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  • What I'm going to talk about here are the characteristics and traits of pandemic pathogens.

  • You just heard my colleague Crystal's talk where she introduced the concept of GCBR.

  • I'm going to try and delve very deep into that concept, to try to understand what is

  • it about certain pathogens that allows them to cause a GCBR?

  • And I think the theme of this conference is to be curious, and that's really what motivated

  • this project, was to be very curious about what goes on there.

  • I have a picture of my blog there, Tracking Zebra, if you're interested in infectious

  • disease, I do write a lot about that, and that's my Twitter handle.

  • The aim of this project was really to develop a whole new framework around the traits of

  • naturally occurring pandemic pathogens that could constitute a GCBR in order to change

  • preparedness activities.

  • In the past, I'm going to talk about this a little bit later, we've really focused on

  • list based approaches, that are largely derived from the former Soviet Union's biological

  • weapons program.

  • There hadn't been a lot of fresh thinking.

  • It was very static.

  • I think that's what we tried to do in this project.

  • So a couple of basic definitions, just because I don't know if everybody has a biological

  • background.

  • Pandemics are infectious disease outbreaks that occur over a wide area and affect a large

  • proportion of the population.

  • It doesn't necessarily have to be severe; 2009 H1N1 was a mild pandemic, but it was

  • still a pandemic.

  • An epidemic is an infectious disease outbreak that occurs over a large number of individuals

  • within a population.

  • So, the SARS outbreak in 2003 would be an epidemic.

  • An endemic is something that occurs regularly within a population.

  • For example, the common cold is endemic in the human population.

  • Those are just things to keep in mind.

  • What we're talking about are specific types of pandemics that are very severe for the

  • GCBR, to meet GCBR criteria.

  • I'm not going to spend much time on this definition because Crystal really went into some great

  • detail, but what I'm going to do is really expand on what is it about those biological

  • agents?

  • What types of biological agents can cause GCBRs?

  • Everybody is very focused on viruses, some people are focused on bacteria, some people

  • on other things, that's what I'm trying to understand is what traits does a biological

  • agent have to have in order to be able to cause something this severe, to cause this

  • massive catastrophic loss of life, disruption of society, that type of analysis.

  • I just want to draw a distinction, because what I'm talking about here are pathogens

  • of pandemic potential, versus what's this distinction that was made in Mike Osterholm's

  • recent book about pathogens of critical regional importance.

  • When you have an outbreak like Middle East Respiratory Syndrome, that doesn't mean...

  • just because it's not a GCBR doesn't mean it's not important or that it's not going

  • to be very disruptive to people's lives and to societies and to governments.

  • But what we're talking about in the GCBR is something that's going to be global, like

  • the 1918 flu.

  • Something that's a lot different in scale than even Middle East Respiratory Syndrome

  • or SARS.

  • Something much different.

  • There's lots of pathogens of critical regional importance.

  • Even the Ebola outbreak in 2014 in West Africa falls under this type of criteria, versus

  • this type of criteria.

  • The specific aim with this project was really to, like I said, move away from this list-based

  • historical approach.

  • People had really just taken the Soviet Union Biological Weapons program and added a couple

  • things here and there, but really hadn't thought much about why were these things on there?

  • Challenge the assumptions that put them on there, and really try to understand what was

  • it that made smallpox so scary?

  • What was it that makes pandemic flu so scary?

  • We really try to go into an inductive manner, trying to make a whole new paradigm, looking

  • at the actual attributes.

  • We tried to do this by being totally microbignostic.

  • What I say microbignostic, that means we didn't go into this project saying, "This has to

  • be a virus.

  • This has to be a bacteria".

  • We said it could be anything.

  • It could be a parasite, a protozoa, it could be a prion.

  • So that was something that was totally new.

  • We really wanted to challenge thinking and then take this paradigm, and hopefully use

  • it to move forward when we think about preparedness and try and think of new infectious disease

  • outbreaks with this new paradigm in mind, to get better at being prepared because we're

  • constantly surprised, which I'll get to later in the talk.

