Speaker 1: We were having hat day at school, and I'm not
Speaker 1: normally a hat person. I had this like numb spot
Speaker 1: on my head all day long and it just was
Speaker 1: like like a not scratchable itch. It was all day,
Speaker 1: all day, all day. But I thought like at first,
Speaker 1: I was like, oh, it's just hat day. Like I'm
Speaker 1: just not comfortable wearing this ridiculous Christmas tree hat at school.
Speaker 1: By the weekend, so that like started midweek. By that weekend,
Speaker 1: it had started to move down my forehead to like
Speaker 1: my eyebrow area, and that's when it just became this
Speaker 1: burning itchy, couldn't really make it go away thing. A
Speaker 1: few days went by, and so this is all at
Speaker 1: Christmas time. That's when we were driving from where we
Speaker 1: live in Buffalo down to my parents on Law Island,
Speaker 1: and that drive, my forehead felt like someone had a
Speaker 1: match to it. I think I kind of lucked out
Speaker 1: with shingles because it was a really small patch that
Speaker 1: I had, But it just feel like someone had a
Speaker 1: lighter on my forehead for as long as it did.
Speaker 1: Was just the craziest thing. I had no idea what
Speaker 1: it was though, So I started doing like the web
Speaker 1: MD thing and I was searching for like, what's a
Speaker 1: large red spot, red spot with blisters, because it started
Speaker 1: to get these really small spots over time. And that's
Speaker 1: kind of when I started to see other pictures of
Speaker 1: people who had the same thing, and people were saying,
Speaker 1: its shingles, shingles at shingles. So I finally called my
Speaker 1: doctor and I said, hey, I have all these symptoms,
Speaker 1: but like, I don't know what this is. And they
Speaker 1: said that sounds like shingles. You need to get to
Speaker 1: you need to come see us right away. But we
Speaker 1: were traveling for Christmas. By the time I kind of
Speaker 1: got all that together, we were already en route from
Speaker 1: Long Island up to r Island for the weekend. So
Speaker 1: that's when I ended up at an out of state
Speaker 1: urgent care and I walked in. The receptionist looked at
Speaker 1: me and she's like, oh, look at that. You have shingles.
Speaker 1: And it was just as fast. And then as soon
Speaker 1: as they saw that, they were able to prescribe medication
Speaker 1: and get it under wraps. So by the time I
Speaker 1: got that, they were like, it's probably too late because
Speaker 1: it had been a week since I started showing the
Speaker 1: first symptom. But the really scary thing that they kept
Speaker 1: sounding the alarm on was this is really close to
Speaker 1: your eye, This is really close to your eye. So
Speaker 1: when I came home, I had follow ups with my
Speaker 1: eye doctors. I had to go back to my primary
Speaker 1: care just to continue watching it to make sure that
Speaker 1: at whatever it was wasn't going to affect the optical
Speaker 1: nerves and all of those forehead things. But like I said,
Speaker 1: it was just the craziest thing because I didn't know
Speaker 1: anybody who had ever had it. I didn't know like,
Speaker 1: was I going to pass this on to my mom?
Speaker 1: Was my sister going to get it? I think everybody
Speaker 1: here is you get shingles from chicken pox, and of
Speaker 1: my generation, like I think I was the end of
Speaker 1: like the chicken pox party. So I was just so
Speaker 1: afraid that I was going to pass this on to
Speaker 1: all of my family members, and they were just kind
Speaker 1: of like, no, You're everything's going to be fine, like
Speaker 1: just kind of cover it up then go about your day.
Speaker 1: So that was my That was my shingles experience, I guess.
Speaker 2: Thank you so much for taking the time to chat
Speaker 2: with us and for being willing to share your story.
Speaker 2: Thanks Hi, I'm Erin Welsh and I'm Aaron Oman Updike,
Speaker 2: and this is this podcast will kill you. Welcome, Welcome,
Speaker 2: this is a fun one.
Speaker 3: I'm honestly thrilled. I don't know. I don't know exactly why,
Speaker 3: but I have been looking forward to covering this for
Speaker 3: a really long time.
Speaker 2: I have two and I've been kind of like daunted
Speaker 2: because I don't I didn't know anything about the history,
Speaker 2: and it turns out there's like kind of not that
Speaker 2: much to it. So I hope you don't fall asleep,
Speaker 2: I'm sure, or if you're listening to this podcast to
Speaker 2: fall asleep, I hope you do fall asleep. But yeah,
Speaker 2: I think it's like it's one of like we all
Speaker 2: have experienced it or know someone that's experienced it. And
Speaker 2: I think Aaron, you and I are part of the
Speaker 2: generation like the last remnants that didn't get the vaccine exactly.
Speaker 3: We definitely are the last cohort that just got chicken pox,
Speaker 3: which is the subject of today's episode.
Speaker 2: There we go plus shingles, slash zoster whatever you want
Speaker 2: to call it, exactly, Yeah, basically the vercella zoster virus.
Speaker 3: Yeah.
Speaker 2: Uh, Erin, when did you get chicken pox?
Speaker 3: I don't remember exactly how old I was, but it
Speaker 3: had to have been after nineteen ninety four or five,
Speaker 3: and we all four got it in a row. It
Speaker 3: went boom boom, boom boom, like down the row of
Speaker 3: older brother than me, than my younger brother, than the
Speaker 3: baby brother. We all got it in age order. And
Speaker 3: I have a very distinct memory of my first poc oh.
Speaker 3: I had my very first chicken pox was on my
Speaker 3: left side, like right on my ribs, on my left side,
Speaker 3: and obviously, like my brother was already sick with it,
Speaker 3: so I knew this is chicken pox. And I showed
Speaker 3: my mom and I was like, Mom, I found this
Speaker 3: is this chicken pox? And she was like, uh, yeah,
Speaker 3: it's chicken pox. And I was like, okay, but can
Speaker 3: I still go to gymnastics?
Speaker 2: Did you go?
Speaker 3: I did? As far as I can remember. Maybe my
Speaker 3: memory is off, but my mom was like, you've already
Speaker 3: exposed everyone. Just keep it covered.
Speaker 2: That's hilarious.
Speaker 3: She might dispute that memory of it. We'll see, mom,
Speaker 3: is that what happened? That's how I remember it. I
Speaker 3: have the scar that I know that that was my
Speaker 3: first pop.
Speaker 2: I really should have called my mom to ask her
Speaker 2: my chicken pox story, because I don't remember, and I
Speaker 2: don't even know if I think I might have been
Speaker 2: too young like to actually remember, but I think it
Speaker 2: was my older sister and I at the same time
Speaker 2: got it, and then my two younger brothers got it,
Speaker 2: and then I honestly don't know about my younger sister
Speaker 2: whether she got it or whether she got vaccine. Yeah. Yeah, anyway, should.
Speaker 3: We should we move on to like actual podcasts, actual
Speaker 3: business of our podcast?
Speaker 2: Maybe is it quarantiny time?
Speaker 3: I think it's definitely quarantin any time. What are we
Speaker 3: drinking this week, Aaron, We're drinking chicken scratch.
Speaker 2: I love this. It works on so many levels. It's
Speaker 2: like people always complain about how doctors have chicken scratch handwriting.
Speaker 2: It's true and also if you have chicken pox, you're
Speaker 2: definitely gonna be scratching.
Speaker 3: Yeah, and what's in a chicken scratch?
Speaker 2: There is tequila, there is kiwi, there is ginger, and
Speaker 2: there is mint.
Speaker 3: Kind of just a fun summary, bev.
Speaker 2: Yeah.
Speaker 3: We'll post the full recipe for that quarantiney as well
Speaker 3: as our non alcoholic plusy Burta on our website. This
Speaker 3: podcast will kill you dot com and our social media.
Speaker 2: And on our website. You can find so many different things,
Speaker 2: like transcripts, like alcohol free episodes, like promo codes for
Speaker 2: all of the ads that we do, like the links
Speaker 2: to Bloodmobile, who does the music for all of our episodes.
Speaker 2: We've also got a Patreon. I mean, it's endless. Just
Speaker 2: go in there, explore it, and I'm sure we'll come
Speaker 2: up with something interesting.
Speaker 3: Definitely. All right, that was the longer intro than we
Speaker 3: usually do. Yeah, it was.
