Speaker 1: My name is Patrick and I live in Orlando, Florida.
Speaker 1: In June of twenty twenty, both of my parents were
Speaker 1: hospitalized with COVID. It started with my mother. My mother
Speaker 1: was seventy two, active and in good health. She ran
Speaker 1: her own cosmetics franchise and practice yoga on a regular basis.
Speaker 1: Her only underlying condition was asthma, which was not severe.
Speaker 1: On June twenty fifth, she walked into the hospital complaining
Speaker 1: of shortness of breath, a persistent cough, and a fever.
Speaker 1: She was admitted and began aggressive treatment with high low oxygen.
Speaker 1: Due to COVID precautions, we were not allowed into the
Speaker 1: hospital and had to communicate with her through the phone.
Speaker 1: As the days progressed, her condition worsened. When she would cough,
Speaker 1: she would gasp for air as if she was drowning.
Speaker 1: We kept our phone calls with her shorts so she
Speaker 1: could conserve her oxygen. Eventually we told her only to
Speaker 1: use text messages. The hospital gave her convalescent plasma, but
Speaker 1: the treatment course was limited and it didn't seem to help.
Speaker 1: On July fourth, she was intubated with my mother on
Speaker 1: a ventilator. Any updates regarding her condition and prognosis were
Speaker 1: dependent upon the nurser doctor on the other end of
Speaker 1: the phone. The information regarding my mother's condition would change
Speaker 1: based on the person observing it. We closely watched her
Speaker 1: ventilator settings, and our hopes and emotions would rise and
Speaker 1: fall with the daily reports. However, there was no true
Speaker 1: guidepost with which to evaluate her progress. We were frequently
Speaker 1: surprised by new conditions, such as her being septic, a
Speaker 1: persistent pneumothorax, and the development of APHEB. On August sixth,
Speaker 1: after thirty two days on a ventilator, the hospital transitioned
Speaker 1: her to compassionate care and removed her from the ventilator.
Speaker 1: Thirty four minutes later, my mother died. Before she died,
Speaker 1: we saw the X rays of her lungs. Instead of
Speaker 1: the shadowy outline of two healthy lungs, it looked as
Speaker 1: if a family of spiders created an impenetrable web that
Speaker 1: showed as white lines criss crossed throughout the arc. My
Speaker 1: father was admitted to the hospital two days after my mother.
Speaker 1: My father has been disabled since two thousand and one
Speaker 1: after suffering a stroke which permanently compromised his balance and
Speaker 1: range of motion. He also suffers from heart disease and
Speaker 1: has frequent bouts of APHEB. Despite his medical history, my
Speaker 1: father's only COVID symptoms were a fever, diarrhea, and extreme exhaustion.
Speaker 1: After five days in the hospital, he was discharged because
Speaker 1: he did not need oxygen. However, he was still testing
Speaker 1: positive for COVID. The convergence of his mobility issues and
Speaker 1: exhaustion meant that he could not even sit up in
Speaker 1: bed and could not care for himself. We struggled to
Speaker 1: take care of him while wearing PPE to avoid exposure
Speaker 1: to ourselves. The same day my mother was intubated, we
Speaker 1: had to have my father readmitted to the hospital because
Speaker 1: the level of care he needed exceeded our capabilities. My
Speaker 1: father spent two more weeks in the hospital and survived.
Speaker 1: January twenty twenty one would have marked my parents' fiftieth
Speaker 1: way anniversary. Throughout this process, we struggled to obtain reliable
Speaker 1: and accurate information regarding my parents' conditions. Before my mother died,
Speaker 1: we were given the opportunity to come into the ICU
Speaker 1: and see her. The images from that day in the
Speaker 1: ICU have stuck with me more than those of my
Speaker 1: mother herself. The entire ICU was COVID patients. Each patient
Speaker 1: was on a ventilator and confined to their room. Outside
Speaker 1: of the door to each room was the IV poll
Speaker 1: with no fewer than six IV bags and pumps. The
Speaker 1: atmosphere was eerily silent. The only sound we heard were
Speaker 1: a faint beeping in the distance and the stifled sniffling
Speaker 1: of nurses who took turns sitting at the nurses station,
Speaker 1: quietly crying with their heads buried in their hands. It
Speaker 1: was clear to us that the doctors and nurses were
Speaker 1: trying to care for all of their patients, but they
Speaker 1: were continuously confronted by the dim, silent reality that most
Speaker 1: every person in the ICU would not go home.
Speaker 2: My name's Rachel and from our toil in New Zealand
Speaker 2: and my husband's My are both working education in Auckland
Speaker 2: and we have two young kits. I wanted to share
Speaker 2: the experience that I have at the moment living in
Speaker 2: a country which is essentially post COVID. We currently have
Speaker 2: no community cases of COVID in only fifty five cases
Speaker 2: in the country as of the eighth of December, which
Speaker 2: are all quarantined at the border, and there is the
Speaker 2: result of people coming back into the country. We went
Speaker 2: into lockdown with the rest of the world in March
Speaker 2: and the lockdown Level four lasted for five weeks and
Speaker 2: during that time we have very strict conditions. Only hospitals, pharmacies,
Speaker 2: petrol stations and supermarkets were open, and we were only
Speaker 2: allowed out of our house for one local walker day
Speaker 2: or for our designated shopper to go get groceries from
Speaker 2: the local supermarket. The idea was that we didn't put
Speaker 2: ourselves at risk anything that we did that might increase
Speaker 2: our chance of interacting with those outside our bubble. We
Speaker 2: just didn't go and then we went to level three.
Speaker 2: We are online. Shopping and takeaways were allowed for another
Speaker 2: fe few weeks and then by May, schools were open,
Speaker 2: businesses were pretty much back to normal. Our Prime Minister
Speaker 2: took the scientific advice that she received really seriously and
Speaker 2: we were rallied as a team of five million to
Speaker 2: protect each other in the United against COVID nineteen. Ashley
Speaker 2: Bloomfield was a Director General of Health and he did
Speaker 2: a press conference at one pm every day to update
Speaker 2: everyone on new cases and which clusters had new cases.
Speaker 2: And even though everyone not everyone agreed with lockdown. We
Speaker 2: had very few cases of people breaking it. People received
Speaker 2: government support and most people got paid at least eighty
Speaker 2: percent of their wage over lockdown, and our borders are
Speaker 2: still closed except for returning citizens in permanent residents and
Speaker 2: they have to undergo two weeks isolation in a government
Speaker 2: funded facility, which is a five star hotel until they
Speaker 2: give return three negative tests. So after that first lockdown,
Speaker 2: we had one hundred days with new cases, and to
Speaker 2: be honest, it really felt like that was that. But
Speaker 2: then we had one relapse where just an Auckland, the
Speaker 2: Auckland region went back into lockdown for three weeks when
Speaker 2: one family tested positive in the community and they were
Speaker 2: able to find out that that was somebody from quarantine
Speaker 2: who had delayed incubation period, so they came up positive
Speaker 2: once they were back in the community. And so contact
Speaker 2: tracing is a huge part of New Zealand's response and
Speaker 2: they now trace all cases genomically to help link the clusters.
