April 20—University of Pennsylvania microbiologist Susan Weiss, PhD, co-director of the Center for Research on Coronaviruses and Other Emerging Pathogens, joins Chief Investment Officer Tony Roth to discuss the origins of the coronavirus, a field Dr. Weiss has researched for more than four decades. Listen as Dr. Weiss walks us through the biology and epidemiology of COVID-19.
Susan Weiss, PhD, Professor of Microbiology, co-director of the Center for Research on Coronaviruses and Other Emerging Pathogens, Perelman School of Medicine, University of Pennsylvania
Please listen to important disclosures at the end of the podcast.
Wilmington WealthWise with Tony Roth
COVID-19:The Cure for What Ails Us
Part I: What Makes This Virus Different From All Other Viruses?
Tony Roth, Chief Investment Officer Wilmington Trust Investment Advisors, Inc.
Susan Weiss, PhD, Professor of Microbiology, University of Pennsylvania Perelman School of Medicine, Co-director of the Center for Research on Coronaviruses and Other Emerging Pathogens
Tony Roth: Welcome to Wilmington Wealth Wise, the podcast dedicated to financial literacy where we take complex ideas from the investment world and make them accessible to everyone. I’m your host, Tony Roth, Chief Investment Officer of Wilmington Trust.
Today we start the first episode of a two-part examination of the deep science underlining the coronavirus. In this episode, we will be joined by microbiologist Susan Weiss from the University of Pennsylvania Perelman School of Medicine, where her lab focuses on coronavirus pathogenesis. She is also a Co-Director of Penn’s newly-founded Center for Research in Coronaviruses and Other Emerging Pathogens. Dr. Weiss is here to discuss the biology and epidemiology of the coronavirus and how the scientific community is working to better understand the intricacies of the virus. Thank you, Dr. Weiss, for joining us today.
Susan Weiss: Thank you. It’s very nice to be here.
Tony Roth: Well, it’s great to have you and we’re excited for the conversation. And we’ve had a lot of conversations with others around the various medicines that many people around the world are working on, whether it be therapies or vaccines, and it occurred to us that we really need to do a primer, if you will, a biology 101 on viruses for our audience since viruses are very unique and tricky creatures. And we thought it would be really helpful to start with some of the foundational elements and understanding what a virus is and how it works.
Susan Weiss: Well, a virus is really a very simple thing that has – but that’s very clever and can do all kinds of things to its host cell. But, the virus itself is actually, the particle is called a virion, and it’s composed of a piece of genetic material that can either be DNA, which you’ve probably heard of, which is our genetic material, or it can have only RNA as its genome. And this RNA or DNA is wrapped up with proteins in kind of a capsid it’s called, and then many viruses, coronaviruses for one, have a membrane around them and that membrane is made out of lipids, which are really just fats, and that membrane comes from the host cell. And in that membrane, it has other proteins sticking out of it and these proteins that stick out are, in the case of coronaviruses, are called spikes.
But many viruses have very similar proteins. And that’s the protein that attaches to the host cell. It recognizes a receptor on the host cell and through this interaction the virus enters the cell. one thing that’s important to note about viruses are they’re not really alive. They’re able to replicate, but only inside of a cell. If you have a virus just sitting on a tabletop or in water or whatever, it can’t really replicate. It’s not really dead or alive. It’s different from a bacteria.
Tony Roth: But, if we touch a surface that’s been where a virus has been recently deposited, we can contract the disease. So, when you say it’s not alive, in what state is it if I can get it?
Susan Weiss: I thought you were going to ask that. So, it’s kind of, I would guess it’s like it’s not – it’s static. It’s not growing and it’s not dead. It’s sitting there and it won’t last there that long. I mean after a period of time it’ll decay. There’s – all viruses will have a half-life. They can be denatured or fall apart from heat or from even UV light or anything like that.
So yes, if you put down some virus on a tabletop and someone else comes by and touches it and puts it in their nose or eyes, yes, they can catch the virus. But it’s not going to actually replicate. The amount that you put down on the table is just going to decrease over time, rather than replicate.
Tony Roth: So then, so the spike somehow enables it to gain entry into the cell in the case of a coronavirus, which has the spike. And then, what happens next?
