In episode 12, President Bob Iuliano and Biology Prof. Steve James ’80 discuss the biology and genetics of COVID-19, its origins, how properties of the virus are affecting the development of a vaccine, and other related topics.
In Episode 12 of Conversations Beneath the Cupola, podcast host, Gettysburg College President Robert W. Iuliano, is joined by Biology Prof. Steve James ’80. Iuliano and James discuss the biology and genetics of COVID-19, its origins, how properties of the virus are affecting the development of a vaccine, and other related topics.
The episode begins with James sharing with Iuliano how he adjusted one of his biology courses to include topics related to COVID-19 when the semester shifted to remote learning. In making a transition to a topic that was relevant to all students, James says he saw performance increase and received positive feedback from students who appreciated knowing more about the disease and having a firm understanding of where it came from, what it is, and its effects on the human body.
The conversation continues with James simplifying the complexity of COVID-19 and explaining how it differs from other coronaviruses. James also further discusses the origin of COVID-19 and what progress is being made toward a successful vaccine. He says that from his understanding, there are as many as 90 vaccine trials underway globally, and we are advancing this at a pace that the world has never seen before.
Iuliano’s last question to James is what he predicts the lasting impact of COVID-19 will be on society. James shares that his hope is that COVID-19 spurs change that substantively addresses income inequality, institutional biases, and brings about a society with better safety nets and opportunities for everyone.
The episode concludes with an anecdotal “Slice of Life” told from the president’s perspective. Iuliano shines light on how Musselman Library staff is continuing to support students remotely during finals week and the conclusion of the spring semester. Some of their efforts included a spirit week, a virtual “study break” with stress relief activities, and “Lattes with a Librarian,” during which students could receive one-on-one research help on their projects and papers.
Guests featured in this episode
Steve James, Prof. of Biology.
Steve James: As this pandemic evolved, it became clear to me that it was just a very logical swerve to bring the Coronavirus to my students. I thought, there’s really nothing more important than this and for their lives right now and for them to understand the circumstances that we’re facing.
President Bob Iuliano: Hi and welcome to Conversations Beneath the Cupola, a Gettysburg College podcast. I’m Bob Iuliano, president of the college and your host. If you’ve tuned into recent episodes of this podcast, you know that we’ve been trying to make sense of the significant changes the pandemic has brought to the way we live and work. We’ve benefited from the expertise of members of the Gettysburg College faculty who have offered thoughts about the political, economic, health-related, and social impact of the outbreak.
President Bob Iuliano: Today we are joined by Steve James, a 1980 Gettysburg graduate and a professor of biology at the College. Steve is a molecular biologist and a geneticist and he will use this background to help us take a closer look at the biology and genetics of COVID-19, it’s origins, how properties of the virus are affecting the development of a vaccine and other related topics.
President Bob Iuliano: So Steve, I understand that when the coronavirus outbreak really became more widespread, you completely revised a course that you were teaching. Say a word or two about that. What did you change, why did you change it and how was it received by the students?
Steve James: Thank you Bob. Thanks for inviting me today. I am teaching a course called Biological Basis of Disease for non-majors. Along with Betty Ferster who is also teaching the course, we have 160 students total in the course. It’s a course that I’ve been teaching for a long time. It’s driven by the afflictions and conditions that biologically affect humanity and hopefully I try to present material that is relevant to students. So it’s designed to help students who are not scientists to understand the biology of disease.
Steve James: In this case, the timing was really serendipitous. We had been covering infectious diseases and had just finished talking about some viruses before spring break. As this pandemic evolved, it became clear to me that it was just a very logical swerve to bring the coronavirus to my students. I thought, there’s really nothing more important than this and for their lives right now and for them to understand the circumstances that we’re facing.
President Bob Iuliano: That’s fascinating. I assume your students are always interested in your course, but did their engagement heighten as the pandemic became more obvious to them? It affected them directly, obviously by virtue of the decisions we made as a college and the experiences they’ve been having outside of the college as well. Did you see a palpable change in their engagement with the material?
Steve James: Yes. Averages on quizzes and exams went up. I’ve received a lot of feedback from students thanking me for bringing this to them. They appreciate knowing more about the disease and having a firm understanding of where it came from, what it is, and what it can do.