Speaker 2: So COVID, is this a weird thing? Right now? We
Speaker 2: know it's out there, we did the work to eliminate
Speaker 2: it from the community, and there's this sort of peripheral
Speaker 2: awareness of it. Because we wear masks on public transport in
Speaker 2: case another case comes through quarantine, and we hear stories
Speaker 2: from overseas and it's by no means completely rosy, like
Speaker 2: it's hard for people with loved ones overseas and you
Speaker 2: can't fly into the country unless you have a spacebook
Speaker 2: to the managed isolation, so there are people that are
Speaker 2: missing out on coming home for Christmas. But we also
Speaker 2: go to concerts and have plans to travel with the
Speaker 2: New Zealand over summer and have big family Christmas celebrations,
Speaker 2: and we see what's going on, but we're not really
Speaker 2: part of that global narrative of quarantine and the ever
Speaker 2: present fear of in fiction or death for us here
Speaker 2: in New Zealand and instead because of how swiftly the
Speaker 2: government acts if there is a community case, we're sort
Speaker 2: of on edge. But it's very easy to forget in
Speaker 2: the day to day that it's out there, because our
Speaker 2: lives are back to normal so to speak. Okaids are
Speaker 2: at school, where at work, and apart from not being
Speaker 2: able to travel overseas, there's not a huge difference to
Speaker 2: how we live now compared to in February, but we
Speaker 2: do have that feeling of how lucky we are to
Speaker 2: be in this situation. So basically all that to say,
Speaker 2: there's a lot at the end of the title. New
Speaker 2: Zealand is proof that testing, contact, tracing, quarantine, and science
Speaker 2: and collective action can prevail, and hopefully we will and
Speaker 2: I've crossed the rest of the world as well.
Speaker 3: Thank you so so much for sharing your stories with us,
Speaker 3: and thank you also to everyone else who has written
Speaker 3: in to share your first hand account of how COVID
Speaker 3: nineteen has impacted you. We absolutely love hearing from you,
Speaker 3: and we feel like telling your stories is such an
Speaker 3: important reminder of how far reaching the effects of this
Speaker 3: pandemic have been.
Speaker 4: Yeah.
Speaker 3: Hi, I'm Aaron Welsh and I'm Erin Alman Updike and
Speaker 3: this is this podcast will kill you.
Speaker 4: Yeah, Welcome to our fourteenth I can't believe we've made
Speaker 4: it this far.
Speaker 5: Oh my gosh.
Speaker 4: I installment of our Anatomy of a Pandemic series on
Speaker 4: COVID nineteen. Today we are revisiting the virus itself, SARS
Speaker 4: COVID two, which we visited first many many.
Speaker 3: Months ago, many many months.
Speaker 4: So today we'll refresh you on what exactly this virus is,
Speaker 4: what new things we've learned about its transmission. We'll touch
Speaker 4: on some of the new strains or rather variants that
Speaker 4: you've probably been hearing about, and we'll talk about the
Speaker 4: different tests for COVID nineteen and how those actually work,
Speaker 4: and honestly, so much more.
Speaker 3: Again, there is a lot of great information in this episode,
Speaker 3: so get excited. I'm excited, But first, are you also
Speaker 3: excited that it is Quarantin any time?
Speaker 4: I'm always excited for quarantine any time.
Speaker 3: Absolutely? What are we drinking this week?
Speaker 4: We're drinking quarantin y fourteen.
Speaker 3: Oo. What a surprise.
Speaker 4: And in Quarantini fourteen we have lime juice, Lemon juice, rum,
Speaker 4: and Marischino liqueur. And we'll post the full version of
Speaker 4: this Quarantini as well as our non alcoholic plus burrita
Speaker 4: on our website. This Podcast will Kill You dot Com
Speaker 4: and all of our social media channels, so make sure
Speaker 4: you follow us there.
Speaker 3: Absolutely. Okay, let's see, we've got a little bit more
Speaker 3: business to cover, so we are still soliciting first hand
Speaker 3: accounts for this COVID nineteen series, and if you would
Speaker 3: like to submit your first hand account, head to our website.
Speaker 3: This podcast will Kill You dot Com and click on
Speaker 3: the COVID nineteen first hand tab on the top of
Speaker 3: the page, and that'll send you over to a Google
Speaker 3: forum where you can fill out some of the information
Speaker 3: for your first hand account. And once again, thank you
Speaker 3: so much to everyone who has submitted their first hand
Speaker 3: account so far.
Speaker 4: Yeah, we also are in the process of getting transcripts
Speaker 4: made yay for all of our episodes. This is long overdue.
Speaker 4: We're very excited. They will be available under the transcripts
Speaker 4: tab on our website This Podcast will kill You dot Com,
Speaker 4: So check back there or follow us on social media
Speaker 4: to know when they're all being released.
Speaker 3: And then there's just the usual business stuff. So we
Speaker 3: have a good Reads list, we have a bookshop affiliate
Speaker 3: account if you want to read more about any of
Speaker 3: the subjects that we mention and that there happens to
Speaker 3: be a book about.
Speaker 4: And we also have.
Speaker 3: Tons of incredible, amazing, beautiful, super cool TPWKY merch. Yeah
Speaker 3: we do, and you can find links to all of
Speaker 3: those things on our website This Podcast will kill You
Speaker 3: dot Com.
Speaker 4: How many times can we say the name of our
Speaker 4: website in this episode?
Speaker 3: My gosh, oh, my gosh.
Speaker 4: Oh. Anyways, let's get into today let's get into today.
Speaker 3: Yes, so our guest today is someone that you are
Speaker 3: likely familiar with because we talked with her all the
Speaker 3: way back in March for our first virology episode. Also,
Speaker 3: she's been like all over amazing, you know, up First
Speaker 3: and other podcasts.
Speaker 4: Super famous at this point.
Speaker 3: She's famous, and we think she's great. We thought she
Speaker 3: was great way back in the day. We still think
Speaker 3: she's great. So we wanted to ask her once again
Speaker 3: all about the virus and what we've learned. Yeah, we
Speaker 3: recorded this interview on December thirtieth, twenty twenty last year,
Speaker 3: last year, and so here she is. We are so
Speaker 3: thrilled to have back on virologist doctor Angie Rasmussen, affiliate
Speaker 3: at the Georgetown Center for Global Health, Science and Security,
Speaker 3: and she is going to answer all of our questions
Speaker 3: about SARS Kobe two, the virus that causes COVID nineteen.
Speaker 3: And we will let her introduce herself right after this break.
Speaker 6: I'm Angela Rasmussen or Angie.
Speaker 5: I am an affiliate and a virologist at the Georgetown
Speaker 5: Center for Global Health, Science and Security. Soon I will
Speaker 5: be a research scientist at Veto Intervac, which is the
Speaker 5: vaccine Research Institute at the University of Saskatchewan.
Speaker 4: Excellent, Thank you so much for coming on again. We're
Speaker 4: thrilled to speak with you. If you could kind of
Speaker 4: just help refresh our knowledge and tell us a bit
Speaker 4: about SARS CoV two, the virus that causes COVID nineteen,
Speaker 4: Like what kind of virus it is, maybe other viruses
Speaker 4: it's related to, and what that tells us about the
Speaker 4: virus and the disease it causes.
Speaker 5: Absolutely so, SARS coronavirus two, as the name implies, is
Speaker 5: a coronavirus. It is a beta coronavirus. So the Stars
Speaker 5: or the coronavirus family is divided up into three major branches,
Speaker 5: the alpha coronaviruses, the beta coronaviruses, and the gamma coronaviruses.
Speaker 5: SARS coronavirus two, like SARS classic, is a beta coronavirus,
Speaker 5: and it's also what's called the sarbeco virus. The Stars
Speaker 5: like beta coronaviruses, which is a subgroup of that particular genus,
Speaker 5: So it's most similar to SARS coronavirus classic. It's also
Speaker 5: related to MYRS coronavirus, which is another beta coronavirus, as
Speaker 5: well as to two of the common cold coronaviruses, which
Speaker 5: are also beta coronaviruses, and the other two common cold
Speaker 5: coronaviruses that circulate in humans are alpha coronaviruses. So it's
Speaker 5: part of this larger family called coronaviruses. And what all
Speaker 5: coronaviruses have in common is they have a single stranded
Speaker 5: RNA genome, so their genome, their genetic material, is encoded
Speaker 5: on one single piece of RNA, a single strand, So
Speaker 5: unlike our genomes, which are double stranded, DNA is just
Speaker 5: one strand of RNA, and it's what we call positive sense,
Speaker 5: meaning that if it gets into a cell, it can
Speaker 5: be directly translated into protein by the ribosomes, which are
Speaker 5: the organelles inside your cell that basically make proteins from RNA.