Speaker 2: It was kind of fun, though, it was.
Speaker 3: That's fun getting to relive my chicken pox story. Anyways,
Speaker 3: should we dive into the biology of.
Speaker 2: This thing, let's do it.
Speaker 3: We'll take a quick break first, so vercella zoster or
Speaker 3: herpes zaster or if you want to be very official,
Speaker 3: human alpha herpes virus three. So this virus that we're
Speaker 3: dealing with is a herpes virus, which I think some
Speaker 3: people might not realize because it's called chicken pox. People
Speaker 3: might think it's a pox virus. It's a herpes virus,
Speaker 3: and in fact it's very closely related to herpes simplex one,
Speaker 3: which is a common cause of oral herpes, can also
Speaker 3: cause genital herpes. Check out our herpes virus episode for
Speaker 3: more on that. And so, like all of the herpes viruses,
Speaker 3: this is a DNA virus. It has a double stranded
Speaker 3: genome blah blah blah. Like many of the human herpes viruses,
Speaker 3: this is a very human specific virus. It doesn't infect
Speaker 3: any other animals, which, as we'll see, is part of
Speaker 3: why we don't have a lot of answers about some
Speaker 3: of the specifics of the diseases that this virus causes
Speaker 3: because we don't have great animal models in which to
Speaker 3: study it.
Speaker 2: That makes sense, Yeah.
Speaker 3: Yeah, this particular virus doesn't have a lot of variability.
Speaker 3: There aren't a lot of different strains of varicella. There
Speaker 3: doesn't seem to be a lot of variation in the
Speaker 3: virulence across outbreaks or over time. It's a pretty stable
Speaker 3: virus and aarin. You asked me something before we started
Speaker 3: researching this, which is why is chicken pox often called
Speaker 3: vericella zoster and shingles is called herpes disaster? Yeah, did
Speaker 3: you find an answer to that?
Speaker 2: Well, so, the only thing I could think of is
Speaker 2: the etymology of it. So vericella is another word for
Speaker 2: chicken pox, like that rash that happens for that initial infection,
Speaker 2: and in a lot of other languages besides English, it
Speaker 2: tends to be not like the equivalent of chicken pox,
Speaker 2: but some sort of variation of vericella, right, And the
Speaker 2: word veriicella might come from like the diminutive form of variola,
Speaker 2: which is the word for smallpox, and so it might
Speaker 2: just be like, you know, there's it's analogous where chicken
Speaker 2: pox is to smallpox as veriicella is to variola. Etymologically,
Speaker 2: does that makes sense?
Speaker 3: Yeah, it totally makes sense. No, I genuinely makes sense.
Speaker 2: And then herpe'saster herpees from herpes is like the old
Speaker 2: you know, word that was used by ancient Greeks like
Speaker 2: Hippocrates and whatnot to describe those rashes.
Speaker 3: So it seems to just boil down to the fact
Speaker 3: that even though we're talking about one single pathogen, we're
Speaker 3: talking about two completely different clinical diseases exactly. Yeah, So
Speaker 3: I think that that's something that's interesting. I feel like
Speaker 3: we've covered a lot of pathogens that just cause like
Speaker 3: one disease, where we're like, here's the disease we're talking about,
Speaker 3: and here's the pathogen that causes it, and then we've
Speaker 3: talked about some things like staph oreas, for example, that
Speaker 3: can cause any number of diseases.
Speaker 2: Yeah, or strip piogenies exactly, right.
Speaker 3: So yeah, I don't know. I just feel like that's
Speaker 3: an interesting aspect of this, that there's this big distinction
Speaker 3: between the pathogen and the diseases or the illnesses that
Speaker 3: they might cause. Yeah, well, let's get into the pathogen
Speaker 3: and both of these diseases, shall we.
Speaker 2: Let's do it.
Speaker 3: So I talked about how similar already this human herpes
Speaker 3: viruses to other herpes viruses. Let's start to talk about
Speaker 3: how it's a little different. Unlike many other herpes viruses,
Speaker 3: Viicella is transmitted primarily via the respiratory route.
Speaker 2: What.
Speaker 3: Yeah, isn't that interesting?
Speaker 2: I want to know? And I didn't find the evolutionary history,
Speaker 2: Like what about it? How did that happen?
Speaker 3: It's a really good question that I still don't fully understand,
Speaker 3: aside from the fact that we've talked on this podcast
Speaker 3: a number of times about the tropism of different viruses. Right, So, viruses,
Speaker 3: because they are dependent on host cells to be able
Speaker 3: to replicate. Oftentimes, specific viruses can only infect a limited
Speaker 3: range of cell type popes. It seems like vericella can
Speaker 3: infect a pretty wide range of cell types. So is
Speaker 3: it just that that's a really easy route of transmission,
Speaker 3: and it happens to be good at invading and replicating
Speaker 3: within not just our respiratory epithelium, but also it's very
Speaker 3: good at invading and replicating in our white blood cells,
Speaker 3: in lymph nodes, and so a big thing where it
Speaker 3: replicates is in the lymph nodes in our chest and
Speaker 3: things like that.
Speaker 2: Oh, that's very interesting because I thought that like it
Speaker 2: also though, does have a tropism towards nerves or is
Speaker 2: that just later?
Speaker 3: Oh? Certainly, certainly, let's let's get into all of this.
Speaker 2: Okay.
Speaker 3: Basically, I think the bottom line is that it can
Speaker 3: infect all of those cell types.
Speaker 2: Interesting, okay, cool, yeah, all right.
Speaker 3: But primarily the way that people become exposed via respiratory.
Speaker 3: So a kid, because it's usually kids who are infected,
Speaker 3: comes up and it's like I don't feel good, and
Speaker 3: like breathes right on your face and you inhale those
Speaker 3: viral particles. They you speak from experience, I guess I
Speaker 3: do it, uh, And they travel, those viral particles travel
Speaker 3: to those regional lymph nodes and they replicate. And what's
Speaker 3: really important about the fact that they can infect these
Speaker 3: white blood cells is from there they can travel anywhere
Speaker 3: and everywhere, right, So they travel throughout our body and
Speaker 3: they're able to continue replicating as they invade different cells.
Speaker 3: In general, the incubation period is about two weeks. It
Speaker 3: can be from ten to twenty days after exposure to
Speaker 3: when you first start to show symptoms. But what's important,
Speaker 3: especially for a respiratory virus, is that you become infectious
Speaker 3: and able to infect others at least two days before
Speaker 3: those first symptoms start.
Speaker 2: Aha.
Speaker 3: And this is quite an infectious pathogen. It's pretty contagious.
Speaker 3: I've seen anywhere from sixty to ninety percent of susceptible
Speaker 3: household contacts are likely to become infected.
Speaker 2: What is the estimated are not?
Speaker 3: According to a lecture from Johns Hopkins School of Public Health,
Speaker 3: the r NOT for chicken pox is nine to ten.
Speaker 3: Oh that's a lot higher than I realized.
Speaker 2: Goodness, So when you say respiratory transmission, is it respiratory
Speaker 2: droplets or is it like aerosolt like air?
Speaker 3: Good question. I didn't find this specific answer to that.
Speaker 3: They just say respiratory route, So I don't know how
Speaker 3: long it can hang out in the air. I don't
Speaker 3: think that it's quite as bad as something like measles
Speaker 3: that can stay airborne for like hours at a time.
Speaker 3: But with an attack rate that's so high, I would
Speaker 3: guess that it's probably pretty well airborne. Like it's aerosolizing
Speaker 3: pretty well. Okay, those chicken pox parties that people used
Speaker 3: to have, those are probably pretty effective. It's spreading disease.
Speaker 3: Oh yes, not a good idea. Let's talk about why
Speaker 3: should we?
Speaker 2: Let's do it.
Speaker 3: So, once this virus has disseminated throughout our body, one
Speaker 3: of the main cells that they tend to infect are
Speaker 3: our epidermal cells, our skin cells. Inside of our skin cells,
Speaker 3: it begins to replicate, and this is what causes the
Speaker 3: typical chicken pox rash that we all know and don't love.
