The following is a rough transcript which has not been revised by The Jim Rutt Show or by Brian Hanley. Please check with us before using any quotations from this transcript. Thank you.
Jim: On today’s Currents episode, we have as our guest, Brian Hanley. Brian’s an independent scientist with published work in economics, epidemiology and he has worked in vaccines, including virus vaccines. Brian is going to talk a little bit. We’re going to discuss first the economic and social consequences of lockdowns, i.e., that it is not cost-free to do lockdowns, and some ideas Brian has on how to get us out of lockdown as soon as possible. So Brian, let’s start with the costs of lockdowns, economic, social, other.
Brian: Okay. So I went and looked for examples of big drops in GDP such as we’ve seen during this lockdown. We hit a 4.3 back in April as the U.S. drop in GDP. And it took a year for the 2008 crisis to get down that low. All of the examples that I’ve seen have been not V-shaped, but L-shaped there. I don’t really like the word L because it doesn’t really describe it very well. It’s a step. You take a step down and then you can get going at the previous rate of growth, but you don’t recover what you lost. So what that means is collectively worldwide, we have lost a total of 12 GDP years, which amounts to a total… It’s held pretty steady at 8 trillion per year, which is a total of 96 trillion. For the U.S. itself, it’s 1.8 trillion and that’s a 21.6, almost 22 GDP years which is equivalent to an entire year’s GDP since the 2008 crisis.
Jim: So we have a significant GDP loss, and based on historical analysis we’re not going to get a V-shape recovery.
Jim: At best, we’ll get a re-establishment to the previous track but from a lower base. Is that a fair way to say it?
Brian: Right. Right. And going forward from here with the Coronavirus lockdown, we do not know what it’s going to be. Now I just read an article today, an interview with Roubini and he’s predicting an L-shaped, in other words a step, for this and that it’s going to be deep because there’s a lot of outstanding consumer debt. And a lot of that is in people who needed to be working continuously. So he sees this as being a real problem, particularly in the U.S.
Jim: Yep. I agree. That will be certainly a problem. And further, we don’t know how far down the down leg is on the L, right?
Jim: It could easily be 15% or 16%, not the 8% or 10% that the data so far shows. So we have to get an L-down we get a rise up. And then in previous recoveries, one of the things that we do know is that the ones that are most strongly affected are young people.
Jim: People first trying to get on the career ladder. They essentially have their heads held down for some significant period of time, and most of the analysis shows they never catch up.
Brian: Right. Because of all those lost opportunities going forward that we talked about with the step. You’re tracking at the same rate but you’re way below what you would have been. So all those younger people will not have those career tracks.
Jim: Yeah. And then also, I think because of the fact that essentially the economy’s on hold for a while, the normal growth you’d have in your career… Like I said, when you’re 25, if you’re good, you’re rising very rapidly in your career in the business world. But if nothing has happened, nobody’s getting promoted for two years, you just lost those two years and you’ll never gain them back.
Jim: All right. So we clearly have a significant economic loss. Most likely and I think it’s reasonable, the L-shaped model then at best will get back on the same growth path. But it’s also show social implications. I know you’ve talked a little bit about that locked down seems to be increasing the suicide rates, at least in some areas. Could you talk about that a little bit?
Brian: Yes. Yes. There’s reports that we have had in the last four months roughly the number of suicide attempts coming to ERs that normally occur in a full year, which is an indication that people are either psychologically stressed or that they are economically stressed and they’re just saying, “I’ don’t want to deal with this.” One or the other or both.
Brian: Personally I’ve been seeing a new crop of what appear to be homeless people sitting around at shopping and things like that. And the reason that they don’t look like they’ve been homeless very long is they’re normally fed, their skin isn’t weathered, all the rest of it. And they’re all young.
Jim: Yeah. We know an awful lot… What 50% of Americans approximately have less than $500 worth of liquid financial reserves.