Susan Weiss: Okay. And that’s a really general thing. So, like a herpes virus has other proteins. They’re not called spikes. But they’re – they have the same function. So, many, many viruses have the same kind of function.
Tony Roth: Okay.
Susan Weiss: And so, that protein, it recognizes a receptor on the host cell. That could be – they’re very – they’re all different proteins for different viruses and they have other functions, these receptors. They just happen to be proteins that the virus can kind of latch onto.
Once it latches onto it, the spike protein undergoes a change or a change in its conformation and the virus, as I said, has a fatty lipid envelope it’s called around it or a membrane. That membrane fuses with the host cell membrane and then the inside of the virus or the capsid can get kind of pushed into the, or released into the, cell and so that it can start replicating. So, it leaves the membrane behind and just the inner part of the capsid gets into the cell and begins the process of replicating.
Tony Roth: And so, within the host cell the virus is actually just growing in the sense that it’s just replicating itself over and over again?
Susan Weiss: Yeah. You wouldn’t call it growing, because it doesn’t get bigger and it doesn’t – it replicates. It kind of takes over the host cell. So, it leaves its membrane. We call it uncoating. So now, the DNA or the RNA and its protein surrounding it are we say sort of released into the cell. And once it’s there, it starts making proteins and then those proteins can start replicating the RNA.
So, it’s not like you get like bacteria. You – they divide, and you get one to two to four to eight. With viruses, they just start spinning off huge amounts, many numbers of thousands of copies of that RNA, of its genome RNA. It replicates itself and it makes messenger RNAs. Those are RNAs that encode for protein. So, it makes lots of RNA and lots of proteins. And then, it reassembles itself into new virus particles that then leave the cell.
Sometimes, they kill the cell. Sometimes, they don’t.
Tony Roth: So, what does the disease consist in? In other words, we’ve got this virus that’s fused into the cell and it’s replicating itself. So, I could understand that if it kills the cell, that would seem – I’m not sure what the right word is – a pathogenic activity.
Tony Roth: But is that what the coronavirus is doing? It’s actually killing the cell or is it – or does the disease consist of something else?
Susan Weiss: Well, it’s sort of a combination. It may kill some cells and not kill other cells. But, in a way, the virus doesn’t want to kill everything, because if it killed everything it couldn’t replicate. It wants to make more of itself and then go onto the next cell and replicate in the next cell and the next cell.
But one of the side effects of infection is the host cell is going to respond to that. So, the host cell is going to make lots of, yeah, like cytokines.
Tony Roth: Right.
Susan Roth: You’ve heard of, probably everyone’s heard of the cytokine storm.
Tony Roth: Yes.
Susan Weiss: So, that cytokine storm is initiated by the cell realizing that it’s infected. It responds by those cytokines are meant to get rid of the virus. But, an overexuberance can be disruptive to the lungs in the case of the coronaviruses, but just can be disruptive to the host.
Tony Roth: So, that’s the basic lifecycle of a virus. That’s our basic foundation.
Susan Weiss: Yeah.
Tony Roth: Okay. So, in the case of the coronavirus, is there anything – and you’ve studied coronaviruses for decades.
Susan Weiss: Yes. Yes, I have.
Tony Roth: What makes this coronavirus fundamentally different than other coronaviruses or is it?
Susan Weiss: The – it’s true. It’s not fundamentally different. If you – if we look at the genome, which is, again, the genetic material, and compare that to SARS coronavirus, the original SARS coronavirus, I call sometimes SARS-1 from the one that was emerged in China in 2002, they’re very, very similar. They’re I think 95% or 96% of their sequences are similar.
So, it’s not like you look at it and say, wow, this one has a new gene that maybe is making it more pathogenic. It’s pretty tricky really, because all coronaviruses have pretty similar genetic material. So, or I shouldn’t say all of them, but these lethal ones. But they’re behaving so differently and to me that’s really mysterious.
So, what you said is absolutely correct. This virus seems to be more transmissible. It seems to be transmissible before someone actually shows symptoms of being sick and it seems to – it actually – the lethality is much lower than the original SARS or MERS coronaviruses, just the percent of infected people. But, it’s so tricky because, yeah, we don’t – we didn’t see with those first two epidemics – there weren’t people walking around on the street with the virus that were not apparently sick. So, and like I said, it really is puzzling that we don’t know why that is from the genetics of the virus, not at all obvious.