Speaker 3: So what's really common is that one to two days,
Speaker 3: like twenty four to forty eight hours before this rash kids,
Speaker 3: I say kids. Of course this affects adults too, but
Speaker 3: most often kids will have like they'll feel kind of
Speaker 3: cruddy for a day or so beforehand, maybe a headache,
Speaker 3: maybe a little tummy ache, maybe like a fever probably,
Speaker 3: But then comes the rash, which is very characteristic and
Speaker 3: kind of what we call chicken pox. The rash starts,
Speaker 3: for anyone who hasn't experienced this, starts as very very itchy,
Speaker 3: red flat patches, and then these patches become raised or
Speaker 3: get little bumps within them, and then those little bumps
Speaker 3: develop into small fluid filled vesicles, tiny little blisters, and
Speaker 3: these tiny little blisters are chock full of virus. So
Speaker 3: this is not only a respiratory pathogen, but it can
Speaker 3: also be transmitted by direct contact.
Speaker 2: Okay, it's just covering all the bases.
Speaker 3: It's covering all the bases exactly. This rash can also
Speaker 3: be present on mucous membranes like in the mouth or
Speaker 3: even the eyes, and there the lesions can kind of
Speaker 3: ulsterrate a bit more and be really quite painful. Not
Speaker 3: unlike the lesions that we see with Herpes simplex. These
Speaker 3: all cause a very similar looking lesion. And these this
Speaker 3: rash spreads anywhere and everywhere. It's pretty common that they
Speaker 3: might start on the head or face, or like centrally
Speaker 3: on the trunk, but will pretty quickly spread across the
Speaker 3: entire body and new lesions this rash essentially continues to
Speaker 3: develop over the course of three to five days, although
Speaker 3: the range can be anywhere from one to seven days,
Speaker 3: where you're continually getting more and more little pox.
Speaker 2: Oh yeah, I mean, I don't remember any of this,
Speaker 2: but sounds obnoxious.
Speaker 3: It's not great, and of course they're incredibly itchy if
Speaker 3: you don't scratch the heck out of them. Then eventually,
Speaker 3: after a few days, these vesicles kind of cloud over,
Speaker 3: so it's not like a clear fluid anymore, and then
Speaker 3: they'll encrust usually if you don't scratch them off. This
Speaker 3: will only take about a day or two per blister,
Speaker 3: kind of and once every vessel is crusted over, that's
Speaker 3: when someone is no longer infectious. So you're able to
Speaker 3: spread this disease from about two days before you got
Speaker 3: that fever and headache, so up to four days potentially
Speaker 3: before the rash, until every blister is crusted over. Now,
Speaker 3: chicken pox is generally considered a very benign childhood disease.
Speaker 3: That's why people had things like chicken pox parties because
Speaker 3: it was generally considered, you know, a pretty benign. Yes,
Speaker 3: your kid is miserable for a week, maybe, but they
Speaker 3: get over it, and most of the time that's true.
Speaker 3: Chicken pox is an annoying but self limited disease.
Speaker 2: But I knew there was a butt.
Speaker 3: If there's always a butt. There are a number of
Speaker 3: potential complications associated with veriicella, and that's before we're even
Speaker 3: going to talk about shingles. Okay, mm hmm, let's just
Speaker 3: focus on this primary infection with Varislla virus aka chicken pox. So,
Speaker 3: first of all, these lesions are itchy, itchy, itchy, itchy, itchy,
Speaker 3: and especially for kids, it's very difficult to not scratch
Speaker 3: at an inch, so this inevitably leads to open wounds
Speaker 3: all over the skin, which can lead to a very
Speaker 3: easy route for a secondary bacterial infection to establish. Our
Speaker 3: bodies are covered in bacteria, especially all over our skin,
Speaker 3: and bacteria like Strep Pyogenes and staff aureus can both
Speaker 3: invade deeper tissues and cause very serious and potentially fatal infections.
Speaker 3: So that's one probably the most common complication.
Speaker 2: Number two.
Speaker 3: Veriicella, like we've talked a lot about, is this respiratory pathogen, right,
Speaker 3: except that for most people who are infected, it doesn't
Speaker 3: actually cause any respiratory symptoms. However, it's certain can and
Speaker 3: in kids who are immuno compromised, especially, but also in
Speaker 3: older teens and adults who are exposed to veriicella for
Speaker 3: the first time, infection tends to be more severe and
Speaker 3: primary infection. This first time being exposed to varicella virus
Speaker 3: can cause a viral pneumonia which can be very severe
Speaker 3: or even fatal.
Speaker 2: Wow.
Speaker 3: Yeah, So the numbers that I saw were that of
Speaker 3: otherwise healthy seeming people who were infected with vericella. Up
Speaker 3: to sixteen percent of those people had radiographic evidence, so
Speaker 3: if you took an X ray of their chest, you
Speaker 3: saw that something was going on in their lungs. So
Speaker 3: even in people who maybe don't have respiratory symptoms, this
Speaker 3: virus is still doing stuff in their lungs. But only
Speaker 3: about a third of those would have any respiratory symptoms. Okay,
Speaker 3: but before the advent of antivirals, so before we had
Speaker 3: any kind of antiviral therapy, mortality from varicella pneumonia was
Speaker 3: as high as thirty percent, and even today with treatment,
Speaker 3: it's still around ten percent. So even though this is
Speaker 3: a small, a very small proportion of people who would
Speaker 3: go on to develop vercella pneumonia. It's pretty serious when
Speaker 3: it doesn't. Right.
Speaker 2: I feel like I have heard, you know, a lot
Speaker 2: of people be like chicken pox vaccine, Like why do
Speaker 2: we need a chicken pox vaccine? Everyone gets it, It's
Speaker 2: totally fine. And I mean I was kind of like, well,
Speaker 2: I had the chicken pox, should I have gotten the
Speaker 2: vaccine somehow? But it totally makes sense.
Speaker 3: Yeah, So I think that's one thing I hope that
Speaker 3: everyone can learn, especially in talking about all these complications
Speaker 3: of veriicella as well as shingles, which we'll get to
Speaker 3: in a little bit. Even though all of these complications
Speaker 3: are very very rare, because vericeella is such or was
Speaker 3: such a wide spread pathogen. Literally almost one hundred percent
Speaker 3: of adults in the US, for example, and in most
Speaker 3: temperate regions across the world were exposed and infected by
Speaker 3: the time they reached adulthood, almost like ninety nine percent
Speaker 3: of the population. And so when you have that large
Speaker 3: of a population that's exposed, even these small numbers like
Speaker 3: proportionally lead to pretty severe morbidity and mortality.
Speaker 2: Yeah, right, because.
Speaker 3: Again it's not just death, there's other complications. So speaking
Speaker 3: of other complications. We haven't even really talked about it,
Speaker 3: but we'll talk about it in more detail. That this
Speaker 3: is a virus that is good at infiltrating our nervous system. Right,
Speaker 3: All herpes viruses are good at kind of getting into
Speaker 3: our nervous system and lying latent. So it's not surprising
Speaker 3: then that neurologic complications are another potential serious complication of
Speaker 3: verricilla infection. Overall, the incidence of neurologic complications is low.
Speaker 3: It's estimated at about one to three per ten thousand
Speaker 3: cases have some kind of neurologic involvement, whether that's encephalitis
Speaker 3: or inflammation of the cerebellum which leads to a taxia
Speaker 3: that kind of wobbly, not being able to walk and
Speaker 3: move normally. And so it's low incidents one to three
Speaker 3: per ten thousand. But of all those neurologic cases, anywhere
Speaker 3: from five to eighteen percent of those are fatal.
Speaker 2: Wow.