Jim: And so being out of work for two months, even at a lower than average consumption rate, because that’s the only good news about this shit show is that our consumption rates are also way down. So we’ve reduced our reserves less than we otherwise would have. But still, if your reserve is $500, there’s going to be a lot of people that are at or near the edge right now. So let’s take both of those elements, potential longterm damage to the economy, social costs in terms of probably mental health, either first order from the stress of lockdown and the threat of disease, and two, from the economic consequences leading to maybe as much as a 300% increase in suicides as long as the lockdown occurs. So if we stipulate-
Brian: And possibly going forward. The economic stress will continue and it will probably increase. We have never had this kind of a dramatic job loss ever in history.
Jim: That is correct. We’re in uncharted territory. Although I do have some reason to be optimistic in that if we go back to our Keynsian analysis of the longterm failure of modern financial capitalism, it tends to be a lack of demand as opposed to lack of supply. One thing I’m looking for that we may have a little bit of V-shape comes from the fact that demand has not been met for a long time. For instance, car sales have fallen by a tremendous amount of sales. When this is over car sales, I suspect, will rebound above their normal baseline for a while. And there may be some other categories that will also rebound. Optional surgery for instance will rebound afterwards, but not for long and probably not enough to produce a V-shape recovery.
Brian: Yeah. That’s what Roubini says.
Jim: Yep. I think that-
Brian: He says there’ll be an initial U-shape start and then that will disappear and it’ll just be an L.
Jim: Yep. Okay. Let’s take that as a given. Let’s just stipulate it for what comes next that the costs of lockdown are very substantial economically, they’re very substantial socially in terms of impact on young people’s career opportunities, and we pay a substantial cost in terms of raw deaths in terms of suicide. So what’s the alternative? At this point, I should add that Brian has experience in viral vaccines, including having made his own COVID-19 vaccine and has given it to himself. So with that, what should we do?
Brian: Let me preface this by talking about vaccines a little bit because there’s more than one type. The original vaccine is Vaccinia, which was the smallpox vaccine, which was the serendipitous discovery that cowpox would infect humans and cause mild disease and then those people were protected from smallpox. There haven’t been very many of those. Well as far as I know there’s been not other such vaccine since. In the fifties, we started developing attenuated vaccines by passaging viruses in cell cultures. And over time those would adapt to the cell culture and they would become mild diseases for humans. That’s how we got the measles vaccine that we use today. That’s how the original Salk vaccine was made. That’s also how the second vaccine was made that followed it.
Brian: The problem with that type of vaccine is it’s kind of a black box. And back then we didn’t do sequencing. We didn’t really know how far it was away. So a vaccine of that type could potentially revert to virulence. And the Salk vaccine did that in a very small number of cases. So we stopped using that. We created regulations to deal with that kind of situation. We haven’t updated them since. Since then, we’ve learned the structure of DNA. We’ve learned how to sequence rapidly. We can get the sequence for a new disease once we identify it pretty quickly. The SARS COV 2 vaccine, the Wuhan strain was sequenced and posted by the 10th of January. And today we can use that data to rationally design vaccines because we also understand the genes of viruses much better. So we can go in and we can look at that and we can make decisions.
Brian: Now, there are several kinds of non-living vaccines and non-living vaccines are inherently safer because they’re not going to cause disease. They’re safe for immunocompromised people. And the original ones were killed vaccines. That’s what the current yearly influenza vaccine is. It’s a killed vaccine. So what I’m going to propose is really an expansion and version of what we already do every year to deal with influenza.
Brian: The next step from killed vaccines is you can take components of the virus, the proteins, and you can combine those with adjuvants and inject those and those will create an immune response. They are pretty good at generating antibody responses. They’re fair, depending on the kind of adjuvant at generating CD8 responses. CD8 T cells are what clears a virus infection. There have been studies done in mice where if you don’t have the CD8s, you can have any amount off antibodies those mice will die. They’ll die more slowly the more antibodies they have, but they will still die because you have to get rid of the factories that are producing the virus in order to defeat it. And that’s what CD8 T cells do.
