds of thousands. Sometimes a million. This is 10 million. It makes an enormous difference in generating data when you have all the, we call it noise, of us humans. We're not colonies of inbred mice, we're very different in our genes and environment and it afforded an enormous opportunity.

 Yes, certainly the robustness of the data is indisputable. I'm curious for you, Dr. Ascherio, to that point, are there plans to continue analyzing those data? What are you hoping that we might be able to elucidate by doing so?

Oh, yes, absolutely. As we speak, my colleagues are working on those data exactly. Looking at the table to dissect the signal more in depth. Our collaboration with the military is continuing. If you notice, the data there were up to 2013 because of the time it takes to get funding to get the machine moving.

I’d like to take the opportunity to acknowledge the wonderful collaboration from our military collaborators, Ann I. Scher, PhD, and David W. Niebuhr, MD, MPH, MSc, of the Uniformed Services University of the Health Sciences, and all the military collaborators. Science is moving slow sometimes, but this is a very exciting time. And I think this will bring in an accelerate and momentum and I hope we can exploit it with full benefit of people with amazing people at the risk of MS.

I just wanted to add one other thing. For the last 4 years, I've been the head of a Research Advisory Committee for our Veterans Administration, on something called Gulf War illness that our veterans who served in that theater of operation. These biobanks turn out to be very helpful for understanding issues like potential toxic exposures on the battlefield. It's not only the military protecting us as the military is supposed to do as our defense. But also, this kind of research can end up helping soldiers and helping people after they leave the military understand some of their afflictions to determine whether they were due to something that happened on the battlefield or something else. It works two ways, but we're very fortunate to have it, since we don't have a national healthcare system. For the rest of us outside the military, there's no simple way of getting these immense set of specimens. So again, it's very fortunate. I always joke that our immunological system is our Department of Defense, so it's working bidirectionally. But it gets to that other metaphor. This kind of research can really also help the people who gave the specimens who are in the military, and were in the military, for some of their future problems.

 Is there anything else that you both think is important to touch on or that that sort of raises any points that you think is important to include?

 I just want to say that this work was a team work on my hand. Kassandra L. Munger, ScD, has been working with me for 20 years and it would not have been possible to achieve this without her collaboration, and Kjetil Bjornevik, MD, PhD, and Marianna Cortese, MD, were the first authors of the 

 paper and have also been fantastic collaborators. We are a team, and I'm here to represent all of us.

 And I would just echo the same. I mentioned my collaborators, Tobias Lanz, MD; William Robinson, MD, PhD; and Peggy Ho, PhD, MS, and many others. And I'm very fortunate because they were—a long time ago—my students, and I still get to collaborate with them. So, I point out that my best teachers are my students.

 Absolutely. I'm glad the two of you have echoed that sentiment and that you both are working toward not only collaborating within your groups, but your groups with each other. Thank you so much for your time. This has really been fantastic. It's opened the doors for I'm sure many future discussions that we'll likely be having, so I just want to thank you both very much again for your time.

For those watching, thank you for sticking around. On behalf of 

®, I'm Matt Hoffman, thank you for watching this Peers & Perspectives conversation.

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