Speaker 3: Yeah. And these complications how usually from encephalitis, okay, Yeah,
Speaker 3: And these complications are most common in very very young
Speaker 3: kids like under five, and then adults over age twenty,
Speaker 3: and then there's a lot of other things. This is
Speaker 3: a virus that can infect almost anyone of our cells,
Speaker 3: so it can infect the liver or the kidneys, cause
Speaker 3: liver failure kidney failure. It can infect your heart muscle
Speaker 3: and cause myocardie or pericarditis. If it infects the lining
Speaker 3: of your heart, it can lead to low platelet counts,
Speaker 3: which can lead to hemorrhage. And all of these complications
Speaker 3: are rare, but they happen, especially for children who are
Speaker 3: immunocompromised or adults who get infected for the first time
Speaker 3: who weren't exposed as children. And if that's not enough,
Speaker 3: veriicella can also cross the placenta and infect a developing fetus,
Speaker 3: So infection during pregnancy is very bad and can result
Speaker 3: in congenital vercella syndrome if it happens early in pregnancy,
Speaker 3: which can lead to neurologic development problems, limb development problems,
Speaker 3: Scarring of the skin can be pretty serious, and infection
Speaker 3: later in pregnancy can result in pneumonia in the newborn
Speaker 3: that is often fatal, Oh my gosh, as well as
Speaker 3: leading to premature delivery. It's not as benign as I
Speaker 3: think people think it is.
Speaker 2: Yeah, definitely, definitely a lot worse than I thought it was.
Speaker 3: Yeah, and all of that is just chicken pox. What
Speaker 3: about shingles?
Speaker 2: What about shingles?
Speaker 3: Okay, Shingles, like other herpes viruses like herpie simplex that
Speaker 3: we talked about, Vericella zoster is able to invade our
Speaker 3: nerve cells, hang out there and chill, just hang out
Speaker 3: in our little ganglia, not be detected by all the
Speaker 3: antibodies that we make against this virus. We make a
Speaker 3: lot of antibodies. Yeah, I want to make that clear.
Speaker 3: It's not like the people who get shingles didn't develop antibodies.
Speaker 3: They totally did. But this virus just hangs out in
Speaker 3: their nerve cell bodies, and eventually, when the time is right,
Speaker 3: this virus can travel back out again along those nerves,
Speaker 3: back up to the skin surface and cause a similar
Speaker 3: but different disease that is shingles. So, shingles starts out
Speaker 3: as a pain, most often a pain or like a
Speaker 3: burning sensation, a tingling sensation, and this nerve pain usually
Speaker 3: is along one nerve route. This is what we call
Speaker 3: a dermatome, which is the fancy word for the area
Speaker 3: of skin that your sensory nerve innervates. Like each one
Speaker 3: of your sensory nerves only innervates like one like triangle
Speaker 3: or one section of your skin, right, and so this
Speaker 3: virus you can think of it as traveling along that
Speaker 3: nerve and irritating just the skin just where that nerve is.
Speaker 2: Gotcha, Okay, that makes sense based on the spread and interesting.
Speaker 3: And then following this pain or this burning sensation, usually
Speaker 3: a few days later, blisters start to appear. These blisters
Speaker 3: look a lot like the initial blisters of chicken pox.
Speaker 3: They have like irregular red borders, these raised fluid filled vesicles,
Speaker 3: and they can be itchy, but they're often just super painful,
Speaker 3: and they're often in that same dermatome where that pain is.
Speaker 2: Yeah, I feel like, if there's one word to describe
Speaker 2: chicken pox, it's itchy, itch And if there's one word
Speaker 2: to describe shingles, it's painful.
Speaker 3: Painful. Absolutely, I agree, hundred percent. And it is possible
Speaker 3: to get lesions like away from just this one dermatome,
Speaker 3: or you could even have like multiple dermatomes involved, but
Speaker 3: most of the time it's just like one. So for
Speaker 3: example T eleven, so like you're tenth and eleventh thoracic
Speaker 3: vertebrae T ten and eleven. That dermatome goes kind of
Speaker 3: right around your belly button right, and you've got one
Speaker 3: nerve on the left and one nerve on the right,
Speaker 3: so it's usually just one or the other. So you'll
Speaker 3: get pain and a rash on one side, going wrapping
Speaker 3: around your belly, wrapping around your back to your belly,
Speaker 3: and stopping at the midline.
Speaker 2: Interesting, isn't it? I feel like that?
Speaker 1: Then?
Speaker 2: Does that make diagnosis like fairly straightforward?
Speaker 3: Yeah, if it looks like clinic classic shingles, it's a
Speaker 3: pretty classic shingles presentation. The other very classic area besides
Speaker 3: the trunk, and of course this can happen anywhere anywhere.
Speaker 3: You have nerves everywhere, but very classically it happens on
Speaker 3: the trunk or on your head because the other place
Speaker 3: that they like to hang out is the trigeminal ganglia,
Speaker 3: So that's your nerve that innervates all of the sensory
Speaker 3: of your face, and there it'll just be in like
Speaker 3: one section. So let's say it's V one that's like
Speaker 3: just the head, forehead and nose, but not probably like
Speaker 3: your cheeks and ears, and most likely just on the
Speaker 3: right side or the left side, but not both sides,
Speaker 3: and as uncomfortable as that probably sounds, shingles can be
Speaker 3: a lot more debilitating than just an uncomfortable, painful rash,
Speaker 3: especially in those who are immuno compromised or the very elderly.
Speaker 3: This rash can become quite widespread, so you could have
Speaker 3: involvement of a number of different nerves, or this reactivation
Speaker 3: can spread beyond just these nerves and cause a disseminated
Speaker 3: disease just like primary infection, just like the first time
Speaker 3: you got exposed to verisella. It can leave those nerves
Speaker 3: and go anywhere, and even in folks who aren't immunal compromised,
Speaker 3: there's a phenomenon called post herpetic neuralgia. This is when
Speaker 3: this pain, this numbness, this pain, this tingling can persist
Speaker 3: long after the rash has come and gone and result
Speaker 3: in chronic, sometimes lifelong pain.
Speaker 2: So this is like reason five hundred why the vaccine
Speaker 2: is so crucial.
Speaker 3: Yeah, So, overall of people who get shingles, I think
Speaker 3: it's about ten percent people might go on to develop
Speaker 3: post herpetic neuralgia, but in people over sixty the risk
Speaker 3: can be as high as forty to fifty percent.
Speaker 2: Now, what proportion of people get shingles.
Speaker 3: About thirty percent of people will go on to develop shingles.
Speaker 2: Okay, if you've been naturally infected, now, if.
Speaker 3: You've been now, if you've gotten chicken.
Speaker 2: Pox, right, yeah, And is there something like is it
Speaker 2: sort of like a stress type thing that triggers it
Speaker 2: or is it kind of question?
Speaker 3: Mark such a good question because my next thing I
Speaker 3: have written is like, the question is how does this
Speaker 3: virus do this? And I can't really answer that. Aaron Dang, Yeah,
Speaker 3: you know, this virus, like many other herpes viruses, can
Speaker 3: have these long latent periods. But exactly how it gets
Speaker 3: into our nerves in the first place, how it's so
Speaker 3: good at evating our immune system, what causes it to
Speaker 3: come back out? And who is going to get shingles
Speaker 3: and who isn't going to get shingles and when and why?
Speaker 3: We don't fully know. Fascinating And like I said earlier,
Speaker 3: a lot of the reason we don't is because we
Speaker 3: don't have super great animal models. So there are a
Speaker 3: number of different sort of theories and ideas out there,
Speaker 3: but we just don't fully understand these exact mechanisms. Yeah,
Speaker 3: the good news is that there is treatment. It's the
Speaker 3: same kind of treatment that we use for Herpie's simplex virus.
Speaker 3: So it's acyclavier or valley cyclavier. It's a specific drug
Speaker 3: for treating these Herpe's viruses. Yeah, it reduces the severity
Speaker 3: of symptoms and can prevent severe complications like verceilla pneumonia.
Speaker 3: But it doesn't ridge your body of the virus, just
Speaker 3: like if you use it to treat herpie simplex right, right, right,
Speaker 3: So that's the biology erin Ooh, there's a vaccine, but
Speaker 3: I'm not going to talk about it yet because I've
Speaker 3: already talked enough. So tell me what's up with this virus?
Speaker 3: Where did it come from? And what's going on?
Speaker 2: I can't wait to try to answer those. We'll take
Speaker 2: a quick break first. So you always ask where does
Speaker 2: this pathogen whatever come from? I always want to know. Well,
Speaker 2: it turns out that we've actually been down this before
Speaker 2: with our Herpes simplex one and two episode that we
Speaker 2: did last season, which was aaron that was less than
Speaker 2: a year ago. Now that was six years ago, I am,
Speaker 2: I know was before we start a podcasting.
Speaker 3: Yeah, But just.