President Bob Iuliano: It’s fascinating. I’ve now spoken with members of the Philosophy Department and the Religious Studies Department and it will not surprise you, Steve, that they both have said that their students engaged in a different way with the material because in both areas, different sorts of questions were being raised and the underlining disciplinary tools that the students were getting, whether in religion or philosophy, were helping them to make sense of a situation that was largely again, not decipherable to them because they’ve not seen anything it. So I’m not surprised to hear that your students have engaged in a different way. As part of the charm of the curriculum, I think in that our students are finding a number of the things that we teach them as means again, of making sense of something that is hard for all of us to comprehend.
President Bob Iuliano: So let’s start at a basic level, if you would. That is, we all read a lot about what the coronavirus is, but I suspect we don’t actually know what it is. So what is it? how is it distinguished from other viruses and how is COVID-19 distinguished from other coronaviruses?
Steve James: Most people will know that viruses are inanimate particles with a protein shell that surrounds genetic material. Some viruses have an additional membrane surrounding that protein shell. That is true of what we’ll call SARS-CoV-2, which is the name of the virus. The disease is called COVID-19. Most people will know also that viruses cannot survive on their own. They can’t make more viruses by themselves. So they need the machinery of a living cell in order to replicate and assemble more virus copies. Some viruses have DNA as genetic material, like all of us do. These include things like adenoviruses that cause upper respiratory infections and pox viruses like chicken pox. But many viruses have a genetic cousin of DNA as their genetic material called RNA or ribonucleic acid. For example, influenza is an example of an RNA virus.
Steve James: The three that are of serious concern are the SARS virus, which emerged in Asia in 2003 with about a 10% fatality rate. However, in patients greater than 60 years of age, it was over 50%. So it was a very, very lethal virus. We now call it SARS-CoV-1 to distinguish it from the current SARS-CoV-2 that emerged. The second deadly coronavirus that emerged in 2012 in Saudi Arabia only caused about 2000 cases, but has a very high death rate as well, over 30%. Now we have SARS-CoV-2, which is the causative agent of the COVID-19 illness, which depending upon region of the world and the way cases are reported, the death rate from this virus is lower or about as low as the two other lethal ones, with a rate of between 0.5% and 15% depending upon, again reporting, conditions, where in the world the virus is occurring, et cetera.
President Bob Iuliano: Steve, maybe you can’t answer this, but those other two examples that you gave did not turn into quite the same global pandemic that this has. What is the reason, if you know, why this has proven to be much more widespread, if a little less fatal as a statistical matter?
Steve James: That’s a super question. We can really help to distinguish in this case. So all viruses have to dock with the target cell that they’re going to infect through a physical lock and key process, in which a protein on the viruses surface locks onto a protein on the surface of the host cell that it will infect. Then once locked on it can be drawn into the cell to begin an infection. In the case of SAR-CoV-2, and in the case of the original SARS, that red spike protein that everyone is so familiar with on the surface of the coronavirus binds tightly with a protein on airway cells called the ACE2 receptor protein, or angiotensin converting enzyme 2 receptor, which incidentally, this receptor protein is also found in the lungs, arteries, heart, kidneys, small intestine, and plays a central role in regulating blood pressure. Some people will have heard about this, I’m sure.
Steve James: Why is so much more infectious, so much more transmissible, such that it is caused a pandemic, whereas SARS and MERS were relatively small localized outbreaks? First, the prevalent strains of SARS-CoV-2 attach 10 to 20 fold more tightly with 10 to 20 fold higher affinity to that AC to protein than does SARS-CoV-2. So that makes it easier, much easier, for the virus to gain entry to infect cells.
President Bob Iuliano: That’s just a byproduct of the biology.
Steve James: Yes it is.
President Bob Iuliano: It is what it is. Okay.
Steve James: Unlike some coronaviruses that attached to ACE2, the spike protein on this coronavirus contains a special region that allows that spike protein to be cut in half by a human enzyme that’s present in our airways after the coronavirus has attached or locked onto the ACE2 protein on the host cell. Cutting it in half keeps the virus particle attached to the cell surface, but cutting it with this enzyme allows it to gain entry into the cells, to be taken into the cells, much more efficiently.
President Bob Iuliano: That’s fascinating.