Speaker 5: And that's their normal function. So that's what coronaviruses have
Speaker 5: in common with each other. They all evolved at some
Speaker 5: point from a common ancestor coronavirus back in you know,
Speaker 5: ancient times, and now there's very diverse. They are very
Speaker 5: diver family. We probably only know a handful of the
Speaker 5: coronaviruses that are out there, and only a subset of
Speaker 5: those actually infect people, so people should keep in mind
Speaker 5: not to scare anybody, but stars coronavirus two is a
Speaker 5: sarbco virus, as I mentioned, and there are quite a
Speaker 5: few of those that have been found circulating in wild
Speaker 5: bat species, and not all of them can probably infect humans,
Speaker 5: but some of them may be able to. So there
Speaker 5: may be other coronaviruses out there floating around in the
Speaker 5: wild that may be potentially human pathogens, but we really
Speaker 5: don't know that much about that, and we I think
Speaker 5: really need to know more about that to prevent future
Speaker 5: pandemics from happening.
Speaker 1: Mm.
Speaker 3: Yeah, So now let's talk what has been all over
Speaker 3: the news lately, and that is strains. So in our
Speaker 3: earlier episode back in I think March, where we talked
Speaker 3: with you about the virology of SARS Kobe two, we
Speaker 3: asked a bit about a couple of the different strains
Speaker 3: that seem to have emerged at the time, calling the
Speaker 3: L and S strain, and we talked about what that
Speaker 3: might mean in terms of disease outcomes. And lately, a
Speaker 3: we have a lot more information about just overall strains
Speaker 3: of SARS Kobe two in general, and then in particular,
Speaker 3: there's been a lot of coverage about the one UK
Speaker 3: strain as it has been called in the news, that
Speaker 3: seems to have now popped up in the US, for instance,
Speaker 3: and popped up all over different countries, and there's some
Speaker 3: indication that it might be more contagious. Could you sort
Speaker 3: of just walk us through what this UK variant is,
Speaker 3: whether this appears to be a new strain, how different
Speaker 3: it is, and whether there are any you know, clinical
Speaker 3: outcomes that we are seeing in regards to the strain.
Speaker 5: Absolutely, So, before I get started, I'll say that, you know,
Speaker 5: even the use of the word strain is somewhat confusing,
Speaker 5: I think for people sometimes because it can be used.
Speaker 6: In a variety of different ways.
Speaker 5: So I tend to call the variant of variants because
Speaker 5: it's not really that different from all the other variants
Speaker 5: of stars coronavirus two that are floating around out there.
Speaker 5: It has I think twenty three different nucleotide substitutions or deletions.
Speaker 5: There are twenty three changes basically to the genome overall
Speaker 5: that make up this new variance, and that basically means
Speaker 5: that it's genetically different. But we expect all these variants
Speaker 5: to be circulating around anyways, because the one thing about
Speaker 5: RNA viruses that you can count on is that they
Speaker 5: mutate every time that they replicate. So this is a
Speaker 5: normal and expected thing to have different variants with different
Speaker 5: properties emerge. Whether there's strains or not is a matter
Speaker 5: of debate, just because sometimes when people say strain they
Speaker 5: mean something that's radically different, either genetically meaning that a
Speaker 5: much larger part of its genome is substantially different from
Speaker 5: the parent virus, or that it might be different immunologically
Speaker 5: meaning that you know your immune system will mount fundamentally
Speaker 5: different responses, make different antibodies to it. And we don't
Speaker 5: have any evidence that that's happening for this. So the
Speaker 5: L and S trains that we talked about, which feels
Speaker 5: like a million years ago, didn't turn out to be
Speaker 5: L and S. I think that the L and S
Speaker 5: stod for I think low, low disease or lethal. I
Speaker 5: can't remember what they stood for, but one was mild
Speaker 5: and one was more severe, and that didn't turn out
Speaker 5: to be true. That was probably just an artifact of
Speaker 5: the population sizes that they sampled. But this variant in
Speaker 5: the UK, which has the extremely catchy name of B
Speaker 5: one one seven is does appear to be more transmissible,
Speaker 5: and that's really based on a couple different lines of evidence.
Speaker 5: One is that it became very prevalent, very very quickly
Speaker 5: in the southeastern United Kingdom, and I should note that
Speaker 5: it didn't really necessarily emerge in the UK, but that's
Speaker 5: where it was first detected because their genomic surveillance program,
Speaker 5: where they're actually sequencing about ten percent of the viruses
Speaker 5: that they identify, and in terms of new cases, that
Speaker 5: made it very easy for them to track the sort
Speaker 5: of rapid takeover, if you will, of this particular variance,
Speaker 5: and it just became it out competed essentially all the
Speaker 5: other variants that were circulating in that population in about
Speaker 5: a couple of months, So that's really fast for a
Speaker 5: single variant to take over. So there was that evidence.
Speaker 5: They also observed that people who were infected with this
Speaker 5: particular variant had higher viral loads at the time of diagnosis,
Speaker 5: and that's a little trickier because people aren't usually being
Speaker 5: sampled every day and tested, and you know, during the
Speaker 5: course of a viral infection, your viral load will change
Speaker 5: as the viral replicating and then as it starts to
Speaker 5: be cleared so it's hard to say if that's the
Speaker 5: mechanism by which it's more transmissible, meaning that people who
Speaker 5: are infected with that are sheddy more virus, But that's
Speaker 5: what this preliminary data seems to suggest.
Speaker 6: And then yesterday I saw that they.
Speaker 5: Had released some data, some epidemiologic data about the secondary
Speaker 5: attack rate, and that basically showed that people who were
Speaker 5: infected with this were more likely to transmit the virus
Speaker 5: to others in their households or in their workplaces. So
Speaker 5: it does appear to be more transmissible. You know, we've
Speaker 5: now found it in the US in Colorado, it's probably
Speaker 5: elsewhere in the US. It's been found in I think
Speaker 5: twenty five twenty six other countries so far. So this
Speaker 5: variant has been emerging and has been spreading globally for
Speaker 5: a while now. We just hadn't picked up on it
Speaker 5: until the week before Christmas.
Speaker 2: Gotcha.
Speaker 3: And so if the mechan is by which it is
Speaker 3: more transmissible is a higher viral load or shedding more virus,
Speaker 3: does that have any sort of clinical outcomes as well?
Speaker 3: Like do we see more severe disease in people infected
Speaker 3: with this variant compared to other variants?
Speaker 5: So that hasn't been observed yet, and it doesn't appear
Speaker 5: that this variant results in increased pathogenicity or increased disease severity.
Speaker 5: You know, we don't know the mechanism by which it's
Speaker 5: more transmissible. That that viral load data is suggestive that
Speaker 5: that might be the case, but other people have shown
Speaker 5: that one of the mutations in the spike protein, which
Speaker 5: is in the receptor binding domain, binds ACE two, the
Speaker 5: receptor for the virus more tightly. It could have something
Speaker 5: to do with that. It could have something to do
Speaker 5: with increased fitness, which basically means that the virus is
Speaker 5: able to replicate to higher tighters. We don't know, but
Speaker 5: the good news is it doesn't appear to be associated,
Speaker 5: at least observationally with more severe clinical disease. And there
Speaker 5: is a mutation that inserts stop code on and to
Speaker 5: be ORF eight protein, and previously with both STARS coronavirus
Speaker 5: two and STARS, classic deletions in ORF eight have been
Speaker 5: associated with attenuation or making the virus less virulent. So
Speaker 5: it may be that this stop codeon and ORF eight
Speaker 5: has something to do with that might not, but people
Speaker 5: are investigating this now.