Speaker 2: Like with every other episode, I end up forgetting so
Speaker 2: much of what we talk about, like as soon as
Speaker 2: the editing is done and the episode is released, and
Speaker 2: it's just like gone from my brain. Yeah, And so
Speaker 2: then I like come across things that I've read or
Speaker 2: I've learned before and I'm like, oh, yeah, that's right,
Speaker 2: which was absolutely the case for this episode. I hate
Speaker 2: to admit, but it's the truth. So maybe you remember
Speaker 2: from the herpes episode, but in case you don't, the
Speaker 2: group Herpes very day, which the Verricella zoster virus is
Speaker 2: part of, is very old, like millions and millions of
Speaker 2: years old group, and this group of viruses in general
Speaker 2: tends to be, like you mentioned, super species specific, meaning
Speaker 2: that a lot of the diversification events where like a
Speaker 2: new species of herpes virus emerges, those happen right alongside
Speaker 2: their host diversifying as well. So that might all be
Speaker 2: a bit of a review, but I did learn one new,
Speaker 2: very fascinating thing. So in the biology section you talked
Speaker 2: about how Vicel's ostrovirus it's a herpes virus, and like
Speaker 2: all herpes viruses, they tend to infect nervous tissue or nerves,
Speaker 2: And it turns out that that characteristic the neurotropism dates
Speaker 2: back almost five hundred million years what, uh huh, which
Speaker 2: kind of like, so that's based on how the abalone
Speaker 2: herpes virus infects nervous tissue, leading to ganglio neritis and
Speaker 2: eventual necrosis of the nervous tissue and ultimately death.
Speaker 3: I'm sorry, avaloni herpes huh. Oh my goodness, I.
Speaker 2: Know, I know it is. It's amazing. And I think
Speaker 2: that that kind of also goes a little bit towards
Speaker 2: explaining why we, like, why this is so good at
Speaker 2: evading our immune system.
Speaker 3: Yeah, it's been doing it for a literally ever forever.
Speaker 2: Yeah, And so that also gives you a sense of
Speaker 2: just how old these are. And to underline that point,
Speaker 2: I read that the alpha herpees virus group, which includes
Speaker 2: herpie simplex one HSV two and Vera Cella's oster virus,
Speaker 2: as well as other mammalian and avian viruses, that dates
Speaker 2: back to around one hundred and eighty to two hundred
Speaker 2: and ten million years ago, stop very old.
Speaker 3: Wow.
Speaker 2: And so like Herpes simplex one and two viruses, it
Speaker 2: seems reasonable then to assume that the chicken pox virus
Speaker 2: Vera Cela's oster virus, I'm gonna use those interchangeably also
Speaker 2: evolved with humans, like alongside humans, right, And that is
Speaker 2: what it was thought for a while that the vera
Speaker 2: cells oster virus originated in Africa, where modern humans evolved.
Speaker 2: This wasn't just like a passing thought, though, it wasn't
Speaker 2: just an assumption. This origin story is backed up by
Speaker 2: several pieces of evidence. First is that this would follow
Speaker 2: the trend of like all herpes viruses co evolving or
Speaker 2: cospeciating with their hosts. Second, the closest relative of varicella's
Speaker 2: ooster virus is the Simian varocell virus, which infects Old
Speaker 2: World monkeys. And so the VZV ver cells ooster virus
Speaker 2: and the Simian varicell virus they share about seventy percent identity,
Speaker 2: which is like pretty similar. And it turns out that
Speaker 2: immunization of monkeys with human vera cells oster virus prevents
Speaker 2: later infections with simian var cell virus, all right, all right,
Speaker 2: So that's like kind of I think suggestive, right. And
Speaker 2: the third piece of evidence is that some genetic dating
Speaker 2: analyzes put the evolutionary origin of veriicel disoster virus at
Speaker 2: about one hundred and ten thousand years ago. Although I
Speaker 2: also saw like older numbers mentioned a few times, like
Speaker 2: in the millions of years. In either case, it was
Speaker 2: before humans started moving out of Africa, which happened around
Speaker 2: sixty thousand years ago. All right, seems pretty straightforward, right, Yeah,
Speaker 2: maybe not so much. A recent paper from twenty twenty
Speaker 2: seems to question this assumption that the Veraceel dixoster virus,
Speaker 2: like other herpes viruses, evolved with humans in this out
Speaker 2: of Africa way. Instead, they present some evidence that places
Speaker 2: the emergence of ver cell's aster virus in Europe and
Speaker 2: also like much more recently, but their estimates were a
Speaker 2: little bit all over the place. So within vari cell's
Speaker 2: aster virus there are several clades, with virus strains in
Speaker 2: one clade more so molar to each other than to
Speaker 2: strains in other clades. Right, And these clades follow some
Speaker 2: pretty strong geographic distribution patterns. So, for instance, clade five
Speaker 2: is found pretty much only in Africa, Clade two is
Speaker 2: found mostly in Eastern Asia, and so on. And the
Speaker 2: authors of this paper then compare these different clades and
Speaker 2: then the strains within them to try to trace, Okay,
Speaker 2: when did they diverge from one another? And what is
Speaker 2: like the oldest one, like, what do we think the
Speaker 2: oldest one was, which led them to conclude that it
Speaker 2: was actually the clades found in Europe that seemed to
Speaker 2: be the oldest. I think there are though, I really
Speaker 2: want to point out a couple of important caveats to this.
Speaker 2: One is that they had very few strains from Africa
Speaker 2: that they included in the analysis, just.
Speaker 3: Like not great sampling.
Speaker 2: No, it was from a very limited geographic range, but
Speaker 2: they had tons of North American and European strains included,
Speaker 2: which of course would have biased those results. And the
Speaker 2: second thing, and the authors noted this one as well,
Speaker 2: is that it's totally possible that of all the clades
Speaker 2: of Verisola's aster virus that are present today, that they
Speaker 2: did originate in Europe, but that even older clades from
Speaker 2: Africa just went extinct, which is I think, like really
Speaker 2: fascinating to think about. We don't talk a lot about
Speaker 2: like extinction, accidental extinction of We talk about eradication, but
Speaker 2: we don't really talk about extinction of pathogens just like happenstance.
Speaker 3: Yeah, just happening, which it totally makes sense that it
Speaker 3: could happen.
Speaker 2: It totally does. And I remember when I was doing
Speaker 2: my PhD. There are like sloth ticks, and there are
Speaker 2: also like ticks that are very specific to certain animals,
Speaker 2: and they're you know, like one of the things as well.
Speaker 2: If this endangered animal goes extinct, then the ticks and
Speaker 2: everything else, and the sloth moths and everything will go
Speaker 2: extinct too.
Speaker 3: Happened with California condors. Right when they rehabilitated California condors
Speaker 3: from a very small population they lost I think it
Speaker 3: was I don't know if it was more than one
Speaker 3: species of Laos bird laos that was specific to the
Speaker 3: California condor, but at least one.
Speaker 2: Yeah, it's so it's so interesting. But yeah, So going
Speaker 2: back to Veracell's ooster virus, like there's there's really only
Speaker 2: I think this kind of just shows how there's really
Speaker 2: only so much we can tell about viral or bacterial
Speaker 2: evolution because so much of it is based on, you know,
Speaker 2: the currently circulating strains and the samples that you collect, right,
Speaker 2: And in the case of Veracell's oster virus, things might
Speaker 2: get trickier as the vaccine strain continues to become more
Speaker 2: widespread and as recombination events might happen that's kind of
Speaker 2: a question mark. I don't I don't know, all right,
Speaker 2: So I don't know if I like gave a satisfactory
Speaker 2: answer for your where did this come from? Question? There's
Speaker 2: a lot of murky origins, but I think I can
Speaker 2: at least try to answer how did we get here? Right, So,
Speaker 2: regardless of where precisely it came from, the vercella zoster
Speaker 2: virus is now globally distributed and probably has been so
Speaker 2: for a long time, like thousands of years. And this
Speaker 2: type of widespread distribution is something we've seen for a
Speaker 2: lot of the typical childhood illnesses or what we would
Speaker 2: think of as childhood illnesses, things like measles, rubella, et cetera.