Brian: The most modern type of vaccine are nucleotide vaccines of which there are two kinds. There’s DNA vaccines, which were invented in the late eighties, early nineties. And I did a year of my graduate school work with Gary Rhodes, who was the inventor of DNA vaccines. One of the things we discussed was how he had never seen… And basically if you keep the design straightforward, keep it simple, you code for proteins that are there in the virus natively without modifying them, or if you modify them do it very, very little, you will get a successful vaccine. He had never seen an instance where this didn’t work with DNA vaccines.
Brian: In this century, we have developed RNA vaccines as a practicality. And because of the way that they develop the technology, we can create RNA vaccines and roll them out as fast as we can DNA vaccines, but we can manufacture them much more quickly. You can manufacture on a table top for RNA vaccines potentially millions of doses, which means that you’ve got something there that scales well for rollout. DNA vaccines, at this point, nobody’s figure out how to make them scale as well.
Brian: My vaccine was a DNA-type vaccine. I probably designed it around the same time Moderna was designing theirs. They had an application into the FDA by early February, and they got approved for a clinical trial in early March. I tested the DNA vaccine that I designed on myself and a couple of colleagues, we were co-developers so we did it under self experimentation rules. It’s certainly safe, which is what we expected because there’s very little reason to think that you wouldn’t have a safe vaccine. It appears to be effective. I have exposed myself multiple times to people who were diagnosed as sick with COVID-19. I have not gotten symptoms. That is, of course, not in itself a proof because a lot of people in the regular population don’t get symptoms, but I am in the high risk category at my age and because I have asthma and have had it most of my life.
Brian: So with this as background, what I’m saying is there is no reason today why we aren’t rolling out vaccines like Moderna’s vaccine right away and do it as a rollout trial. You monitor it. You look at it. But you always evaluate it from the point of view of we have a disaster here, essentially it should be war time rules not the kind of rules you have when you’re assuming that everything has to be absolutely perfected and all the T’s crossed and all the I’s dotted. Because for vaccines, particularly for vaccines that aren’t alive, there’s very little reason to think that there’s going to be a serious problem, particularly in adults.
Jim: Now we had a previous conversation about this topic, a little side conversation, and I was kind of surprised by the data on how many Americans have died from vaccines since 1950. That might be an interesting data point to bring up here.
Brian: Yeah. I’ve done my best to come up with a number and that number is below 200. It’s probably on the order of 100. The majority of the real serious casualties were in… Well, the early ones were with the Salk vaccine. There was thousands of children who got polio from it. There are people who have gotten Gillain Barre Syndrome, which is arguable whether or not is related to vaccines. It has been accepted kind of provisionally as possibly related to vaccines, but it’s far more common and likely that it was related to an actual illness with an actual virus.
Jim: So the bottom line is the risks from modern vaccines are, in terms of deaths at least, minuscule.
Brian: Very, very low. There was a, there was a killed RSV vaccine. It came out ’56 which was pulled because there was some instances of children under the ages of two who appeared to have a worse course of disease because they had the vaccine. That wasn’t true for anyone over the age of two. So it could have been, as with some other vaccines, it could have been simply not used in children of that age group. But that kind of thing is pretty darn rare. The rest of it… One of the interesting things about the anti-vaccination people is that virtually all of what they cite is just basically made up. It’s not real stuff or it’s wildly exaggerated.
Jim: So the argument is that modern vaccines are relatively safe, but the other half of the FDA standard for any kind of medication is that it also be effective. How would we make sure, or I guess we can’t make sure but how will we have any reasonable confidence, that these new startup vaccines of which there’s been human trials on small numbers are actually effective?
Jim: We don’t want to vaccinate a whole bunch of people with a vaccine that doesn’t provide actual immunity.
Brian: Right. Now there are with all vaccines, except one, the smallpox vaccine, there is a range of immunity that is provided by them. The yearly influenza vaccine based on epidemiology it’s estimated that somewhere around 30% of everyone who’s vaccinated actually gets the flu, but they get such a light case that they don’t even know it. Those people can potentially infect others for a short period of time. Measles vaccine, which is even a live attenuated vaccine, has had failures. Now some of those failures are probably because of poor storage conditions. The measles vaccine is a live attenuated vaccine. And if it’s not kept at the right temperature under the right conditions and all the rest of it, it’ll die. So you won’t get an effective vaccination from that. There are instances where there have been people who had the measles vaccine who were later infected by people who didn’t have it and got measles and were spreading the virus all over. Now those people were protected.