Speaker 6: But the good.
Speaker 5: News in the bottom line is that it doesn't look
Speaker 5: like this variant is more pathogenic.
Speaker 4: That is good news. I guess you mentioned that there
Speaker 4: are a lot of other variants kind of floating around,
Speaker 4: and I know that that's something that a lot of
Speaker 4: people have expressed questions or concerns about. Do we have
Speaker 4: any evidence of any other variants that do seem to
Speaker 4: cause more severe disease or even potentially affect different populations
Speaker 4: differentially than more common variants.
Speaker 6: So not really.
Speaker 5: Initially this UK variance, it was said that that it's
Speaker 5: infecting children more, and today some data came out that
Speaker 5: in a preprint that showed that maybe not. So it's
Speaker 5: really hard to say, but to my knowledge, there haven't
Speaker 5: been any variants described that are more virulent than others
Speaker 5: apart from that L and S paper way back when
Speaker 5: that doesn't mean that they're not out there, but right now,
Speaker 5: at least in the US and in most countries besides
Speaker 5: the UK, we just aren't doing enough genomic surveillance overall.
Speaker 5: So it's really difficult to associate particular variants with particular
Speaker 5: disease severities if you're not actually sequencing a big portion
Speaker 5: of the variance that you're seeing. I mean, in the US,
Speaker 5: if somebody goes in and gets a COVID test, you know,
Speaker 5: if they're very sick, they'll go to the hospital. But
Speaker 5: that doesn't necessarily mean that somebody's going to be doing
Speaker 5: the sequencing that's required to say, Okay, this person's infected
Speaker 5: with this variant versus that one. So it's not to
Speaker 5: say that there aren't variants out there that are ass
Speaker 5: with more severe disease, but to my knowledge, we haven't
Speaker 5: found any yet. There are other variants that have been
Speaker 5: said to be more transmissible. There's one currently that was
Speaker 5: reported right around the same time as the UK variant
Speaker 5: in South Africa that also may be more transmissible. They've
Speaker 5: said that it might also have some impact on virulence,
Speaker 5: but right now there's not a lot of data about that,
Speaker 5: or at least I haven't seen any to indicate whether
Speaker 5: or not that's the case. So the take home message
Speaker 5: for me with this is we would maybe have more
Speaker 5: information about this if we did more genomic surveillance, So
Speaker 5: we should really think about finding ways to do that.
Speaker 3: Yeah, and so you know, in a general sense, where
Speaker 3: do all of these new variants come from.
Speaker 5: They don't come out of thin air. They come from
Speaker 5: the place where all viral variants come from, and that
Speaker 5: is evolution. When RNA viruses, like coronaviruses replicate their genome,
Speaker 5: they usually make mistakes, and that's because the enzyme that
Speaker 5: replicates or copies their genomes essentially makes typos. It's called
Speaker 5: the RNA dependent RNA polymerase or RDRP. Coronaviruses actually have
Speaker 5: an advantage, probably not from an evolutionary standpoint, but it's
Speaker 5: good for us. They have a lower mutation rate than
Speaker 5: many other RNA viruses because even though they're rdrps are
Speaker 5: still very error prone. They have another enzyme that is
Speaker 5: an exonuclease that basically can do partial spell checking essentially,
Speaker 5: so it can correct some of the errors that the
Speaker 5: RDRP makes.
Speaker 6: When it copies the genome.
Speaker 5: But nonetheless, mutation does occur, and some of those mutants,
Speaker 5: which occur randomly, will be in a place that results
Speaker 5: in some sort of competitive advantage to the virus. Either
Speaker 5: it makes it replicate better, it allows it to enter
Speaker 5: cells more easily, it allows it to evade the immunes
Speaker 5: system more easily. There's a lot of different ways that
Speaker 5: a mutation could have that sort of impact on a virus.
Speaker 5: But if it does give the virus some sort of advantage,
Speaker 5: it's said to be under positive selection. So these new
Speaker 5: variants are the results of basically these mutations being acquired,
Speaker 5: providing some kind of advantage to the virus, and then
Speaker 5: getting passed on because they are under that positive evolutionary selection.
Speaker 5: People ask me a lot, how do we stop the
Speaker 5: virus from mutating? How do we prevent these variants from emerging.
Speaker 5: The best way to do that is to keep the
Speaker 5: virus from replicating, and the best way to do that
Speaker 5: is to keep it from finding new hosts to replicate in.
Speaker 5: It all comes back basically to masks and social distancing
Speaker 5: and staying home and washing your hands and avoiding getting
Speaker 5: infected in the first place.
Speaker 3: I have a quick question about, going back to B
Speaker 3: one one seven and about the mechanism of transmissibility. How
Speaker 3: much do you think behavior could play a role in that. So,
Speaker 3: for instance, if that variant is less virulent than the
Speaker 3: other circulating more common variants, and that means that potentially
Speaker 3: more people who are infected with it are still walking around,
Speaker 3: maybe shedding virus asymptomatically and don't know, so could that
Speaker 3: be one of the major drivers of this apparently increased transmissibility.
Speaker 5: It could, and I don't think we have enough data
Speaker 5: to answer that directly, but I'm going to try to
Speaker 5: speculate a little on how behavior might be involved.
Speaker 6: It could be because people.
Speaker 5: Are more commonly asymptomatic and infecting people when they don't
Speaker 5: know that they're sick, but that happens for normal variance
Speaker 5: of Stars two as well. It could just be that
Speaker 5: because it's more transmissible. The UK also relaxed some of
Speaker 5: their restrictions in preparation for the holidays, which I think
Speaker 5: is kind of a dumb idea, because if Christmas is
Speaker 5: coming up, the virus doesn't care.
Speaker 6: It doesn't take the holidays off.
Speaker 5: So if you relax your restrictions and people think that okay,
Speaker 5: it's safe, like I can get together with my family,
Speaker 5: I can go to work, I can go have dinner
Speaker 5: in a restaurant or a bar or something like that,
Speaker 5: you're in a situation that's going to be more conducive
Speaker 5: to transmission anyways. And if you have a variant that's
Speaker 5: more transmissible, then you're going to see transmission in those
Speaker 5: riskier circumstances increase. And I think that that could explain
Speaker 5: it just as well as anything else. We already know
Speaker 5: that there's a lot of pre symptomatic transmission, and a
Speaker 5: lot of the literature doesn't really distinguish asymptomatic from pre symptomatic.
Speaker 5: So there are people who are asymptomatic completely through the
Speaker 5: entire course of their infection, and then there are people
Speaker 5: who are diagnosed while they're asymptomatic, but they later become symptomatic.
Speaker 5: Those people already drive a fair amount of transmission. So
Speaker 5: if people are in a situation where they're more relaxed,
Speaker 5: they're not being as vigilant about these non pharmaceutical interventions
Speaker 5: intended to reduce exposure risk, and you have a more
Speaker 5: transmissible variant added into the equation, and whether they're more
Speaker 5: asymptomatics or not is probably not as relevant as just
Speaker 5: the fact that a situation in which you would have
Speaker 5: maybe had five people get infected now is resulting in
Speaker 5: ten people getting infected.
Speaker 4: Yeah, that makes sense. So I think one of the
Speaker 4: big questions that a lot of people are concerned about
Speaker 4: with all this talk of new variants is what do
Speaker 4: these new variants mean for the effectiveness of all these
Speaker 4: new vaccines that have been developed, So could you kind
Speaker 4: of explain whether these new vaccines will work against these
Speaker 4: new variants and how.