Speaker 2: And in many ways it follows the same epidemic pattern
Speaker 2: two Right, you get a critical mass of susceptible individuals
Speaker 2: in a population and then boom, like one exposure, the
Speaker 2: virus just races through, especially with an r not of
Speaker 2: nine to ten. Oh my gosh.
Speaker 3: Oh mg.
Speaker 2: Yeah. But there's one key difference between chicken pox and
Speaker 2: these other childhood diseases, and that is that, unlike measles,
Speaker 2: for instance, which it needs a certain population size in
Speaker 2: order to in order for it not to go extinct,
Speaker 2: which is why like measles and these other crowd diseases
Speaker 2: took off after the agricultural revolution, chicken pox doesn't need
Speaker 2: that because aaron, because shingle, because shingles. Yes, so, because
Speaker 2: this virus, like herpies simplex virus one and two, it
Speaker 2: hangs out in US forever and it can pop up
Speaker 2: later in life as shingles slash zhauster. It has this
Speaker 2: amazing survival strategy that allows it to persist in these
Speaker 2: and even small nomadic populations rather than needing the agricultural
Speaker 2: revolution to take hold.
Speaker 3: Because if we didn't say this already, and if listeners
Speaker 3: you didn't realize this, shingles rash is absolutely contagious by contact. Yes,
Speaker 3: so the virus can persist in a population even in
Speaker 3: decades later. Mmm mm hmm.
Speaker 2: But where Varicell's oster virus is like other human herpes
Speaker 2: viruses in this way, in this sort of like latent
Speaker 2: period and then reactivation. In another sense, it's kind of
Speaker 2: an outlier alongside Herpes simplex two, I guess because of
Speaker 2: its transmission so many herpes viruses like HSV one cytomegalavirus
Speaker 2: human herpesvirus six and epstein bar virus is are often
Speaker 2: or mostly transmitted vertically within the first few years of life,
Speaker 2: often through saliva transmission, like for instance, premastication of solid
Speaker 2: food or through breast milk. But like you said, the
Speaker 2: Varicell's ooster virus doesn't follow this pattern, and it's you know,
Speaker 2: it's respiratory transmitted, which I just thought is so fascinating
Speaker 2: because instead of being vertically transmitted like so many other
Speaker 2: herpes viruses, this is still a horizontally transmitted pathogen. So
Speaker 2: from like an unrelated adult with zauster to some kid
Speaker 2: to then give them chicken pox.
Speaker 3: Yeah, and then from that kid to like ten other kids.
Speaker 2: Yeah. Yeah. Literally. So with seemingly no minimum population size
Speaker 2: and this incredibly high transmissibility, it seems like the Veraceella
Speaker 2: zoster virus would have made itself pretty well known among
Speaker 2: humans for as long as it's been around.
Speaker 3: I mean, I could see it going one of two
Speaker 3: ways here, Aaron.
Speaker 2: Okay, well, what did people say about it. It's kind
Speaker 2: of like not much, to be honest.
Speaker 3: Yeah, that was going to be my fear.
Speaker 2: Yeah yeah, it was my fear too. And then it
Speaker 2: was realized I was like, oh boy, here's the history.
Speaker 2: So the link between chicken pox and shingles wasn't really known,
Speaker 2: or at least it wasn't widely suspected until the eight
Speaker 2: eighteen hundreds, and I'll get to that later. But both
Speaker 2: diseases had been recognized long before that. So we get
Speaker 2: the first mention of chicken pox, or rather veriicella as
Speaker 2: it was first called, in the fifteen fifties, when an
Speaker 2: Italian physician named Giovanni Filipo Engracia differentiated it from scarlet fever.
Speaker 2: The first thorough description, though, came from English physician William
Speaker 2: Heberden in seventeen eighty five, and at the same time
Speaker 2: he distinguished it from smallpox. And I already went through
Speaker 2: like the etymology so veriicella as this diminutive form of
Speaker 2: the word variola. But why do we call it chicken pox?
Speaker 2: I didn't go through that etymology.
Speaker 3: Yeah, can you tell me?
Speaker 2: I mean, no, one really knows for sure, but there
Speaker 2: are plenty of guesses. One popular guess is that the
Speaker 2: bumps resembled chickpeas, and so it was called chicken pox.
Speaker 2: That was like not very well supported. Yeah, But another
Speaker 2: like more popular one is that chicken pox kind of
Speaker 2: resembles smallpox but is way less deadly and horrible, and
Speaker 2: so it was called chicken pox as like the lesser version,
Speaker 2: the small fry version of the big bad smallpox.
Speaker 3: Like you're just a chicken, yeah, pop.
Speaker 2: Yeah, I mean chicken. Chickens are cool, though, Like, I
Speaker 2: don't know why they get such a like. I wonder
Speaker 2: why the negative connotation of chicken began.
Speaker 3: It's a good question.
Speaker 2: It's a good question anyway, let us know if you know.
Speaker 2: But shingles goes even further back than chicken pox in
Speaker 2: terms of its name, So Herbie's zaster, the reactivation of
Speaker 2: the virus was named by Hippocrates from the words for
Speaker 2: to creep and girdle zoster meaning girdle, and shingles, which
Speaker 2: is the other name for this reactivation is from the
Speaker 2: Latin word singulus for belt, where it typically happened.
Speaker 3: Yeah, girdle, Yeah, very common.
Speaker 2: But I also want to mention that in Norway they
Speaker 2: had a bit more colorful or evocative description for the rash,
Speaker 2: the belt of roses from Hell, which I love. I
Speaker 2: love that. It's great. So I'm not sure exactly when
Speaker 2: the first like description of shingles was but by the
Speaker 2: eighteen sixties it's neural qualities were recognized and its focus
Speaker 2: in the dorsal root ganglion was identified.
Speaker 3: Wow, that's impressive. I know, I am.
Speaker 2: I was very surprised by that too. It was sort
Speaker 2: of like, you know, autopsies were still if you remember
Speaker 2: from our people for episode.
Speaker 3: It's just so interesting that they were able to find
Speaker 3: like I mean, they didn't know virus, right.
Speaker 2: No, they didn't know virus, but I think it was
Speaker 2: like actually physical change, like changes, right.
Speaker 3: Yeah, like the inflammation and things that you exactly starting there.
Speaker 3: So they were like, well, this is obviously the root
Speaker 3: of the route. Yeah.
Speaker 2: Wow, that's pretty that's pretty cool. It is in this period.
Speaker 2: Like so from the eighteen sixties on sort of kicked
Speaker 2: off a growth in the interest of zoster and chicken pox,
Speaker 2: which you know probably was just sort of alongside the
Speaker 2: growth of interest in all diseases that appeared to be infectious, right,
Speaker 2: And so it makes sense then, given this high interest
Speaker 2: that it was around eighteen seventy five that the transmissibility
Speaker 2: of chicken pox was first demonstrated through inoculation of human
Speaker 2: quote volunteers.
Speaker 3: Quote quote volunteers.
Speaker 2: We all know what vounteers. And then in eighteen ninety two,
Speaker 2: the link between chicken pox and zoster was first suggested
Speaker 2: after the Viennese physician Jano's von Bouke noticed that chicken
Speaker 2: pox tended to pop up in susceptible children in a
Speaker 2: household where there happened to be a zoster.
Speaker 3: Casek Hey, I was wondering how they finally made that connection, because.
Speaker 2: Yeah, I mean, it makes sense, but it was still
Speaker 2: at that point a hypothesis, right, Yeah, And it did
Speaker 2: gain a bit more support when the next year the
Speaker 2: antigens for the two diseases were shown to be similar,
Speaker 2: but it wasn't until the nineteen forties that it was
Speaker 2: finally shown that chicken pox and zauster were caused by
Speaker 2: the same virus.
Speaker 3: Wow.
Speaker 2: So I talk a lot on this podcast about germ
Speaker 2: theory and how that reshaped our concept of disease, really
Speaker 2: altering the way that people saw the world and themselves.