  • What are the essential traits?

  • The next slide is a little busy.

  • I'm going to walk through it one by one.

  • Thinking about what does it have to have?

  • Talking to people and doing a lot of literature review, there's a whole bunch of different

  • things that make up the alchemy of a pandemic pathogen.

  • I'm going try and explain what this equation means and all of this as best I can.

  • The first thing you need to do, is you have to have a pathogen that can efficiently transmit

  • from human to human.

  • You can have a disease that can be really bad like Tetanus.

  • That doesn't transmit between humans, so it can't be a pandemic pathogen.

  • When you're talking about a pandemic pathogen, it has to be able to get from people to people,

  • so that's number one.

  • It has to have a moderate fatality rate.

  • It doesn't have to be really, really horrible like a 90% fatality rate or 100% like rabies.

  • It has to be something that's kind of in a sweet spot that it allows enough death to

  • occur that it causes disruption in the society.

  • Remember that the 1918 Influenza pandemic, which killed 50 to 100 million people, only

  • had a fatality rate of two percent.

  • But because it was so widespread, it led to disruption.

  • Contagious during incubation period.

  • I have bolded this because in multiple modeling studies, and in experience, and Crystal alluded

  • to this earlier when she talked about smallpox, if a disease is contagious during the incubation

  • period, when you're not sick, it's very, very hard to control.

  • That's why the H1N1 pandemic had spread everywhere before anybody even knew about it because

  • people were contagious one day before symptoms.

  • If a disease is contagious in that period, it becomes very, very difficult for public

  • health interventions to have any impact.

  • The same goes with mild illnesses with contagiousness.

  • When you have the flu or the common cold and you're out shopping, doing your normal daily

  • life, you spread that to other people.

  • It's very hard to stop that, versus something like Ebola, when you're sick and highly contagious

  • you are in bed and you can't really move, and move about in society.

  • So this is another key factor.

  • An immunologically naïve population.

  • Again, reflecting back on Crystal's talk when she showed the map of the indigenous populations

  • in the Americas, in the pre-Columbian area in 1492.

  • That was an immunologically naïve population to smallpox, which allowed smallpox to spread

  • very rapidly through that population.

  • That's what a pandemic pathogen would require.

  • No vaccine or treatment.

  • You don't have any way to stop this.

  • That's another thing that fits into this.

  • Correct atmospheric and environmental context.

  • Infectious diseases happen in a context.

  • Is it happening during World War I like the pandemic flu did in 1918?

  • Is it happening where there's been societal disruption?

  • Like, for example, Yemen right now and the Cholera outbreaks?

  • All of that's going to play a major role in how prolific an infectious disease outbreak

  • is.

  • There's a lot of biology that has to go into this too.

  • Not every pathogen can infect every type of human.

  • You have to have a proper receptor.

  • So you've got to have some receptor that lots of humans have that this virus or this bacteria

  • can actually cling onto.

  • It's also going to explain which organs it affects, because obviously some organs are

  • more important.

  • If it affects your brain, your kidney, your liver, your lungs, those are what you really

  • see with these pandemic pathogens.

  • And then it has to be able to evade the host immune response.

  • It has to be something that is not easy for the immune system to mount an effective response

  • against.

  • This is a fancy equation that showed up.

  • The point of this equation is not to memorize it or to think about it, it's just that you

  • can take all of these things and give them values, and come up with pandemic potential

  • of a pathogen.

  • You can look and vary them.

  • If you look at some other things, for example, the more host types a pathogen has, the more

  • chance it is to emerge.

  • That's another thing that comes up, that these things can infect more than one type of species.

  • That's where the concept of zoonosis comes about, where something comes from an animal

  • species into humans.

  • But the more hosts something has, the more likely it is to be able to infect humans and

  • cause a problem.

  • Thinking deeper about this.