Tony Roth: And is it puzzling at all that there’s such a wide spectrum of individual responses to it? I mean, obviously, you’re always going to have people that have compromised immune systems or potential people that are more elderly I would imagine are always more susceptible. But even within the range of individuals that we see that tragically are felled by this virus, you know, you see people that are seemingly young and healthy in certain cases or even if they’re not ultimately killed by it they get very, very ill. Then there are other people that I mean we hear the 70% or 80% of the people that contract it have no symptoms whatsoever. Is that typical or is that a bit unusual compared to the other coronaviruses?
Susan Weiss: Compared to the other coronaviruses I think it’s very unusual. The people, like I said, people that had SARS were very sick and something like 10% of them died, much more than we’re seeing with this coronavirus. But, because people were so sick, they were put in the hospital, they were isolated, and it was easy to contain the virus or relatively easy. It lasted for eight months and then it was gone. And I don’t think anybody thinks that’s going to happen with this one.
And that was also true with MERS coronavirus – well, MERS coronavirus is still infecting people in the Middle East, but again, people are really sick. And I think here the issue is that we just can’t tell when – we just can’t tell who has the virus. And I asked a friend of mine who’s a medical doctor – I’m not a physician – does this seem really surprising, because to me it did. And he said, well, you know, for example, other viruses, like some of the flaviviruses, West Nile virus or Zika virus, you can have very inapparent infections and then every now and then somebody gets really sick.
So, maybe it’s not that unusual. It is unusual for a coronavirus. And one of the reasons –
Tony Roth: To have such a varied impact.
Susan Weiss: I think so. And one of the reasons that it’s so dramatically that people are getting so sick is that we have no immunity to SARS coronavirus. We’ve never seen it in the U.S. before. And even in – I don’t know of people that had the original SARS if they were – if they would be immune or semi-immune, if they were sort of immunized against this future SARS virus by having the original one. I don’t really know.
But there’s – it’s sort of like when flu comes around most people have had some flu or a flu shot. So, even if they get infected, they may not get that sick. Whereas, here we’re completely naïve to it. So, we’re like sitting ducks, I think.
Tony Roth: Right. That’s interesting, the idea that there could be some immunity from a – another virus that may be very similar but not exactly identical to this virus, a different kind of coronavirus. But very few people would’ve even had exposure to those earlier coronaviruses.
Susan Weiss: But it would have to be relatively close. I’m – I said, for example, SARS coronavirus. Like, if there were a vaccine, had been a vaccine, maybe that would’ve worked against this virus. I think MERS coronavirus is going to be too far. I don’t think it would give any kind of immunity to this virus,
Tony Roth: So, we have some basic stages of the lifecycle we’ve just defined, which is, at least in terms of its relationship to its ultimate host, it’s the entry and then there’s the replication, and then it moves onto the next cell. So, when you think about those stages, are there particular stages from an intervention standpoint that medicines try to target to try to stop the activity? And are there certain stages that tend to be more successful than others?
Susan Weiss: Well, there – we don’t know who – we don’t know what’s successful yet. Everyone’s trying to figure that out. But I mean we know from other viruses.
So, the first step that’s often targeted is viral entry. I talked about how the viral, the spike protein attaches to its receptor and then it mediates what we call fusion, which is fusion of the viral membrane envelope with the cell envelope and release of the capsid into the cytoplasm of the cell or into the interior of the cell. And for coronaviruses, they – there are two possible pathways they can use to enter. This may get a little detailed, but I’ll try to explain it simply.
Tony Roth: No, that’s okay.
Susan Weiss: The spike attaches to the ACE2, which is the angiotensin converting enzyme or the receptor, and it can either at that point just fuse right into the cell, right at the membrane there or it can be endocytosed into the membrane. That means that a vesicle kind of envelops it into itself and it’s deposited into the cell in a vesicle, like in a bubble kind of thing. And then, from that vesicle it fuses into the cytoplasm. And that may seem like kind of a subtle difference. But, the reason why that’s important is that that second, the second method through that bubble is – requires a low pH or an acidic pH and there’s some enzymes in that vesicle called cathepsin that has to be activated to release the virus particle and that only happens at low pH.