Speaker 5: Yeah, so that's really the million dollar question and the
Speaker 5: short answer to that right now is that we don't know,
Speaker 5: but those experiments are in progress, and it's actually fairly
Speaker 5: easy to assess this. Basically, what you do is you
Speaker 5: take plasm or serum, the liquid component of blood which
Speaker 5: has antibodies in it, from somebody who was either vaccinated
Speaker 5: or has recovered from being infected. We call that convalescent
Speaker 5: plasma convalescent serum, and you take that and you incubate
Speaker 5: it with the variants or with another virus that has
Speaker 5: the spike protein from the variants on top of it.
Speaker 6: That's called the pseudovirus.
Speaker 5: You take those antibodies and then you take the virus
Speaker 5: and you incubate them together and see if the antibodies
Speaker 5: can still neutralize that virus. So, this variant from the
Speaker 5: UK has I believe seven nucleotide changes, specifically in two
Speaker 5: deletions and the spike protein, and that that could change
Speaker 5: the virus's ability to bind antibodies that were produced for
Speaker 5: the vaccine.
Speaker 6: It also might not.
Speaker 5: And one thing that's important I think for people to
Speaker 5: get to keep in mind is that it's very unlikely
Speaker 5: that just a couple of mutations are going to completely
Speaker 5: evail the overall immune response, because with the vaccines are
Speaker 5: made with are they direct antibody responses to the full
Speaker 5: length prefusion spike protein, which is the protein that's on
Speaker 5: the surface of the virus particle. That protein is obviously
Speaker 5: pretty small to us, but it's pretty large to your
Speaker 5: immune system, and different antibodies will bind all over the
Speaker 5: surface of that spike protein. It's thought that the antibodies
Speaker 5: that bind to the specific part of the spike protein
Speaker 5: that binds the receptor, which is called the receptor binding domain,
Speaker 5: are the most neutralizing, meaning that they will be best
Speaker 5: able to render the virus non infectious. But not always virus.
Speaker 5: Virus proteins can undergo conformational changes, changes in their shape
Speaker 5: and structure that occur when an antibody binds to a
Speaker 5: different part of the protein. So it's unlikely that you know,
Speaker 5: unless the mutations themselves are inducing sort of radical structural
Speaker 5: changes to the entire protein, that a few mutations are
Speaker 5: going to completely avoid the entire broad repertoire of antibodies
Speaker 5: that are going to be raised against it by your
Speaker 5: immune system. However, ultimately we won't know until we do
Speaker 5: the experiments to actually find out.
Speaker 6: To a certain degree.
Speaker 5: A lot of these mutations that distinguish different variants are
Speaker 5: just kind of like a fingerprint.
Speaker 6: They're just mutations that were acquired.
Speaker 5: They don't necessarily offer any type of advantage to the virus,
Speaker 5: but because they're incorporated and they get replicated, they're preserved, so
Speaker 5: you can use them sort of as genetic fingerprints to
Speaker 5: see how a particular variance has evolved if you're doing
Speaker 5: enough sequencing. But they're not always functionally important. The other
Speaker 5: thing people should really keep in mind about this is
Speaker 5: that even if the vaccines are less effective against these variants,
Speaker 5: these vaccine are synthetic and they're easy to change. You
Speaker 5: could make new mRNA vaccines very quickly, and I think
Speaker 5: that it would be very easy to adjust these to
Speaker 5: accommodate for new emergent variants. And over the long term,
Speaker 5: people have asked me, are we going to have to
Speaker 5: keep getting COVID shots over and over again because it's
Speaker 5: like the flu Well, stars coronavirus two is not like influenza, fortunately,
Speaker 5: and there are other reasons why we need to get
Speaker 5: different flu shots every year. First and foremost, because there
Speaker 5: are a lot of different influenza viruses, including strains and
Speaker 5: multiple subtypes that are circulating and they can all reassort
Speaker 5: with each other, which makes things even more complicated. But
Speaker 5: we are aware that we need to make new flu
Speaker 5: shots every year because of this exact issue. So if
Speaker 5: we can do that annually with an inactivated influenza vaccine,
Speaker 5: we can certainly do that, probably less than annually to
Speaker 5: accommodate for evolving stars coronavirus two.
Speaker 3: Yeah, So, speaking of the spike protein, what additional things
Speaker 3: have we learned about the structure or surface proteins of
Speaker 3: SARS CoV two that maybe have given us some more
Speaker 3: insight into how it causes disease or some of the
Speaker 3: widespread effects that it has on the body.
Speaker 5: Well, that's a good question, and the short answer is
Speaker 5: not that much. Is still a very active area of research.
Speaker 5: But one thing I thought was interesting is that people
Speaker 5: who have more severe disease have been seen to have
Speaker 5: more antibodies to the end protein, which is also another
Speaker 5: viral protein. It's not spike, but it might suggest that
Speaker 5: maybe they're sort of developing different immune responses than people
Speaker 5: who are able to successfully control the infection, in which case,
Speaker 5: many of those antibodies are neutralizing antibodies that are specific
Speaker 5: for the spike protein. And it's not really clear why
Speaker 5: that is. I mean, it could be for a variety
Speaker 5: of reasons. Be because the antibodies targeting end just aren't
Speaker 5: as effective at neutralizing the virus, and so people have
Speaker 5: more widespread infections, or it takes them longer to clear
Speaker 5: the infection. It could be because that's inducing immune responses
Speaker 5: that are associated with more disease severity rather than with
Speaker 5: virus clearance. So the T cells in your body can
Speaker 5: be polarized. They call it to act in a few
Speaker 5: different ways. Th one polarization is thought to be anti viral.
Speaker 5: So that's basically your T cells saying all right, we're
Speaker 5: going to start telling the B cells to crank out
Speaker 5: a bunch of neutralizing antibodies. We're going to tell the
Speaker 5: CD eight T cells to go out and start killing
Speaker 5: infected cells. We're going to tell the CD four cells
Speaker 5: to start thinking about anti viral immunological memory.
Speaker 6: We're going to control inflammation.
Speaker 5: There are other responses that are associated Typically they're supposed
Speaker 5: to be for clearing your body of parasites like worms
Speaker 5: and things like that THH two response that are very
Speaker 5: heavy on antibodies and these other types of specialized immune
Speaker 5: cells called granulocytes, including eosinophils and mass cells, and it's
Speaker 5: thought that airway hyperreactivity can often be the result of
Speaker 5: an inappropriate THH two response to a virus. And that's
Speaker 5: a very simplified way of putting a really complicated process.
Speaker 5: But that's just one example of how sometimes the wrong
Speaker 5: type of immune response can lead to more disease severity
Speaker 5: rather than the immune system doing what it's supposed to
Speaker 5: do and clear out the virus. So those anti n
Speaker 5: antibodies have been a hot topic of discussion for that reason,
Speaker 5: just because it's not clear if that's even important, but
Speaker 5: it is an observation that's been made, and it maybe
Speaker 5: explains why some people go on to develop ards or
Speaker 5: acute respiratory distress syndrome that's associated with severe COVID nineteen,
Speaker 5: and why some people have very mild infections that they
Speaker 5: that they can control and clear and and don't have
Speaker 5: any problems with. And then there's the whole issue which
Speaker 5: we still really don't know very much about at all
Speaker 5: of long covid, which is not due to a persistent
Speaker 5: infection most likely, but due to sort of a reprogramming
Speaker 5: of inflammatory responses. We don't really know much about what
Speaker 5: causes that, why some people get that and not some
Speaker 5: people don't, why some people get that when they have
Speaker 5: pretty mild disease. So there's a there's a lot that
Speaker 5: we need to do here to look at, you know,
Speaker 5: the types of immune responses. And I realized this doesn't
Speaker 5: have a lot to do with your original question, which
Speaker 5: was what do we know about antibodies to other viral proteins?