  • We have that recipe there.

  • When you think deeper, there's a couple of things that come out of this.

  • When you look at the way these things transmit, the most likely way to cause a pandemic is

  • for it to be done through the respiratory or the airborne route.

  • There's much, much less you can do to stop an airborne virus or a respiratory droplet

  • spread virus.

  • If I had measles right now, you would all be exposed.

  • It's very, very hard to do that.

  • But if it was something that was spread through, for example, fecal/oral, like Hepatitis A

  • or Cholera, you can really delimit that with sanitation.

  • Remember, there was a couple of cases of Cholera in Mexico about five years ago, and everybody

  • panicked.

  • But there was just even a modicum of sanitation - stopped Cholera.

  • It did not spread in Mexico.

  • You can't do that with respiratory viruses and airborne viruses.

  • It's much, much harder through the respiratory or airborne bacteria.

  • A vector borne transmission, so that means through mosquitoes, through ticks, that's

  • something that's very interesting and it is something that I think we struggle with trying

  • to figure out exactly how bad a vector borne outbreak can get.

  • They are, in general, limited by the vector range.

  • For example, mosquitoes frolic in places that are going to be much more conducive to their

  • habitat, so it's going to be very hard for them to live in a temperate climate.

  • I live in Pennsylvania, we don't have mosquitoes year round there.

  • But there are parts of the world that mosquitoes thrive in all year round.

  • That's why I talked about specifically aedes mosquitoes, which are the mosquito that's

  • responsible for spreading Dengue, Chikungunya, Zika, Yellow Fever.

  • They are basically covering half the population of the globe.

  • That is something that's a little bit different with vector borne.

  • In general, we don't think vector borne could do this because the host range, the range

  • of the vector, is kind of limited.

  • The other thing to think about is, talking about global catastrophic biological risk,

  • we talk about deaths, but is fatality everything?

  • This is a question to pose to yourself.

  • There's two purposes for an organism.

  • To survive and to reproduce.

  • What if you had a disease like Zika?

  • It was much more widespread.

  • Or Rubella?

  • Pre-vaccine.

  • If you decrease the reproductive fitness of a species, could that lead to a GCBR?

  • I think the answer is yes.

  • I don't think that Zika or Rubella really make that criteria, and maybe if we were talking

  • about this, if Rubella occurred now, maybe it would fit in the GCBR.

  • But back in the 1960s, people coped with Rubella, but it is one way to think about a GCBR that

  • doesn't end up killing everybody.

  • The other thing is, there's another virus, HTLV, which as been in the headlines a lot

  • in the last couple of weeks because of some studies that have come out of Australia.

  • HTLV is the most carcinogenic virus.

  • It causes human t-cell leukemia.

  • This was the first human retrovirus that was discovered.

  • What if an infectious agent causes cancer in everybody?

  • Would that lead to a GCBR?

  • That's something just to think about, that it's not always going to necessarily be death.

  • I think you have to be very broad and active minded about this.

  • There's also something I wanted to talk about called sapronotic disease.

  • That's a term that we found from the plant world and the animal world, where you have

  • this idea that if an infectious agent is killing everybody that it's infected, it's not very

  • good because it's going to run out of people to infect.

  • But what if it doesn't care?

  • What if that's a secondary source?

  • What if it's an amoeba that eats things in pond scum, but only intermittently infects

  • humans?

  • Like the brain-eating amoebas that always grab headlines?

  • How does that fit into this?

  • If it doesn't necessarily need to be in humans to thrive.

  • That it has other things.

  • It could eat dead bark on a tree, or it can eat stuff on the bottom of the forest floor.

  • That's another way to think about a pandemic pathogen, I think is really interesting that

  • came out of this talk.

  • The first set of conclusions we drew from this project were, the traits that are most

  • likely to be possessed are going to be respiratory droplet transmission, fecal/oral much less

  • likely.