Okay. So, chloroquine is one of the drugs –
Tony Roth: Yeah and hydroxychloroquine.
Susan Weiss: And hydroxychloroquine are drugs that have bandied about and probably in clinical trials now as an antiviral drug. And the way that chloroquine works is it prevents that acidification of the endosome. So, it’s a kind of general mechanism. So, any virus that requires that low pH CEPT should be sensitive to chloroquine or we’ll find out if it is.
Tony Roth: Do we know that the coronavirus gained entry or fusion through that second method?
Susan Weiss: It’s a little more complicated. So, coronaviruses can use both pathways. The first pathway doesn’t require the low pH, but it may require an extra protease step. So, the spike protein has to be cut or cleaved in two places to activate it. This gets a little bit complicated, too. And those cleavages depend on sequences in the spike protein and they also depend on enzymes on the cell that makes the virus and the cell that the virus is entering. So, it’s a kind of a complicated mixture of what the sequence of the spike is and what enzymes are available to cut the virus.
So, some coronaviruses will enter mostly through the cell surface. Some will enter mostly through the endosome and the low pH CEPT and some can do both. And on top of that, it’s even more complicated, because different cell types express different enzymes so they may – so this virus may be more likely to use one pathway or the other in one cell type or the other. Does that kind of make sense?
Tony Roth: But essentially what you’re going to tell me I think, unfortunately, is that we don’t know yet which COVID-19 is in terms of how it gains entry, right?
Susan Weiss: Well, we know a little. There’s some data about that. There’s some studies that say that it – that this enzyme called TMPRSS is important for entry of SARS-CoV-2 and that may be only on a particular cell type that it was tested on. So that if the virus uses TMPRSS it would suggest that it’s going to go in through the membrane directly and not through the endosome.
But, if it were to do that, then chloroquine really shouldn’t work. So, to me, if you use chloroquine you might kind of force it to go in through the membrane. If you use a TMPRSS inhibitor, you might kind of force it to go in through the endosome, because maybe it can go in by both pathways. Some viruses can go in through both pathways.
So, my prediction is that probably you’d – and this is just a prediction – that you’d probably have to shut down both pathways if you want to really shutdown viral entry.
Tony Roth: Well, so there’s been, as I think we all know, pretty I think at best we could say mixed results with the chloroquine. Certainly, it’s been far from a slam dunk. But that doesn’t mean that perhaps if it was used in conjunction with one of those other drugs that block the other path, maybe the two of them together could be effective.
Susan Weiss: I would think theoretically yes. I don’t know that – I don’t know if we exactly that chloroquine only acts by disallowing low pH. Maybe it does other things as well. I’ve heard that it may have other mechanisms. But I don’t really know.
But, yeah, I would think that if you shutdown both pathways really well, that that would be like a combination therapy to prevent viral entry.
Tony Roth: Are there any other medicines or compounds, if you will, that are in – either being used off-label or in development that you’ve heard anything about in terms of being effective at this stage?
Susan Weiss: For entry?
Tony Roth: Yeah. For entry for COVID-19.
Tony Roth: Whether it’d be – I mean I think the Remdesivir, we’re going to talk about that’s more of one that targets replication, right.
Susan Weiss: Yeah. Right. I mean there are inhibitors of TMPRSS. But that’s theoretically one way to go to try to inhibit that. There’s also furin is another one of the enzymes that actually it’s an intracell. It’s inside of the cell, but it also cleaves that spike protein to get it sort of semi-activated for entry. So, if you treated cells with a furin inhibitor – this is all theoretical. I don’t know whether that really drugs like that exist or that they work or anything. But, if you could inhibit that furin stage, you might end up producing virus that was unable to infect the next cell.
So, I think that these host cell proteases are probably a good potential target.
Tony Roth: You and your team have spent so many years looking at coronaviruses and evaluating or defining these processes and mechanisms. I would imagine that the work that’s going on now to try to identify inhibitors, if you will, antivirals, inhibitors for these activities.
Susan Weiss: Yeah.