Steve James: Yeah. The other point I would make has to do with where these ACE2 receptors are located. When a flu virus infects or a common cold virus infects, it is capable of infecting airway cells and the upper respiratory tract. So we think of these flu and colds as upper respiratory viruses, but the ACE2 receptors also found deep down in the lower part of the lungs and especially on the air sacs we call alveoli. These are clusters of cells that form air sacs where gas exchange occurs, where oxygen can enter the bloodstream, and where carbon dioxide can leave the bloodstream. So in addition to its enhanced affinity, if for the ACE2 receptor, this coronavirus is capable of infecting deep in the lungs, so a lower respiratory infection.
President Bob Iuliano: So you may have answered my next question, which was going to be, what’s the biological mechanism by which this is more lethal? Is it exactly what you just said, that unlike other forms of the coronavirus, this one, by blocking that gas exchange, presents a greater risk to the health of the subject?
Steve James: Right. It often causes a pneumonia. So what’s happening is sort of a three stage process in which the virus infects and spreads through the lungs and starts to damage and kill cells of the lungs. Because as a virus reproduces and replicates inside a host cell, the host cell is typically doomed. That brings about an immune response. The immune system reacts and says, we’ve got a problem here. Let’s start mopping up these virally infected cells. Then what happens is that... Really interesting in the case of this coronavirus…those immune system cells release chemicals called cytokines, which promote inflammation, which cause a number of things, one of which is to make capillaries, that is the small blood vessels, leaky, so that fluid leaks out of the circulatory system into the air spaces in the lungs and fills the lungs with fluids. This is part of what we call a cytokine storm. When the immune system overreacts or reacts because it itself is being attacked by the coronavirus and it releases large, large amounts of these pro-inflammatory signaling molecules we call cytokines, which then loosen blood vessels and allow fluid to leak into the lungs and cause a more severe pneumonia, which is a characteristic of the final stage of the disease and people who succumb to the disease.
President Bob Iuliano: That’s very helpful. So let’s move back a little bit in time when the virus first manifested itself in China. Should we have known then? Obviously with the benefit of now studying the virus, we understand that it is a very efficient machine. Should we have understood immediately the global risks that this presented and did we as a result, fail to respond adequately given what we should have known from the first case on?
Steve James: Right. I thought about this and my answer would be a yes and a no. Yes, the Chinese government was slow to react initially. From my reading it seems that they hid, or at least the local officials in Wuhan, hid or dismissed the threat initially. In that sense we lost precious time. By the time China imposed those strict lockdowns, the virus had already boarded airplanes and had disseminated widely across the world. Had the local officials reacted more aggressively sooner, then I think that the spread of this disease could have been slowed considerably, whether it could have been slowed sufficiently, I don’t know.
President Bob Iuliano: That makes a lot of sense. Right now a lot of people have on their mind the question of the future of course, and a belief that an important way in which we’re going to respond to this is through a vaccine. Should anticipate that there can be an efficacious vaccine at some point? And what do you have the sense of, from your perspective, of where we are on that timeline to the extent that you have any information about that?
Steve James: Right. I’ve been trying to follow some of this as have many people. My understanding that there are as many as about 90 vaccine trials underway across the world right now. Maybe as many as 30 or 40 or 50 different approaches being taken. We’re advancing this at a pace that the world has never seen before, largely because there’s never been a better research infrastructure in the world, a more advanced technology that’s permitting this very rapid attack on the problem.
Steve James: There are a few that have risen to the surface at this point as possibly going forward. Britain is fast tracking what we call a recombinant vaccine that they have tested in monkeys and they’re now proceeding to human trials. So this is an interesting way of... There are a couple of interesting new technologies. So this is a case where they’ve taken an adenovirus, which causes common upper respiratory infections. They’ve crippled it so that it can’t reproduce itself inside cells. It can get into cells, but it can’t reproduce. They’ve attached the gene for the spike protein in the coronavirus in the genome of this adenovirus. What happens is the adenovirus gets into, or simply you put this adenovirus injected into an individual and the immune system sees the spike protein on the surface of this harmless, adenovirus and creates antibodies against the spike protein. That’s shown some promise in monkeys so they’re moving to human trials.
Steve James: The other that’s really interesting, I think is this Moderna approach. This is a company in the US that was just given almost half a billion dollars by the US government to keep developing what are known as mRNA vaccines or messenger RNA vaccines. These are vaccines in which you literally inject RNA that encodes a viral protein. So in this case, Moderna is injecting into muscle tissue in people or in animals, a piece of RNA. But this RNA isn’t the whole genome of the coronavirus. It just contains the spike protein gene, with the idea that gene will be expressed in certain kinds of cells that take up the RNA, that they will display that spike protein on their surfaces so they’re not virus particles, they’re human cells that are displaying this spike protein on their surface and that would be recognized as a foreign invader by the immune system and would raise an immune response. This is a technique that’s never been used before to create a viable antibody, so we don’t know if it’s going to work, but if it does work, it would eliminate the need to raise traditional vaccines using chicken eggs and it would speed the process greatly.