Speaker 5: But it may be that responses to other viral proteins
Speaker 5: by your immune system or interactions with the virus can
Speaker 5: determine outcome.
Speaker 4: M HM fascinating. So in terms of kind of transmission,
Speaker 4: I think there's a lot of discussion about transmission of
Speaker 4: stars kov two at this point. Is there indication that
Speaker 4: the virus is truly airborne? In terms of transmission, do
Speaker 4: we have any evidence? I know early on there was
Speaker 4: talk of like fecal oral transmission with the diarrhea. Do
Speaker 4: any of these routes seem to be playing a role.
Speaker 6: So by inhalation.
Speaker 5: Definitely, short range transmission by droplets and aerosols is clearly
Speaker 5: an important route of transmission that really drives transmission. This
Speaker 5: has been an incredibly frustrating conversation to have in the
Speaker 5: public domain because the term airborne itself, I think, could
Speaker 5: be really confusing for people. In the strictest sense, means
Speaker 5: that the virus is borne by the air and we
Speaker 5: get it from breathing it.
Speaker 6: To some people, that might mean that, oh God.
Speaker 5: It's going to get into the a fac system and
Speaker 5: people are going to be breathing it like from long
Speaker 5: distances away, and you know, is it safe anywhere, because
Speaker 5: we all need to breathe, And the reality is like, yes,
Speaker 5: it's in shared air. So if you're in a room
Speaker 5: with a bunch of people, like say, I don't know,
Speaker 5: you got together with your extended family for the holidays,
Speaker 5: and you're all having dinner in your poorly ventilated dining room,
Speaker 5: then yeah, that's going to be a huge risk of
Speaker 5: transmission by inhalation. I don't like calling it airborne though,
Speaker 5: just because a lot of people, I think hear that
Speaker 5: and they think like that seen and outbreak, where Dustin
Speaker 5: Hoffman is like it's gone airborne and like looks up
Speaker 5: at the vents in the hospital and it's not transmitted
Speaker 5: that way. There have been a couple reports of people
Speaker 5: in stacked apartment buildings that share plumbing lines having infections.
Speaker 5: They can't rule out infection from congregating, for example, in
Speaker 5: shared spaces in those buildings, but I think that if
Speaker 5: that were happening all the time, we would have a
Speaker 5: lot more people infected, especially in New York. Having lived
Speaker 5: in New York in some terrible apartments, I can guarantee
Speaker 5: that we would have seen COVID spreading like wildfire in
Speaker 5: New York City. In apartment buildings that are sharing sewage
Speaker 5: lines and I'm sure are not perfectly sealed, we would
Speaker 5: have been seen a lot more of that. So I
Speaker 5: think that this is opportunistic airborne in that in certain
Speaker 5: circumstances it's very easy to transmit this by inhalation. And
Speaker 5: that really is thinking about shared air. So anytime you're
Speaker 5: in an enclosed space with people who are breathing and
Speaker 5: putting out respiratory droplets and aerosols into the environment, and
Speaker 5: you can breathe them, particularly cumulatively over a period of time,
Speaker 5: that's going to really increase that risk. And that risk,
Speaker 5: of course, can be mitigated by doing things like wearing
Speaker 5: masks to prevent you as source control, to prevent you
Speaker 5: from emitting particles yourself into the environment when you breathe
Speaker 5: or speak.
Speaker 6: It can be mitigated by increasing.
Speaker 5: Ventilation in those enclosed spaces, by avoiding them altogether. It
Speaker 5: can be mitigated by taking it outside where there's obviously
Speaker 5: no enclosures anymore. It cannot be mitigated by taking it
Speaker 5: to like a temporary plastic tent that really closed, that's
Speaker 5: not outside, but it's definitely transmitted by inhalation. I just
Speaker 5: think that the term airborne is not really helping the discussion.
Speaker 5: COVID is transmitted through shared air without a doubt, and
Speaker 5: that's a major mode of transmission, much more than fomites
Speaker 5: or contaminated surfaces.
Speaker 3: Yeah, so, now shifting a bit to talk about testing
Speaker 3: for SARS KOV two. Can you walk us through what
Speaker 3: these various test experiences are like.
Speaker 5: The testing that we've had since the beginning of the pandemic.
Speaker 5: The sort of gold standard for diagnostic testing is PCR,
Speaker 5: and this is basically a technique where you take you
Speaker 5: essentially are photocopying part of the virus biochemically to see
Speaker 5: if you have it, and if you have it, then
Speaker 5: you will amplify that through the PCR reaction. If you
Speaker 5: have a lot of it to start out with, then
Speaker 5: you will develop a signal on that PCR test sooner
Speaker 5: than later. And that's what if you've heard people talking
Speaker 5: about the CT or the cycle threshold value, that's what
Speaker 5: that refers to. So a lower CT, meaning the sooner
Speaker 5: you got to identifying a positive signal with the PCR test,
Speaker 5: the more.
Speaker 6: Virus you had to start out with.
Speaker 5: So that's the gold standard, and that's a very specific test,
Speaker 5: so there's not a lot of false positives, contrary to
Speaker 5: popular belief. Now, the problem with the PCR test is
Speaker 5: that it's quite sensitive, but it's not perfectly sensitive. So
Speaker 5: if you don't have very much virus, if you just
Speaker 5: were infected, you won't necessarily detect that it'll be a
Speaker 5: false negative. Essentially, if you just got over having COVID,
Speaker 5: you might be shedding viral RNA, which is what the
Speaker 5: PCR test detects for a long period of time, and
Speaker 5: that I think is what some people have referred to
Speaker 5: as a false positive. It's not actually a false positive,
Speaker 5: because you are detecting a real signal from viral RNA.
Speaker 5: It's just that the PCR test can't test for infectious virus.
Speaker 5: And so it's really important in that regard to have
Speaker 5: an understanding of when you were actually infected, because a
Speaker 5: positive test in somebody who's recovered doesn't mean that you're
Speaker 5: actually still infectious over a long period of time, and
Speaker 5: that's been shown by multiple streams of experimental evidence and
Speaker 5: epidemiological evidence. So that's the PCR test. There are PCR
Speaker 5: tests that you get by the nasopharyngeal swab, which is
Speaker 5: the big long Q tip. Some people are now doing
Speaker 5: those tests with the anteriornaries, which are the nostrils basically only,
Speaker 5: and some people have also developed PCR tests that use saliva,
Speaker 5: which are actually more sensitive than the nasopharyngeal swabs, and
Speaker 5: certainly I think probably a more pleasant experience to give us,
Speaker 5: like an example, than to.
Speaker 6: Stick a giant key tip of your nose.
Speaker 5: So those are all the PCR tests, the so called
Speaker 5: high complexity molecular diagnostics. Now you probably have also heard
Speaker 5: about the rapid tests, or sometimes they're called antigen tests,
Speaker 5: and these are tests that are looking for the viral
Speaker 5: proteins what are called antigens, So the antigen test detect
Speaker 5: the viral protein.
Speaker 6: There are a couple of different ways that they can
Speaker 6: do that.
Speaker 5: There's some other rapid tests and development too, LAMP, which
Speaker 5: is a rapid nucleic acid amplification method that looks at RNA,
Speaker 5: it just doesn't go through the whole PCR cycling process.
Speaker 6: Some people have developed a test.
Speaker 5: That has not been authorized yet but that uses crisper
Speaker 5: technology to look for viral genetic material. But the main
Speaker 5: tests that are available now are the PCR test and
Speaker 5: then these rapid tests that look for antigen in a
Speaker 5: very short period of time. The main disadvantages to the
Speaker 5: rapid tests is that they are for diagnostics anyways, They're
Speaker 5: less sensitive than the PCR tests, and they're also less specific.
Speaker 6: They are more likely to give you a false positive.