Tony Roth: It has to stand on the shoulders of all the work that’s already been done over the years so that had we not had MERS, had we not had SARS, we wouldn’t be as far along in hopefully getting closer to a solution, whether it’s a generic solution that works against all the coronaviruses or something even just specific around against COVID-19. All the work that’s already occurred has got to be very important in moving us along.
Susan Weiss: Yes. Just to correct you that COVID-19 is the disease. The virus is actually called SARS-CoV-2.
Tony Roth: Okay.
Susan Weiss: And the reason it’s called SARS-CoV-2 is it’s almost the same as the original SARS. So, just to be more precise about the nomenclature.
Tony Roth: Got it. It was – the original SARS was SARS-CoV-1?
Susan Weiss: Well, it was just called SARS-CoV, because we didn’t know there was going to be another one, right.
Tony Roth: Got it. Okay. Of course, SARS-CoV, okay.
Susan Weiss: So, severe acute respiratory syndrome, right. And then MERS is Middle East Respiratory.
Tony Roth: Yes.
Susan Weiss: Right. So now, this one, there was a lot of controversy about the name, but it was named SARS-CoV-2 because genetically it’s pretty close to SARS-CoV-1 or SARS-CoV.
Tony Roth: So, all that work that you’ve done and others around the world is very critical as a building block upon which people are now putting many times more energy into trying to develop these inhibitors or antivirals for the processes that you’ve just described.
Susan Weiss: Yes. Well, let me go – can I go back a little further? I’m not to SARS. So, SARS was 2002. But I’m going back to the ‘60s and ‘70s. We knew about human cold coronaviruses, OC43 and 229E. They were – people worked on them. They didn’t work on them super-hard, because they were cold viruses and they weren’t that – of that much concern.
But there are a lot of animal coronaviruses that were worked on quite a lot, like IBV chicken virus, BCV cow virus and some porcine viruses. And we worked on mouse hepatitis virus, because it was just a model. So, it was all those work on those viruses before even knew about SARS that really built up. That’s how we know about viral proteases. That’s how we know that they make this long polyprotein and 16 nonstructural proteins.
All of that was, a lot of that was known before SARS, so that when SARS arose in China I can tell you everyone in my field was absolutely amazed. We couldn’t believe it. We were just – we were shocked, because there had been no evidence up until then that coronaviruses could cause severe diseases in humans, which is kind of strange in a way, because we knew they could cause severe diseases in other animals.
But it was because of all that knowledge, I mean when SARS arose it was sequenced. The genome was sequenced really quickly. It was cloned so that people could work with it. Just it was, yeah, I mean there’s an amazing amount of work that went on before that. And then, once SARS arose, many, many, many people started working on these viruses in a way that it was shocking actually.
The field was very small before SARS and then it grew enormously at that time and we learned a lot more of the details, like these enzymes I’m talking to you about. People were – had actually figured out the crystal structures of them and that’s important, because if you know the structure you can kind of model what kind of inhibitor might combine with it and prevent it from having its activity.
Tony Roth: So, what is the relationship that you and your team play as what I’m thinking in my mind is extremely basic fundamental science vis à vie the specialists that are trying to develop these antivirals? Are they – do you interact with them and, you know, are the different drug companies asking you questions about the behavior of this virus? How is the collaboration work across these different specialties?
Susan Weiss: You know, in the time before 2002 I think the field was pretty much ignored. After SARS, I gave more seminars than I’ve ever given in my life and I was – I did talk to some drug companies about, you know, like just wanting advice and stuff like that. So, there was a burst there.
I personally am a really, really basic science. Some of my colleagues are doing more like actually drugs, not really drug studies but, yeah, but looking for inhibitors in their own labs, but on a kind of a smaller level. My colleague, Sara Cherry, now at Penn is doing massive drug screening against this virus. So, you know, if she finds something, I assume a drug company would pick up and wanting – want to develop it.
But, again, like we define what some of these proteins are initially, not just we but we, our field, and that’s incredibly important. Like Remdesivir, the reason that people even tried it on coronaviruses is it was originally designed or used for Ebola. And the reason why you might even think it would work on this virus is that it turns out that RNA polymerases, that’s the enzyme that copies RNA into RNA, they’re kind of structurally similar, even among different viruses. Coronaviruses all have these 16 proteins they make that are conserved. Some of these sort of protein domains you might find similar ones in other viruses.