Speaker 2: But what I haven't really given much time to unless
Speaker 2: I'm forgetting that I've talked about it, which is entirely possible,
Speaker 2: is where viruses fit into all of this. Because microscopes
Speaker 2: and microbiology labs in the eighteen hundreds, when germ theory
Speaker 2: first really gained traction. Those allowed researchers to grow cultures
Speaker 2: primarily of like bacteria or fungi and visualize them under
Speaker 2: either the scope or in the dish, and colonies and parasites,
Speaker 2: which are another big contributor to disease, were also pretty
Speaker 2: easily seen. But where does that leave viruses? Very difficult,
Speaker 2: very difficult, And so there's this whole chunk of diseases measles, smallpox, polio,
Speaker 2: yellow fever, influenza, at chicken pox, diseases that were super prevalent,
Speaker 2: but they still lacked a tangible causative agent. You couldn't
Speaker 2: see it what was causing it. The infectiousness of these
Speaker 2: diseases could be demonstrated again mostly through these human quote volunteers,
Speaker 2: but what exactly was being transmitted remained a mystery for
Speaker 2: decades after the rise of germ theory, in part because
Speaker 2: human beings and other animals and plants are riddled with bacteria,
Speaker 2: and so it was really easy to culture bacteria from
Speaker 2: someone's sputum who was sick with like influenza and assumed
Speaker 2: that the bacteria you cultured were the responsible ones. And
Speaker 2: also in part because we lacked the technology that would
Speaker 2: let researchers actually visualize these causative agents of disease, these viruses.
Speaker 2: But that didn't stop some people from digging deeper when
Speaker 2: their proposed bacterial species failed to meet all four of
Speaker 2: cox postulates, which is what happened in the late eighteen
Speaker 2: hundreds when a disease was sweeping through tobacco farms in
Speaker 2: the Netherlands, leaving plants withered with patches of dead and
Speaker 2: living tissue. The farmers were understandably distraught about this, and
Speaker 2: so they enlisted the help of a scientist named Adolph Meyer.
Speaker 2: And Meyer couldn't find any bacteria or fungi or parasites
Speaker 2: on the disease plants that weren't on the healthy ones,
Speaker 2: but he knew there had to be something, so he
Speaker 2: injected SAP from diseased plants into healthy ones, which then
Speaker 2: also grow diseased. But the bacteria he isolated from the
Speaker 2: SAP wasn't the culprit, and so he grew frustrated and
Speaker 2: dropped the project, which was then picked up a few
Speaker 2: years later by a couple of other scientists who decided
Speaker 2: to grind up the plants and pass them through a
Speaker 2: filter that would block plant cells and bacteria and fungi
Speaker 2: and parasites, so like what was even left?
Speaker 3: Right?
Speaker 2: They then injected that fluid into healthy plants, and voila disease.
Speaker 2: So they called this contagious living fluid a virus or
Speaker 2: transmissible filterable agent, which is what the term was for
Speaker 2: a lot of these viral diseases later.
Speaker 3: On filtered transmissible agent.
Speaker 2: I love it. I love it. And then there like
Speaker 2: that is when the field of virology was born, basically
Speaker 2: what it's It just really was the first time doing
Speaker 2: this episode where I actually thought, wait a second, like
Speaker 2: we just assume we lump viruses in with bacteria and
Speaker 2: parasites and fungi as like you know, human pathogens of disease.
Speaker 2: But it took a lot longer than these other ones.
Speaker 2: It's terms of like germ theory.
Speaker 3: It's just so fascinating that they thought to do that.
Speaker 3: I know, you know, they thought, let's let's use a
Speaker 3: filter that we know is going to keep back all
Speaker 3: of the plant tissue, all of the bacteria even, and
Speaker 3: just see what's left. What an idea, I.
Speaker 2: Know, I know, it's it's amazing. It is amazing and
Speaker 2: so you know, at this time, though, like when virology
Speaker 2: was first started as a field scientist, virologists still lacked
Speaker 2: the tools to actually see what they were working with, right,
Speaker 2: But it didn't stop them from writing papers or books
Speaker 2: about these viral diseases. But in nineteen thirty one, the
Speaker 2: of the electron microscope by Ernst Ruska and Max Noll
Speaker 2: would change all of that. And also, I have to
Speaker 2: shout out X ray crystallography one of my favorite things still.
Speaker 2: Go and listen to our radiation episode. That also helped
Speaker 2: in terms of like somewhat of the structure of viruses
Speaker 2: or their composition. Okay, But anyway, so Ernst Ruska employed
Speaker 2: his brother Helmut, who was a medical doctor in his
Speaker 2: lab and had him look at some various samples under
Speaker 2: this new electron microscope. Among these samples was tobacco mosaic
Speaker 2: virus okay, and vesicle fluid from chicken pox and zoster rashes.
Speaker 2: And so a Helmut Ruska became the first person to
Speaker 2: see the varicella zoster virus and to definitively link the
Speaker 2: two diseases together.
Speaker 3: That is so cool.
Speaker 2: It's very cool to think about, like the first time
Speaker 2: seeing that yeah, oh my goodness, and the development of
Speaker 2: the electron microscope would reveal that viruses in general were
Speaker 2: not just like particles of protein, which is what had
Speaker 2: been thought, but that they had complex and varied structures,
Speaker 2: which was an enormous step forward in virology and molecular biology,
Speaker 2: and it earned the two inventors the Nobel Prize in
Speaker 2: nineteen eighty six, like a long time after yeah wow, yeah,
Speaker 2: And this Nobel Prize would not be the last one
Speaker 2: associated with veracell zoster virus, which was very surprised to
Speaker 2: learn the development of the electron microscope was a pretty
Speaker 2: incredible new tool for this already rapidly growing field of virology,
Speaker 2: and other molecular biology techniques like tissue culture made it
Speaker 2: just a matter of time really before various viruses were
Speaker 2: isolated and then characterized, and one of these, of course,
Speaker 2: was the Veracell's oster virus in nineteen fifty two, which
Speaker 2: was given its name by the virologist Thomas Weller, who
Speaker 2: Nobel Prize number two was given a Nobel Prize along
Speaker 2: with John Enders and Frederick Robbins for their viral discoveries,
Speaker 2: primarily poliovirus. That's why that name is familiar, yeah, from
Speaker 2: our vaccines episodes way back in the day. And while
Speaker 2: the Vicella zoster virus may not have been as like
Speaker 2: sexy of a thing to research as something like measles
Speaker 2: or smallpox, it still did attract a fair bit of attention.
Speaker 2: A researcher named Edgar Hope Thompson spent fifteen years, so
Speaker 2: from nineteen forty seven to nineteen sixty two, studying this
Speaker 2: virus in a small, isolated community and from this amazing
Speaker 2: data set, I imagine made a ton of really important
Speaker 2: observations about its incidents, rate, its pathogenesis, the reactivation of
Speaker 2: latent virus leading to zoster, and the role of the
Speaker 2: immune system in infection. And then Nobel Prize number three,
Speaker 2: our last Nobel Prize in nineteen seventy seven, Gertrude Elion
Speaker 2: discovered a cyclavier as an effective treatment for herpes viruses,
Speaker 2: which that Nobel Prize was awarded in nineteen eighty eight.
Speaker 3: Wow.
Speaker 2: Okay, yeah, so that's like three Nobel Prizes linked in
Speaker 2: some way to this virus which doesn't have like much
Speaker 2: of a big oh, and then it caused this pandemic
Speaker 2: in this epidemic, but still I think it's really cool
Speaker 2: because it shows just how many different fields of research
Speaker 2: are involved in understanding, like gaining and understanding about a disease. Yeah. Absolutely,
Speaker 2: But we still have one more major development in the
Speaker 2: history of Arisol's osterrovirus before I turn it back over
Speaker 2: to you, which is the vaccine.
Speaker 3: The vaccine.
Speaker 2: In the early nineteen seventies, a Japanese researcher name Michiaki
Speaker 2: Takahashi isolated a strain of the vari cell's oster virus
Speaker 2: from a three year old boy and developed a live
Speaker 2: attenuated vaccine, aka the Oka vaccine, which was after the
Speaker 2: last name of the boy. Within a few years, Maurice Hillman,
Speaker 2: if you remember that name from our Vaccines episode.
Speaker 3: Maurice, Let's hear it from Maurice.