  • The aedes vector-borne agents, those mosquitoes, have a special status because there's widespread

  • mosquito prevalence and there are certain viruses that get very high levels in your

  • blood that these mosquitoes can just kind of pick off.

  • That's why we've seen explosive outbreaks of Dengue, Chikungunya, Zika, why we've seen

  • Yellow Fever resurface.

  • So they are a special category.

  • They probably don't fall as high as respiratory/droplet, but that's something to keep in mind, that

  • these could possibly do that.

  • So then the next thing we try to do is think about, okay, we've said respiratory/droplet

  • transmission.

  • So we have to make a choice, we have to think: is it gonna be virus, bacteria, fungi, parasite?

  • So I say there's no agnostics in a foxhole.

  • We had to push people that we talked to in this thing, and push ourselves to think, what

  • would it really be?

  • So I think that viruses are very formidable in this realm.

  • They mutate much, much more rapidly than bacteria.

  • The transmission and replication cycle in a human is much faster than in bacteria.

  • And you heard this earlier today, that there's no real broad spectrum antiviral agent.

  • I have a picture there, this is from Epcot Center, for penicillin.

  • So when we think about bacterial infections, we can usually, even in the face of antibiotic

  • resistance, craft together some regimen that works.

  • And lots of them are nonspecific, they kill wide varieties of bacteria.

  • They have a spectrum.

  • We don't have that so much with antiviral agents.

  • We've got a certain drug for flu, a certain drug for Hepatitis C, a certain drug for HIV.

  • We don't have broad spectrum antivirals.

  • And that's a major chink in the armor against viruses.

  • When you think about bacteria, they really are limited.

  • Because of broad spectrum antibiotics, they're slower, they're less mutable.

  • There are some caveats.

  • We do have multi-drug resistant bacteria that can be challenging, and antibiotic resistance

  • is probably one of the most pressing public health threats that we face.

  • But they still don't rise to the fact of causing a GCBR.

  • Because even if you think about everything becoming resistant, we would be pulled back

  • to the pre-penicillin era.

  • But people still lived during the pre-penicillin era, in a way that they were still flourishing,

  • human populations were still growing pre-penicillin.

  • So I think that's important to remember.

  • But we have seen a major outbreak.

  • For example, we talked about Yemen and the cholera outbreak that's occurring with the

  • bombing that's going on, and the infrastructure problems, it's been the worst cholera outbreak

  • in history.

  • And we had a bad plague outbreak just a couple of years ago in Madagascar, with 1200 people

  • infected.

  • So in certain resource-poor areas, you can see bacteria get very close to causing a GCBR.

  • But it would be hard for it to do anything.

  • So you think back to the Black Death back in the 1300s and 1400s.

  • There were no antibiotics and I think that's why the Black Death probably does qualify

  • for a GCBR at that time.

  • So the other thing, what about fungi?

  • Fungi are everywhere in the environment, there's tons of them everywhere.

  • But the fact is, they're temperature restricted.

  • They don't like to grow at human temperatures.

  • And there's a lot of hypotheses about why this is.

  • They think that humans actually came through what's called a mammalian filter, that we

  • evolved the ability to have a 98.6 degree Fahrenheit or a 37.5 degree Celsius temperature

  • as a way to avoid fungi.

  • And we see fungi decimating salamanders and frogs, and all of these other types of species

  • that have lower body temperatures.

  • And it's very, very hard for fungi to infect humans, they usually have to be immuno-compromised.

  • There's been a few scary things, like candida orus, which is a multi-drug resistant fungi

  • that preys on hospitalized patients.

  • Cryptococcus gattii, which is one that kinda is around the soil and trees.

  • And then there was this Exserohilum outbreak.

  • That was related to contaminated steroids, which you might've heard about that getting

  • injected directly into people's backs.

  • But again, they needed something to be able to do that.

  • Some of these fungi are sapronitic and they can be very, very high mortality rate because

  • they don't transmit well between humans.

  • But the temperature restriction makes it very hard for them to cause a pandemic.