Tony Roth: So, when you put it all together and you think about, from what you’ve seen, and I know that your vision is not comprehensive – nobody’s is.
Susan Weiss: No, it’s not.
Tony Roth: Is there, right, is there a particular class of antivirals or a couple drugs or anything that you think at this very early stage seems to be most promising?
Susan Weiss: I can’t really assess that. I can really talk more theoretically. I mean to me, you know, not only about Remdesivir, but a drug like that seems like a pretty good starting point.
I mean, these viruses don’t change that much anyway. The proteases, I mean if you inhibit the protease, you really have to stop the infection. So, I don’t really have a prejudice as to which one might be better than the other. It really just depends how well the inhibitor works on – because all of these functions are required for replication.
Tony Roth: Okay. What’s the difference between – changing gears a bit here – the difference between preventing the virus from entering the cell in the first place and what I would think a vaccine is, which would be something that would somehow prevent the virus from getting into my cells? There’s obviously a difference between a medicine that’s aimed at preventing that initial stage of entry, like chloroquine that we talked about, versus, excuse me, a vaccine. How do you compare those?
Susan Weiss: Well, a vaccine obviously is prophylactic. A vaccine should do – should really theoretically prevent viral entry, too, because if you make antibodies that are so-called – you’ve heard of maybe neutralizing antibodies. That means that they’re neutralize the virus and prevent it. They usually are directed against the spike protein. So, if they’re really good neutralizing antibodies, they should prevent that infection.
So, I mean in a sense it’s kind of targeting the same step. But also, but if it leaks through and it does get – if the virus does infect, cause some kind of infection, because nothing’s 100%, the new virus will still have to deal with the antibody response from the vaccine. So, maybe in a sense it’s looking at both entry and then spread as well. But, so is the entry inhibitor.
Tony Roth: In the case of a therapy it’s the actual medicine that’s preventing – changing something in the human body to prevent the entry. But in the case of a vaccine, it’s actually stimulating the body to create the antibodies or whatnot to prevent the entry. Is that – ?
Susan Weiss: Yeah. I guess, yeah, you could, yeah. So, it’s a different mediator of the block and entry. But, it’s still both kind of trying to – the goal is to prevent the virus from getting into the cell. The vaccine also will work on any virus that does leak through the cell. If you have a T-cell response, as well as an antibody response, you might also kill infected cells. So, that’s an added step that you wouldn’t have with a drug, but only with a vaccine. It depends if the vaccine is inducing a good B-cell and/or T-cell response.
Tony Roth: If you think about the groundswell of interest after SARS relative to previous where there’s many, many more people focused and interested on this, even compared to that, the number of people that are focused on it now is probably an order of magnitude of many, many times.
Susan Weiss: Oh, yeah. Or two orders of magnitude maybe, yeah.
Tony Roth: Right. So, given that massive interest now of course, the world is trying to solve this, how do you see your work changing or progressing in a different way than it might have had this not happened?
Susan Weiss: Alright. Well, we have a new virus to work on. We want to know why this virus is different. So, one of the things, like I said, I’m still doing very basic research because that’s where my strength is, I think, and that’s where I can be helpful. So, we study how the viruses antagonize the host innate immune response. We didn’t really talk about the innate response very much. That’s interferon and that’s a really early response, not really specific to that virus, but any kind of when a cell sees double-stranded RNA, which is a product of virus replication,
that’s seen as a danger signal by cells and it – and they see that, and they make interferon and they also activate some other antiviral pathways, antiviral activities and coronaviruses are really good at stopping that or antagonizing that innate response. So, what my lab’s been interested in the last ten years or so is like how does – how do viruses do that? We’ve done it with – we work on that with the MERS coronavirus and the mouse virus. And so, we want to do that with SARS-CoV-2 and we also want to create a mouse model. So, in order to infect mice with this virus, you have to make transgenic mice that express the SARS-CoV-2 receptor or ACE2, human ACE2. And so, once you have that, we can actually make mutant viruses and try to probe, try to determine which parts of the viral genome are really causing pathogenesis. So, in that sense we get towards the disease process. And if we uncover things that the virus does to the cell, it will help us figure out what steps to target. Like there you can also target host cell pathways and boost them up, rather than just trying to, excuse me, inhibit the virus. So, that’s where I’m – my interest is, like how does this virus prevent the host cell response.