Brian: So in vaccinology we talk about protection and we talk about sterilization. So the goal is a sterilizing vaccine. And what that means is that you will have not just CD8 T cells, but high enough antibody levels that if you get a normal dose of the virus you’ll essentially get no infection or there’ll be nothing seen.
Brian: And so, for example, in mouse studies what they would do is they would expose a bunch of vaccinated mice to a virus. And then two days later they would kill the mice and they would look in the lungs to see if there’s any evidence of virus in the lungs. And a really good vaccine will have no evidence of virus in the lungs. So what we’ve seen in most mammals, if you use a DNA vaccine or an RNA vaccine on them they will get a good antibody response and a good CD8 response. For reasons that are not fully understood, when you inoculate primates with a DNA or RNA vaccine, and we are primates, this is sometimes called the primate barrier and nucleotide vaccinology, you will not get a great antibody response. You may get some but you’re not going to get a really strong one, but you will get a good CD8 T cell response. So what that means is that this kind of vaccine is considered protective for the individuals who get it but it may not be sterilizing.
Brian: If you combine a DNA or RNA vaccine with a later component vaccine that has a protein in it, those are good at generating antibody responses. And since the body has been primed to respond by the DNA or RNA vaccine, it will give you a good antibody response. And something else to remember when I’m talking about these roll-outs is that just because you’ve been inoculated with one vaccine does not mean you can’t be inoculated with another one. Vaccinology is full of multistage inoculations that improve the antibody response and improve the CD9 response each time.
Brian: Something else to understand is that the current regulations are built around the antibody response. And this is a combination of history. That was the first thing we found out about was antibodies. And we had developed Antisera and Horse Serum and all those, and that was a revolution in medicine, but then that hasn’t been updated. And even today, I run into physicians all the time who are not aware that antibodies don’t cure a disease that it’s only the CD8 T cells that do it. So we have not yet adapted the regulations to looking at T-cell responses in people. It’s a harder assay. It’s a much harder assay to execute. It’s a bunch more work so that makes it more expensive, but it’s also the measure that really, really matters for us.
Jim: Follow-up question thought. If I’m understanding you correctly, and it’s quite possible that I am not, that if we are able to boost the CD8 T cells will keep people from getting sick, but we won’t reach the herd immunity to keep it from spreading to the whole population.
Brian: Well, when you are conducting a vaccine campaign you have to get to 95%-plus vaccination rate in order to say that you have effective herd immunity. When a disease goes through a population you have to get to around 70%. Now why is that? The reason is that the transmission networks through which viruses communicate have particular pathways. They’re not completely flat. Some people have a lot of connections that they can transmit through. Most people have very few. That’s why in epidemiology nowadays our zero is not really considered to be a proper measure because it’s basically a mathematical fiction.
Brian: Most transmission of disease is done by what are called super-spreaders. And that’s true in most diseases. And that’s true in the case of this SARS COV 2 epidemic. There are some people who transmit it to 10, 50, maybe 100 or more. The median is somewhere between zero and one. And then when you average all that out after the fact and look at the curve, you see something that is called R0, but it’s not something that’s actually out there in the real world.
Brian: Does that answer the question?
Jim: Well, not really. That’s a side story.
Jim: You’ll still get propagation presumably.
Jim: But I suppose your point is that it doesn’t matter?
Brian: Well, my point is that if you’re using vaccines to stop an epidemic, you either have to do ring vaccination or you have to get 95%-plus of the population immune. And, as an instance of that, we don’t do that currently with influenza because influenza is not a vaccine that everybody gets every year. And so that’s one of the reasons we have between 30,000 and 50,000 people a year dying of influenza as a normal course of events. Because that’s a pandemic that happens every year, we don’t really pay attention to it like we are with this one. Which is the same kind of thing but at a higher death rate.