  • Prions, you probably heard of mad cow disease, it's probably the most famous prion disease.

  • Those don't spread very well between humans, unless there's cannibalism.

  • This is a graffiti in Pittsburgh, there's a guy who writes kuru all over the city of

  • Pittsburgh.

  • Kuru was a disease that was found in Papua New Guinea among the indigenous tribes there,

  • where they were engaging in ritualistic cannibalism of each other after someone died, and that

  • kuru was really decimating that population.

  • But unless you have people directly exposing themselves like that, in that manner, prions

  • are unlikely to do that.

  • We've seen scrapie for example, in the sheep species, and then chronic wasting disease

  • in elk.

  • Those things have done - because there's so much different saliva contact between people

  • and the way these animals eat and interact with each other, that don't really apply to

  • humans.

  • It's interesting, because when you think about prions, chronic wasting disease, they actually

  • had to burn down a forest to stop it from spreading, because it was so endemic in those

  • elk and in deer in that region.

  • So that's a testament to what a prion can do, but it's very restricted when you think

  • about how this could do this in humans.

  • This is something that most people don't know about.

  • So we look to try to see, was there ever an extinction event from an infectious disease

  • in any animal species?

  • And there's one.

  • This is the Christmas Island rat, and it basically was driven to extinction, by a vector-borne,

  • so mosquito-born, trypanosome.

  • Trypanosomes are parasites, much bigger than bacteria viruses.

  • And the Christmas Island rat basically was rendered extinct because of it.

  • But does this apply to humans?

  • I don't think it does, because the poor Christmas rat couldn't go anywhere, it was on an island,

  • there was nowhere for it to run.

  • Humans can outrun a vector, and like I said, vectors are limited in where they can actually

  • cause disease and where they can spread infections.

  • And if you can outrun that vector, if you can move to places where it isn't there, you

  • can probably avoid it.

  • I think that when you look at the human trypanosome diseases, they haven't done anything near

  • what they did to the Christmas Island rat.

  • There are some concerns when you talk about parasites and protozoa, about certain drug-resistant

  • forms of malaria, especially if they make it from Asia to Africa, being able to maybe

  • cause something on a GCBR level.

  • But we haven't seen that yet.

  • There's lots of other things to think about when you think about infectious disease.

  • Helminths, ectoparasites, amoeba, non-carbon based, so that's something when you talk about

  • the mission to Mars, and thinking about how you're going to deal with organisms that may

  • or may not come back there.

  • So there's lots of different things to think about, but really our consensus was that viruses

  • are most likely going to be the GCBR agent, because of their mutability and their rapidity

  • of spread, and their lack of an antiviral.

  • But when you get into viruses, there's so many viruses.

  • There's lots of different rules and exceptions.

  • Would the virus, would its genes be RNA, or DNA?

  • Will it copy itself in the cytoplasm of a cell or will it be in the nucleus?

  • Will it have a segmented genome like flu?

  • Flu is one of the most prolific viruses, and the reason why it's so good at infecting people

  • is because it can shuffle its genes, because they're all on a segment, and it can basically

  • be like a deck of cards that switches different genes.

  • So that's something that is really important to think about, whether it's segmented versus

  • non-segmented.

  • Does it have a really big genome like MERS and SARS?

  • Or is it a very small genome?

  • And then what about these ones that are spread by mosquitoes?

  • They get very high levels of the blood in people, are those the kind of viruses that

  • are gonna be able to cause?

  • In just a couple of headlines a monkey pox, which is a DNA virus that people are very

  • nervous about in the wake of the smallpox eradication, people aren't vaccinating for

  • smallpox routinely anymore, now monkey pox has resurged and the vaccine used to be, it

  • was protective against monkey pox.

  • So when you think about viruses, there's lots of different things to think about.

  • Probably when you think about GCBR-level risks, flu probably goes to the top of this list,

  • because it's done it so many times before.