President Bob Iuliano: I’ve heard about this. I hadn’t understood that was the reason for its attractiveness. That’s fascinating. Before all of this happened, I was scheduled to go to Philadelphia, as part of my introduction to the alumni community particularly. I was going to talk about the importance of science in that setting. One of the things, and we’re at a moment in time in society where at least there’s some skepticism about the scientific method, but as you were explaining your prior answer about how the vaccine is going to work and the really innovative techniques that people are using, it is yet a reminder of the importance of science and the importance of the scientific method and research and the facts and how our lives are influenced by the work that people are doing in research universities and in industry.
President Bob Iuliano: Just a digression, but it’s a plug for the importance of science, Steve.
Steve James: Thank you Bob.
President Bob Iuliano: Last question from me, and that is, I’m asking everybody this. You can either answer this as someone who studies Biology or as a citizen of the world. What do you see as the lasting impact, if any, of this virus and the way we live and the way we work, the way we organize ourselves as a society?
Steve James: I’m thinking non-scientifically with respect to this answer. You can look at this virus and say well is this virus somewhat of an equalizer in the sense that no one is potentially spared? None of us, prior to this pandemic, were immune. It’s a super transmissible virus. In some people it has devastating effects. That said, in the US at least, it’s very clear now that social and economic factors, poverty and so forth, are a major driving factor that determines who of us is going to get hit hardest, who of us is at higher risk, who is better shielded? First from contracting the virus and then once sickened, who is more likely to recover and who is more likely to die. So I think it is laying bare the social and economic inequalities that exist in our society. My hope is that somehow this pandemic, and I don’t know how yet, I’m not the political scientist or the sociologist, but I am hoping that it may spur some kind of real change that substantively addresses income inequality, institutional biases, especially institutional racism, and brings about a society with better safety nets and better opportunities for everyone and better attention to some of these diseases of civilization that I talked about early on that have a much more devastating impact on some sectors of our society than others.
President Bob Iuliano: Well, that is a wonderful way to end this conversation, with a call to action, that as you say, isn’t just about the biology but about what it is that brings us together as a society. I think you will be hardened to know that as I’ve talked to Amy Dailey and Char Weise and Bruce Larson, also of our faculty, and asked them this question, their answers were a lot like yours, which is this has revealed inequalities in the system that warrant attention and perhaps will be a spur to it. With that, Steve, thank you. Thank you for shedding light on the mechanics of this disease. I think our listeners will be better off for it, so I appreciate your time with me today.
Steve James: Thank you very much, Bob. It’s been a pleasure.
President Bob Iuliano: Let me conclude with a slice of life from Gettysburg College. As we record this, we are in the first few days of finals and the semester is rapidly coming to a close. It has been so inspiring for me to see the way our entire community has responded to this most unusual academic semester. From students to faculty, the resilience and perseverance throughout the semester has been worthy of note.
President Bob Iuliano: Right about now we would normally be on campus and see students flocking to Musselman to get in that last bit of studying they probably should’ve done early in the semester, but they’re certainly trying to get done now. They’re not obviously on our campus right now as we engage in our remote learning, but the spirit that the library brings to bear on what it does for our students is very much tangible. Musselman has done so many different things. For example, from April 27 through May 1 they hosted a spirit week, where each day of the week there was a different theme. It could have been silly socks, Hogwarts house colors, superheroes, throwback Thursday, and other things of school spirit. They’ve had a virtual research help desk. They’ve also hosted lattes with a librarian, which students could sign up for a time slot and receive one-on-one research help on their project and paper. Bravo Musselman. Good luck to our students as they wrap up the semester. We’re looking forward to having you back on campus soon.
President Bob Iuliano: Thanks for listening. If you’ve enjoyed this conversation and want to be notified of future episodes, please subscribe to Conversations Beneath the Coppola by visiting gettysburg.edu or wherever you get your podcasts. If you have a topic or suggestion for a future podcast, please email email@example.com. Thank you, and until next time.