Brian: So the point here is that what we’d want to do is we want to protect initially like first responders, medical personnel, the elderly, the people who are the most likely to be exposed from it and potentially die. And the people who are risking the most. After that, we can roll it out to anybody who wants it and that should be a huge number of people. Now there will be some people who won’t. This gets to how you can say, Okay, we won’t necessarily need to have a lockdown because most people will be protected who would be the ones who are at greatest risk, and then everybody else can potentially decide for themselves.
Brian: And so nucleotide vaccines, killed vaccines and component protein vaccines can all contribute to that pretty well. And a combination of those can do really well. But if you want the most robust, longterm immunity then you want to have some type of a live vaccine. And that would be a recombinant engineered vaccine, such as Adenovirus with the spike protein attached to it, or you would want to try to rationally engineer an attenuated vaccine which could potentially be done with this particular virus. There is some specific proteins that, for example, there’s ORF3a which produces a protein that prevents the individual cells from producing interferon, which is one of the reasons why this virus tends to last so long because it’s stopping the body from responding to it as effectively.
Jim: So can I re-summarize your strategy and the reasoning again, and correct me if I’m wrong which I may well be. We’re paying a high cost for lockdown economically, socially, and in raw deaths through things like suicide driven by both stress and economic loss, modern RNA-type vaccines can scale easily, are very safe, surprisingly so, and are effective at at least keeping people from getting sick through CD8 T-cell development. So therefore there’s no reason we shouldn’t roll those out at scale right away, presumably with at least some curation on which ones go out I would hope.
Brian: Yeah. You’re going to want to follow it. Okay?
Brian: As a kind of trial. Currently, as an example, there’s a vaccine that was produced for Rotavirus by Wyeth and it had five cases of what’s called Intussusception in infants who had gotten it. And this is an easily treatable condition. It’s where the intestine telescopes in on itself.
Brian: It happens pretty regularly. It’s easily treated. And because of this, Wyeth decided to pull the vaccine, which meant that there were, in the interim years before there was a new vaccine, over a thousand deaths of children in the West. And worldwide the death toll was over half a million during that time. And this is a readily-vaccinatable disease.
Brian: Now that is an example of corporate liability avoidance because of the climate towards vaccines at that time, which was still very… The anti-vaccine people have been astonishingly successful at pedaling, their lies and juries are easily convinced. So we’ve lost vaccines because of that sort of thing.
Brian: So what I’m getting at here is that when we do these roll-outs yes, we should log things, but we shouldn’t be deciding to stop because of something like that, because of something that is probably unrelated that nobody in a military situation would blink an eye at.
Jim: Yep. So I think that’s the fundamental distinction. Wartime rules. We know there’s some risk, they’re not zero but we’re paying huge costs by not doing anything. So whatever we have to do from a legal or administrative or indemnification perspective to get it rolling, we should do. Does that sum up your argument pretty well?
Brian: Yeah. With the caveat that the real risk is really, really low. Probably so close to zero that is’ indecipherable.
Jim: Okay. Well, I think that’s been a very interesting perspective, very different from anything we’ve heard from anybody else, either on this show or in general. That we should take some reasonably curated set of the vaccines and just go with it. Accept some risks, probably very tiny and get various benefits from either actual immunity or at least people not getting the disease and be able to open the economy up for probably everybody but those in a high risk category.
Brian: Those two things are not different. Okay. You can have immunity and still get sick. This happens on a regular basis. For example, I had rubella twice. Once when I was a kid and once when I was in college. And the second time I got it, I had much lighter case of the disease. But immunity does decline with time. It can also decline because, for example, if somebody gets a serious case of measles that will destroy a lot of, or all of, some of their populations of memory T cells and memory B cells. So if they are exposed to that virus again, it’s as if they had never been exposed before.
Jim: Got it. Thanks for that clarification and thanks for being on the show. I think people will find this an intriguing idea, and maybe the idea will get out and get thought about seriously by those people working on our policy. So with that thanks.
Production services and audio editing by Jared Janes Consulting. Music by Tom Muller modernspacemusic.com.