  • And we do have this scare right now that's been going on since probably the 1990s, regarding

  • avian influenza.

  • That's a picture from my local county fair in my hometown outside of Pittsburgh.

  • And when you think of avian flu, one of the scariest versions of this is H7N9.

  • We're right now in the sixth wave, but in the fifth wave we saw some very, very scary

  • things happen.

  • You saw changes showing this virus being more likely to be able to transmit between humans,

  • we've seen antiviral resistance in this strain, we've seen the genetics of the strain change

  • so much that the vaccine that's stockpiled, there was a mismatch.

  • And we've seen it evolve high pathogenicity in chickens.

  • This is the CDC's ranking of viruses.

  • A and B are both H7N9.

  • So it's at the highest risk for emergency impact.

  • So this is probably one of the scariest viruses that we face.

  • And it meets a lot of those criteria that we talked about.

  • When you look at the steps in pandemic emergence, there's a bunch of steps that a virus has

  • to do, this is specific for influenza.

  • We're already down to around 3 to 4.

  • The infection is replicating sufficiently to produce infectious virus, but we're seeing

  • very stuttered human transmission.

  • But we're getting down that road with H7N9.

  • So this isn't something that's very theoretical, what I'm talking about, this is something

  • that we're dealing with today, now, in China, with H7N9.

  • I think what the CDC does is they actually rank the different properties of the virus,

  • which I think is a very good thing to do.

  • It might not always be accurate, but it does definitely give you some framework for how

  • to evaluate viruses, and that's what we were doing with this framework, was trying to take

  • this type of an assessment tool of viruses, of influenza, and apply it to the whole microbial

  • world.

  • And that's what this new paradigm that we tried to do was going to try to accomplish.

  • So what do you do when you come up with these ideas, when you come up with these types of

  • lists of things that might cause this?

  • You can do what CEPI did.

  • CEPI is the Coalition for Epidemic Preparedness and Innovation.

  • It's a major funder for vaccine research, and what they did is they came up with a list

  • that they took from the WHO blueprint for research, and picked some to actually go after.

  • I think that's one way to do this, where you have diseases that meet this criteria, then

  • you invest money to go into it, to develop vaccines.

  • A couple of other things, just a couple other headlines just to show you.

  • People did think about space bacteria, but it's unlikely that space bacteria, if they're

  • adapted to Mars, are going to be able to do very well in humans on Earth, because there's

  • totally different conditions that would allow them to flourish on one planet, that wouldn't

  • apply to another planet.

  • We talked to lots of people that were thinking about salamanders and frogs, which are being

  • decimated by these sapronotic pathogens, but don't necessarily affect humans.

  • So a couple more conclusions there.

  • Any microbe is capable of causing a GCBR.

  • But we believe that RNA viruses are the most pressing and likely threat, because of their

  • mutability, their zoonotic potential.

  • Bacterial antimicrobial resistance unlikely to reach GCBR levels, and GCBR level of widespread

  • fungal disease is unlikely due to its temperature restrictions, and very select conditions for

  • a prion-caused GCBR.

  • The last part of the talk, I just want to emphasize a few things.

  • We're always surprised about infectious disease, and I list a bunch of them here.

  • H1N1 coming from Mexico, Zika, SARS, MERS, and there's lots of people investing in surveillance

  • and prediction approaches.

  • I think there's two basic approaches.

  • There is this global virome approach, where people will go out and sequence everything

  • that they want to do, and try to find a list of viruses that are out there.

  • It tells you maybe what's coming, but it's very expensive, and 99 percent of those viruses

  • are probably not gonna pose any threat to humans.

  • What if the next GCBR or the next pandemic is not viral?

  • So that's one way to do it.

  • Or there's another way to do it.

  • I think this is the way I favor.

  • It's looking at people that are getting infected by novel diseases.

  • Looking at people like bush meat hunters, people who work in abattoirs, looking for

  • what's called viral chatter, things that go from the first forays of a pathogen into humans.