Speaker 5: There's been some controversy about this because some people have
Speaker 5: proposed using rapid antigen testing daily so that people can
Speaker 5: monitor their own status. And I think that there is
Speaker 5: a place for that, and this is where we're getting
Speaker 5: into just my opinion, but I don't think it replaces
Speaker 5: molecular diagnostics or PCR testing. I think people should have
Speaker 5: the ability to test themselves, but they should also have
Speaker 5: clear guidance for what to do, and that is they
Speaker 5: should call their doctor, make sure that their case can
Speaker 5: be reported, and then make sure that they have all
Speaker 5: the information and support that they need to actually isolate
Speaker 5: themselves and put contact traces in contact with people that
Speaker 5: they have then and you know, in close physical proximity
Speaker 5: with recently to make sure that those people can quarantine
Speaker 5: and get access to testing as well.
Speaker 3: Yeah. So our last question is is pretty general, and
Speaker 3: that is, so, what do you think this pandemic has
Speaker 3: taught us about virology, whether that's you know, virologists working together,
Speaker 3: or communication about virology, or anything specific related to stars
Speaker 3: Kobe two, what do you think this pandemic has taught
Speaker 3: us about the field of virology?
Speaker 6: Oh?
Speaker 5: God, Well, it's taught me that there's a lot of
Speaker 5: people who are not virilogists who think that they are.
Speaker 5: It's also taught me that people, including very educated people,
Speaker 5: including some of my colleagues.
Speaker 6: I mean, it's really been telling Like it's brought out.
Speaker 5: I think in some people the worst in people, and
Speaker 5: it's brought out in others the best in people, and
Speaker 5: It's really taught me that in general, scientists and our
Speaker 5: society human beings keep making the same mistakes over and
Speaker 5: over again. And I've seen that in so many ways,
Speaker 5: like I keep having to explain the same concepts to people,
Speaker 5: I keep having to debunk the same misinformation, and I
Speaker 5: think that's because to some degree, people don't actually want
Speaker 5: to learn. We live like in a world right now
Speaker 5: where people they want facts, they want them immediately, and
Speaker 5: if those facts aren't there, which in science is usually
Speaker 5: the case. You know, we are as scientists are trained
Speaker 5: to say this is very uncertain.
Speaker 6: We don't know. It may be this, it may be
Speaker 6: that in general.
Speaker 5: People have very little patience for that now, and it
Speaker 5: can be very very difficult to communicate that, you know,
Speaker 5: we don't know this right now. Here's some of the possibilities.
Speaker 5: We're looking into it. We'll let you know as soon
Speaker 5: as we find out. But people want things now, and
Speaker 5: it's been very surprising to me to see how that
Speaker 5: vacuum has been filled for me. It's certainly taught me
Speaker 5: that the way that I was trained to do virology
Speaker 5: through analyzing data, developing hypotheses and testing them and then
Speaker 5: if they're wrong, revising my hypotheses and testing those new
Speaker 5: ones is still the correct way to do that. But
Speaker 5: I've learned that I really have a long way to go,
Speaker 5: as do most of my colleagues in communicating that uncertainty
Speaker 5: to people. It's taken me a lot of experimentation, and
Speaker 5: I still haven't got it right in terms of how
Speaker 5: I communicate. You know, like we don't know if antibodies
Speaker 5: are going to work against these new variants that are merging.
Speaker 5: For example, I can tell you how we'll go about
Speaker 5: looking into that. I can tell you, I can teach
Speaker 5: you all about the spike protein and antibody binding and
Speaker 5: how the immune system works. Although still the the immune
Speaker 5: system is like the most complicated thing in the world.
Speaker 5: So I think we've all learned that even though we
Speaker 5: already knew it. But you know, it's really really hard
Speaker 5: for me to communicate to people that there's still probably
Speaker 5: going to be a lot of knowledge.
Speaker 6: Gaps even after we do this one critical.
Speaker 5: Experiment, even after this one paper comes out in this
Speaker 5: big elite journal, there's still going to be a lot
Speaker 5: of things that we don't know. And I think the
Speaker 5: real challenge that all of us have faced from you
Speaker 5: know an individual like me all the way to like
Speaker 5: the New England Journal of Medicine, is that sometimes getting
Speaker 5: an answer fast is not the same and it's not good.
Speaker 5: That maybe we should figure out a way to communicate
Speaker 5: to people like we should slow down, we should take
Speaker 5: our time with this because it's too important to get wrong.
Speaker 5: It kind of does matter if that answer is the
Speaker 5: right one or if it's based in evidence. But for me, anyways,
Speaker 5: the most important thing I've learned, I think, is that
Speaker 5: we were not only unprepared, grossly unprepared to deal with
Speaker 5: the generational pandemic even though we knew what was coming,
Speaker 5: but we were also grossly unprepared to engage the public
Speaker 5: in fighting it. And that's something that absolutely has to change,
Speaker 5: and that's something that I'm probably going to be thinking
Speaker 5: about for the entire rest of my career, if not
Speaker 5: the rest of my life.
Speaker 4: Thank you so so much, Angie, doctor Rasmusen for coming
Speaker 4: on and talking with us again. I learned so much
Speaker 4: from this episode, so as always in this series, we
Speaker 4: want to go back and cover the top five things
Speaker 4: that we learned.
Speaker 3: Aaron, Yes, we'll start with number one. All viruses mutate
Speaker 3: basically random mutations can happen every time a virus replicates,
Speaker 3: and those mutations are what can lead to new strains,
Speaker 3: or rather new variants, and so it's completely normal and
Speaker 3: expected that a virus, and especially an RNA virus, will
Speaker 3: have multiple variants. It's something that we were all expecting.
Speaker 3: And in the case of coronaviruses like SARS Kobe two,
Speaker 3: the mutation rate actually isn't as high as we see
Speaker 3: in some other RNA viruses like influenza, and that's a
Speaker 3: good thing. It means that it doesn't change as quickly
Speaker 3: or as dramatically, and so while we have seen a
Speaker 3: number of different variants pop up and spread across the globe,
Speaker 3: these variants represent very small changes in the virus genome
Speaker 3: and they aren't drastically different viruses. Many of these mutations,
Speaker 3: in fact, mean nothing at all really biologically, and have
Speaker 3: no biological implications. We have, however, seen that at least
Speaker 3: one variant, the so called B one one seven, which
Speaker 3: is the one currently making headlines, does seem to be
Speaker 3: more transmissible than other variants, but we still don't know
Speaker 3: the precise mechanism for this apparent increased transmissibility, and at
Speaker 3: least some of its rise in prevalence could be due
Speaker 3: to the lowering of restrictions on things like public gathering
Speaker 3: and indoor dining and so on that led to just
Speaker 3: a whole lot more transmission in general. Unfortunately, this B
Speaker 3: one one seven variant, and actually other variants so far
Speaker 3: observed don't appear to be associated with more severe disease.
Speaker 3: But the bottom line is that we also probably aren't
Speaker 3: doing enough surveillance overall to know for sure exactly how
Speaker 3: many variants there are, or whether some are more virulent
Speaker 3: than others, meaning more likely to cause severe disease. So
Speaker 3: the big question is how do we stop this process
Speaker 3: of mutation of new variants emerging? I mean, and we
Speaker 3: can't stop it, but we can slow it down. We
Speaker 3: can slow it down by reducing transmission. Fewer new hosts
Speaker 3: for the virus means less replication and thus fewer opportunities
Speaker 3: for new variants to arise and spread.