Tony Roth: Interesting. So, let me try to summarize quickly what I think we’ve covered today.
Susan Weiss: Okay.
Tony Roth: And I’m going to talk about three key takeaways and the third one I’m going to add a little bit and you have to tell me if I’ve got it right.
Susan Weiss: Okay.
Tony Roth: So, I think the first one, the first two really are around providing a basic foundation of knowledge for our listeners to understand that when we talk about different therapies that are being developed, whether they’re being – whether they’ve already – it’s preexisted and they’re being used so-called off-label for this particular virus or whether they’re new medicines that are being created, they’re typically either targeting the entry stage or the replication stage of the process, the lifecycle of a virus. And that, to the extent that we can think about those therapies in those terms, it helps advance our understanding and put things in perspective in terms of the development of these medicines.
But, the third thing that I think I find fascinating is that to me this is a double-edged sword in a way from the perspective of what we all want, right, which is a solution to this horrible problem that we’re all confronting, is that there’s still a tremendous amount of basic science occurring and on the one hand that is incredibly reassuring that there are people like yourself, doctor, that are working to better understand the most basic processes and mechanisms of the virus and those insights may lead to the medicine or the therapy that ultimately gets us out of this predicament. But at the same time, that’s a long process.
Susan Weiss: Yes.
Tony Roth: And it’s probably the case that the medicines that would come from or will come from the basic science that you’re engaged in today are not 30 or 60, 90 days away. They’re probably –
Susan Weiss: Correct.
Tony Roth: – quite a bit further out on the horizon than that.
Susan Weiss: Correct.
Tony Roth: So, it’s great to know the basic science is happening. But it suggests there’s still so much we don’t know at the same time.
Susan Weiss: Yeah, you’re right. But suppose in 2002 we hadn’t stopped studying SARS or we hadn’t let that lag. Had we really pushed on vaccines or antiviral drugs at that time, maybe it wouldn’t – we would be there now, right?
Tony Roth: That’s right.
Susan Weiss: So, it is true that basic science is slow. But it’s important because if you look back to even, you know, 40 years ago, if we hadn’t done any of that work when SARS first arose, we would’ve been clueless. We wouldn’t have known how to deal with it at all. So, I think what you said is absolutely correct. But I also think that it’s important to keep plugging on the basic science forward.
Tony Roth: Oh, yeah. Of course.
Susan Weiss: Slowly forward.
Tony Roth: I mean, we may be lucky and find a, hopefully we will find a vaccine. But that doesn’t negate the fact that there are going to be many aspects and facets of how these viruses operate that we don’t understand. Just because we find a vaccine, doesn’t mean that we’ve unlocked our unlimited knowledge of the vaccine. And so, we continue with the basic science regardless. But, as we advance the basic science, it really increases the chance over time of coming up with therapies and medicines, because we understand how they operate better, and we know what to go after.
Susan Weiss: Yeah. That’s absolutely true. But I mean I think a vaccine would be really, really wonderful. I mean that’s what’s really going to make people be – feel safe when they go out on the street, you know, now. I mean even when we start relaxing staying home, I think that having a vaccine would make me feel a lot safer.
Tony Roth: Yes. Me too. So, well, thank you, again, for joining us today, Dr. Weiss. It’s been really absolutely fascinating. And I want to ask our audience to please stay tuned for part two, where we’re going to be joined by Dr. Ofer Levy from Harvard Medical School to discuss advances in therapeutics and vaccine development in terms of specific therapies. Armed with the knowledge that we’ve taken today from our conversation today with Dr. Weiss, we’ll be able to apply that to the conversation with Dr. Levy in a couple of days when our next episode is released.
So, thank you everybody, again, for joining us today. Please send your feedback or any suggestions for future podcast topics to email@example.com. And finally, I encourage everybody to go to wilmingtontrust.com for a roundup of our blog posts and media contributions related to coronavirus for market, economic, and global health perspectives. Thank you all so very much for joining us today.
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