  • And then, looking at different hot spots.

  • Instead of trying to sequence things, focus on things that are actually causing infections.

  • And then you think about unknown diagnoses, 50% of our septic shock cases, even in the

  • United States, don't have a diagnosis, and I think that people just treat for symptoms

  • and not necessarily for fevers.

  • So I think that going about this, we're going about this a little bit wrongly.

  • I think going after these unknown etiologies, all over the world, trying to figure out where

  • these infections are occurring and actually running things down to specific diagnoses,

  • instead of just saying, "You've got some viral syndrome."

  • I think that's the way to go about it.

  • And I think the... this headline just came out of Nature a couple of days ago, that really

  • validates what we're saying that pandemics, you should spend much more on surveying actual

  • infections, not on trying to predict things by viral cataloging.

  • I'm just gonna, in the interest of time, just one or two more slides I want to show you.

  • So, what's out there, is lots of biological dark matter.

  • We've got lots of viruses out there, lots of bacteria out there that nobody knows about.

  • And I think we're at the stage now, that we have this tricorder culture, that Captain

  • Kirk is holding there from Star Trek, where Bones, the doctor, would just scan someone

  • and know exactly what they have.

  • We've got lots of new technologies, and I think that you can start and figure out what

  • disease X is going to be, and that's the new WHO nomenclature for the unknown unknown.

  • And I do think we're at that point now, but only if we actually harness these diagnostic

  • tests.

  • And just to conclude here that, when you think about infectious disease risk, you have to

  • also think about human actions and that there are human actions that can enhance pandemic

  • potential.

  • Mistakes, political or scientific, fears of the unknown and also, complex disasters.

  • So, if there's a war, for example, at the same time as an infectious disease, it can

  • raise something to a GCBR-level.

  • So I'm gonna conclude here, people keep asking me for books to read.

  • There are lots... that are first trying to get into this field.

  • These are some of the ones that I could think of, that I think are interesting.

  • This is an article I wrote for The Atlantic, Why Hasn't Disease Wiped Out the Human Race?

  • If you just Google that, you'll find that under my name in the Atlantic, where I try

  • to summarize some of the stuff that I talked about here.

  • And then, these are some interesting books that I think are really... that really give

  • you a flavor for this, and a few other ones that I didn't have pictures of.

  • A Viral Storm by Nathan Wolf and Level 4: Virus Hunters of the CDC by McCormick, that's

  • the book that really got me interested in all of that.

  • It came out in 1996 and this is the book that really started for me when I was a little

  • child.

  • That was the one that my parents read me over and over and over again, which is the story

  • of the rabies vaccine.

  • So, thank you for your interest and I'm happy to take any questions in the time that's remaining,

  • and I have office hours as well and feel free to follow me on Twitter or read my blog.

  • Thanks again for your attention.

  • All right.

  • Thank you.

  • That was an awesome presentation and we do have some questions coming in via the app.

  • We've got a few minutes, so we'll see how many we can get through.

  • So, first question, what are the challenges in creating a broad-spectrum antiviral?

  • You alluded to it a bit, but, tell us more.

  • So, in general antiviral therapy has lagged antibacterial therapy by a long shot.

  • We haven't had many antivirals ever, until actually the modern era with HIV and hepatitis

  • C. Viruses are much trickier to make an antiviral agent against, because remember that viruses

  • don't have their own machinery, they're inside a human cell, so they're going to be using

  • your ribosomes, all the stuff that you use to make protein.

  • So, many of these things can be very toxic because they're going to be hitting things

  • that your cells do as well.

  • So you have to find something on the virus that only affects the virus and minimally

  • impacts your own cellular function.

  • So that's very hard.

  • Whereas, in a bacteria or a fungi, they're doing their own thing, so you can find things

  • that target just them.

  • With antivirals, it's very hard, you have to make sure, the toxicity would be too high

  • if it's actually blocking your proteins synthesis and not just the virus's.