Speaker 4: Exactly Number two. The question of will these new variants
Speaker 4: affect how effective the vaccines that we have will be,
Speaker 4: And the truth is we don't one hundred percent know. However,
Speaker 4: it is highly unlikely that the small changes in the
Speaker 4: these new variants will mean that the vaccines that we
Speaker 4: have are not effective. So we learned in our vaccines
Speaker 4: episode that the mRNA based vaccines produced by Pfizer and Moderna,
Speaker 4: as well as the viral vector vaccine that's produced by Astrozenica,
Speaker 4: all encode the entirety of that spike protein. That's the
Speaker 4: protein that SARS CoV two uses to actually enter our cells.
Speaker 4: So when you get vaccinated and your body starts producing
Speaker 4: this spike protein, you then start making antibodies against it,
Speaker 4: a whole bunch of them, which target multiple parts of
Speaker 4: that protein. And the spike protein, it turns out, is
Speaker 4: a pretty large protein. It's like over twelve hundred amino
Speaker 4: acids long. And the changes that we're seeing in these
Speaker 4: viral variants are super small. In the case of B
Speaker 4: one one seven, we're talking twenty three nucleic acids out
Speaker 4: of their whole genome. Not all of those twenty three
Speaker 4: changes are in that particular spike protein. So while it
Speaker 4: is possible that small changes can affect vaccine effectiveness, it
Speaker 4: is overall unlikely. But that's probably not super reassuring to
Speaker 4: a lot of people. So we do have two other
Speaker 4: better pieces of news that we learned. People are doing
Speaker 4: the research to answer this exact question of vaccine effectiveness
Speaker 4: as we speak. So that's awesome. And now that we
Speaker 4: have this vaccine technology, it's not going to be difficult
Speaker 4: in the future to make small changes as necessary to
Speaker 4: these vaccines going forward to make them effective against new variants.
Speaker 4: In fact, in the case of mRNA vaccines, is actually
Speaker 4: a lot easier to produce new proteins or new mRNA
Speaker 4: than it would be to produce a new entire whole
Speaker 4: killed viral vaccine like we already do every year for influenza,
Speaker 4: for example.
Speaker 3: Yeah, that's really important and pretty reassuring.
Speaker 4: I feel very reassuring. Yeah.
Speaker 3: Number three, we learned that the term airborne gets confusing
Speaker 3: and it's probably not the best term to use in general.
Speaker 3: But what we do know is that for sars KOV two,
Speaker 3: inhalation of viral particles is still the driving factor behind transmission,
Speaker 3: and that means that any place where you are sharing
Speaker 3: air with other people, like in a restaurant or a bar,
Speaker 3: on a plane, or at your Aunt Judy's house, you
Speaker 3: have a risk of transmission and ways to mitigate this risk.
Speaker 3: I mean, we've covered them over and over again, but
Speaker 3: just to reiterate. That includes wearing a mask, increasing ventilation,
Speaker 3: being outside being further apart. But if you are in
Speaker 3: shared air, whether inside a building or inside a plastic
Speaker 3: tent outside at a restaurant, distance alone does not cut
Speaker 3: it because you are still sharing air. Overall, other forms
Speaker 3: of transmission, like from surfaces or fomites or fecal oral
Speaker 3: transmission don't seem to be big drivers of virus transmission,
Speaker 3: which is great news. But that doesn't mean that if
Speaker 3: you rub your nose and then shake someone else's hand
Speaker 3: and then they touch their nose, that they can't get
Speaker 3: infected through that root. So that's why we still have
Speaker 3: to wash our hands and not touch our faces when
Speaker 3: we can help it. It's the Swiss cheese approach all
Speaker 3: over again. The more layers of protection you have, both
Speaker 3: literally and figuratively, the lower the risk of transmission.
Speaker 4: Yeah. Also, does anyone shake hands anymore? I feel like
Speaker 4: that's we're never going to shake hands again.
Speaker 3: I yeah, I'm okay with that.
Speaker 4: I'm okay with it.
Speaker 3: Yeah.
Speaker 4: I have a fan of the elbow bump. I don't know.
Speaker 3: Yeah, I like just the wave.
Speaker 4: Yeah. Number four, So we learned a lot about the
Speaker 4: difference between PCR based tests which are looking for viral RNA,
Speaker 4: and then the rapid tests, which are detecting antigen and
Speaker 4: are overall less sensitive and specific than the PCR based tests.
Speaker 4: We also learned that these at home tests that have
Speaker 4: recently been approved are these antigen based tests, and while
Speaker 4: they are excellent in a number of ways, we do
Speaker 4: need to make sure that there's really good communication and
Speaker 4: guidance around what to do with the information that these
Speaker 4: tests provide. Right now, that guidance is severely lacking, and
Speaker 4: without it, wide implementation of at home testing with rapid
Speaker 4: tests could really backfire. False negatives and false positives are
Speaker 4: possible with any test, but a positive test really needs
Speaker 4: to be followed up in some way, and we need
Speaker 4: to have guidance or some sort of protocol as to
Speaker 4: exactly how to follow up if we're going to be
Speaker 4: using these tests at home.
Speaker 6: M hmm.
Speaker 3: Yeah. And number five are last point, and this point
Speaker 3: seems to be a highly recurring theme in these COVID
Speaker 3: nineteen episodes.
Speaker 4: The number one theme of these episodes yep.
Speaker 3: I think it's been in every episode so far, but
Speaker 3: that just underlines how important this particular theme is and
Speaker 3: that is communication. Communication during a pandemic is hard, but
Speaker 3: it's also essential in this country, especially in the US,
Speaker 3: but truly around the globe. We need to be able
Speaker 3: to communicate truthfully and directly among scientists, public health professionals,
Speaker 3: healthcare workers, and communities. And one of the biggest challenges
Speaker 3: we've faced in this pandemic is how we communicate uncertainty.
Speaker 3: So much of this last year has been uncertain and
Speaker 3: the scientific process works to wade through uncertainty to find answers,
Speaker 3: but it takes time, and this pandemic is one of
Speaker 3: the first times that a lot of people have gotten
Speaker 3: a front row seat as to how slowly and incrementally
Speaker 3: knowledge can grow and how rarely things in science seem
Speaker 3: black and white. We don't know all of the answers
Speaker 3: when we start the process, and jumping to conclusions either
Speaker 3: discarding or disseminating information early without evidence just makes everything
Speaker 3: more confusing in the long run. It's hopefully something we
Speaker 3: can learn from moving forward, how to better communicate this
Speaker 3: process and the uncertainty surrounding it to the wider public.
Speaker 4: Yeah, big time. Yeah, we're learning as we go.
Speaker 3: Oh yes, thank you again so much, Doctor Rasmussen. Angie like,
Speaker 3: we're we're all friends and I right, we're best friends.
Speaker 4: We're gonna go to a Zoom happy hour eventually.
Speaker 3: Yeah. Yes, thanks again for taking time out of your
Speaker 3: busy schedule. We love chatting with you, and your explanations
Speaker 3: are so great and like easily understandable. It's fantastic.
Speaker 4: Yeah. Also, if you want even more detail about the
Speaker 4: variants of sars Kov two that have been all over
Speaker 4: the news, Angie wrote a really awesome article in The
Speaker 4: Guardian that we will link to in our show notes
Speaker 4: and on the website that explains these variants in a
Speaker 4: lot of detail, and also talks about why things like
Speaker 4: travel bands aren't effective in stopping the spread of new variants.
Speaker 4: It's definitely worth a read.
Speaker 6: Yeah.
Speaker 3: Absolutely, thank you to Bloodmobile for providing the music for
Speaker 3: this episode and all of our episodes.
Speaker 4: And thank you to Exactly Right Network, of whom we
Speaker 4: are proud to be a member.
Speaker 3: Yes, and thank you to you listeners for listening. We
Speaker 3: appreciate it. Send us your COVID questions whatever we can
Speaker 3: these things going.
Speaker 4: We really have a lot more in the works and mine.
Speaker 3: We do all right. Well, until next time, wash your
Speaker 3: hands
Speaker 4: You filthy animals,