  • So I think that's the biggest challenge, is the fact that viruses use your stuff to actually

  • do their functions and you can't explicitly target a virus the same way you can target

  • a bacteria or a fungi or a worm or whatever else it could be.

  • How does monoculture kind of fit into this?

  • I mean, farming of animals mostly, maybe other things that humans cultivate as well that

  • kind of become global.

  • Does that increase our risk in a material way?

  • So that was something that we thought, with the monoculture you're thinking about, we

  • were thinking mostly about humans here, so are humans a monoculture?

  • And I don't think that that's the case, because it's said that the human immune system, within

  • all the different humans that live on earth, can actually respond to any type of antigen.

  • There's been some papers written about this, that the diversity of the human immune system

  • globally, is enough that there's nothing that could really drive humans to complete extinction

  • on its own.

  • But, when you think about monoculture for other things, for animals or for plants, that

  • clearly makes them vulnerable to a pathogen that could wipe them out, but not so much

  • for humans.

  • I think that there's enough genetic diversity, that we would be able to survive, at least

  • a good proportion of us, with an infectious disease outbreak.

  • How about things that may be dormant for a long time or asymptomatic for a long time,

  • how does that kind of change the analysis of this stuff?

  • That's an interesting question.

  • So when we talked about GCBR and the definition that we use to bound this, we talked about

  • sudden, the word sudden.

  • And when you think about a disease like HIV, what gave HIV the ability to cause this global

  • pandemic like no other, basically, was the fact that it has this long latency period

  • where people were still infectious, for 10 years about, from infection to when they would

  • start showing symptoms, and in all that time they were contagious.

  • So, that was very advantageous for HIV.

  • When you're talking about GCBRs, then we're talking about the speed of it, but I do think

  • that when you talk about this long latency and dormant period where someone can transmit

  • a disease, that's a very, very huge advantage that a pathogen would have, and able to disseminate

  • through a population.

  • It's unclear whether that would qualify as a GCBR because there would be time to prepare

  • there, there would be people looking at it the way HIV is.

  • And I think we struggled a lot with our definition of GCBR because HIV meets a lot of these criteria,

  • but in terms of its rapidity, it's much different than the black death or 1918 flu.

  • Couple of questions about synthetic biology and apparently ever-lowering barrier to entry

  • into synthetic biology with now kind of hacker spaces for biology.

  • How much does that worry you and how much should it worry me?

  • So, synthetic biology and the democratization of biology and the biohacker culture, is kind

  • of a two edged sword.

  • You got a lot of great minds now being engaged in awesome research and that could probably

  • lead to new treatments, new cures, new discoveries, new types of knowledge, and I think that's

  • a great thing.

  • But the issue, I guess, is that there are people that would try to use this for nefarious

  • purposes and I think that there's a fine line that has to be walked there.

  • And I would say that, although it's becoming very, very simple to do synthetic biology,

  • it's not easy to do.

  • It's still not something that someone can do in their back yard or without any kind

  • of proper training.

  • So, I do think that, some of that risk is a little bit misplaced, because I don't think

  • that people can just concoct these chimeric, crazy things in their garage and release them.

  • But I do think that it's important that they start to respect norms of biosafety and understand

  • that when you work with these pathogens, even if you're not going to create the Andromeda

  • strain, you need to be careful and actually understand that there is a science of biosafety

  • and it's really important that you actually follow that so that you're not going to expose

  • yourself or others to risk.

  • So I think that this is something that people have been engaging with this community to

  • try and teach them this type of stuff, but I do think they should be able to flourish.

  • I think it's really great that they're able to do this type of work without the confines

  • of a traditional academic career.

  • Cool.

  • Well, unfortunately, that is all the time we have here, but you will be available for

  • office hours around the way in our next break, which begins now.

  • So, how about another round of applause for Dr. Amesh Adalja.

What I'm going to talk about here are the characteristics and traits of pandemic pathogens.

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