Speaker 2: Let's hear it from Maurice. Maurice and colleagues worked on
Speaker 2: one in the US based off of this Oka strain,
Speaker 2: and in nineteen eighty four, the first v CELLA vaccines
Speaker 2: became commercially available. But this was a pretty controversial vaccine
Speaker 2: at the start, with many scientists in disagreement about the
Speaker 2: duration of immunity, whether the virus was attenuated enough, and
Speaker 2: the modeling showing that there might be an increase in shingles,
Speaker 2: which Aaron, I know you'll go into.
Speaker 3: I'm so excited to talk about it.
Speaker 2: But ultimately, study after studies showed that the vaccine was
Speaker 2: safe and was effective, and so the vaccine was introduced
Speaker 2: to Korea and Japan in nineteen eighty eight and eventually
Speaker 2: became available in the US as of nineteen ninety five.
Speaker 2: And I think it's really cool that we're doing this
Speaker 2: episode now, twenty six years after it became routine in
Speaker 2: the US, because it's probably only now that we're getting
Speaker 2: a true sense of the impact that it's had. Aaron,
Speaker 2: tell me about that impact. Where do we stand with
Speaker 2: chicken pox and shingles today?
Speaker 3: I am literally so excited. We'll take a quick break
Speaker 3: and then talk all about it. Okay, So let's just
Speaker 3: talk about vaccines, all right, because it turns out, like
Speaker 3: you kind of mentioned Aarin, there's a lot of nuance
Speaker 3: to this discussion, and I'm excited about it.
Speaker 2: I am too.
Speaker 3: So the vaccine that we use against verriceella in the US,
Speaker 3: like you mentioned Aarin, it was licensed in nineteen ninety five.
Speaker 3: Since two thousand and six, two thousand and five, two
Speaker 3: thousand and six. The recommendations in the US are for
Speaker 3: two doses, the first at age like twelve to fifteen
Speaker 3: months and the second dose at age four to six.
Speaker 3: When they first started giving this, they found it was
Speaker 3: pretty effective, but there were still a good number of
Speaker 3: like breakthrough infections, and so that is why about ten
Speaker 3: years later they added that second dose, and it's much
Speaker 3: more effective after two doses. Okay, And like you mentioned, AARIN,
Speaker 3: this vaccine is a live attenuated virus vaccine. That means
Speaker 3: it's a live, whole real virus. But even though Verceella,
Speaker 3: like wild type vercella, is benign, this virus is even
Speaker 3: more benign. It doesn't cause disease, but it does provide
Speaker 3: you with the antibodies that protect against wild type Verceella.
Speaker 3: At this point, like you said, Aarin, we have pretty
Speaker 3: good long term data that shows that in a lot
Speaker 3: of populations immunity actually is quite good up to twenty years.
Speaker 3: So amazing, it's very good immune and that's awesome. But
Speaker 3: the biggest question.
Speaker 2: There's always a butt.
Speaker 3: That's the title. The biggest question that I hear from
Speaker 3: people is if you get the vericella vaccine instead of
Speaker 3: getting chicken pox as a kid, are you more susceptible
Speaker 3: to shingles later on in life because you only got
Speaker 3: the vaccine? And I think that that idea itself is
Speaker 3: a little bit off base, and I'll talk about why,
Speaker 3: but I think that this idea came about because of
Speaker 3: these math models that you mentioned aarin. So when this
Speaker 3: veriicella vaccine was first introduced, and even before it was
Speaker 3: introduced in the US, but after it was shown to
Speaker 3: be quite effective, there were a lot of math models
Speaker 3: that suggested that by introducing this vaccine, what would happen
Speaker 3: is that we would see a huge increase, a very
Speaker 3: rapid increase in shingles in adults. Because the prevailing thought
Speaker 3: is that part of what protects you against the development
Speaker 3: of shingles is repeat exposure to veriicella in the population.
Speaker 2: Oh my gosh, that makes sense, right, right, So it's
Speaker 2: like a natural booster that, like, you're an adult, you're
Speaker 2: exposed to kids coming home with chicken.
Speaker 3: Pox, and your body's like, hey, I remember that chicken
Speaker 3: pox because the kid just breathed in your face. And
Speaker 3: then your body's like, well, I'm going to make sure
Speaker 3: to just re up my immunity and then you're less
Speaker 3: likely to get shingles.
Speaker 2: But is that? Is that how it works?
Speaker 3: So there is data that suggests that people who have
Speaker 3: frequent or have higher numbers of exposures to varicella are
Speaker 3: less likely to get shingles, And so that was the
Speaker 3: data that these math modelers used to predict this increase
Speaker 3: in shingles. And these math models had such strong data
Speaker 3: that that's part of the reason that it took quite
Speaker 3: a long time before this vaccine was introduced into childhood
Speaker 3: vaccination campaigns, well after it had been shown to be
Speaker 3: safe and effective against preventing vericella disease. So, now that
Speaker 3: this vaccine has been introduced for so long, what has
Speaker 3: happened with shingles? That's the question, right, Yeah, let's talk
Speaker 3: about it big picture since the introduction, and I'm focusing
Speaker 3: on the US because first of all, I have good data.
Speaker 3: There was a lot of studies published on the US,
Speaker 3: but also not every country, Like there's not a ton
Speaker 3: of countries that have had this as part of their
Speaker 3: regular childhood vaccine campaign for as long. So anyways, that's
Speaker 3: why a lot of this data is from the US.
Speaker 3: Since the introduction of the vaccine in the US, the
Speaker 3: cases of chicken pox vericella have declined by like ninety
Speaker 3: five to ninety seven percent. And these declines have even
Speaker 3: been seen in a adults over the age of twenty
Speaker 3: as well as in infants. And what that tells us
Speaker 3: is that not only have we prevented illness in the
Speaker 3: people who have been vaccinated, but we have in fact
Speaker 3: done what these math models predicted, which is decreased the
Speaker 3: potential for community exposure because infants under age one and
Speaker 3: anyone over twenty something likely was never vaccinated. So what's
Speaker 3: going on with shingles? Well, shingles rates have been increasing,
Speaker 3: but age specific rates of shingles were increasing before we
Speaker 3: even started any vaccination campaigns, before any of these vaccines
Speaker 3: were used widespread in the US.
Speaker 2: Well, that is fascinating, isn't it?
Speaker 3: And we don't know why since the introduction of these
Speaker 3: vaccines there haven't been any additional increases in this already
Speaker 3: increasing incidence. Like, there's no acceleration of shingles since the
Speaker 3: introduction of the vaccines.
Speaker 2: What kind of increase are we talking about?
Speaker 3: Oh gosh, I don't have good numbers on it. And
Speaker 3: the truth is, we just don't have good numbers for
Speaker 3: shingles overall, because not everyone who gets shingles is going
Speaker 3: to go to the hospital. It's not necessarily a reportable disease,
Speaker 3: et cetera, et cetera.
Speaker 2: Okay, but it's like a is it a mild slope
Speaker 2: or like a you know.
Speaker 3: Clush, it's a relatively mild slope. I will link to
Speaker 3: the paper which was published in twenty nineteen called do
Speaker 3: Varicella vaccination programs change the epidemiology of herpe' sauster? It
Speaker 3: was a really comprehensive review.
Speaker 2: Its great.
Speaker 3: So to make things even a little bit more complicated,
Speaker 3: we don't just have one vaccine. We also have vaccines
Speaker 3: against shingles.
Speaker 2: Yeah, how does that work?
Speaker 3: Yeah, so we have two different vaccines against shingles. The
Speaker 3: first came out in two thousand and six, and this one,
Speaker 3: like the vericell vaccine, was a live attenuated vaccine. But
Speaker 3: there's been a newer one that has come out in
Speaker 3: twenty seventeen, and this one is a recombinant vaccine. So
Speaker 3: it's just I think, just one of the surface proteins
Speaker 3: of veriicella, and so it's not a live virus. It
Speaker 3: doesn't replicate in you. Okay, and that one came out
Speaker 3: in twenty seventeen. But the roll out in the US
Speaker 3: especially has been very slow. There's been a lot of
Speaker 3: like backlog where people just couldn't get vaccines because there
Speaker 3: just wasn't enough supply. But in the last like five
Speaker 3: years or so, there has actually been a slight decline
Speaker 3: in the incidence of shingles. But we don't know why
Speaker 3: that is either, and it's probably not just because of
Speaker 3: these shingles vaccines.
Speaker 2: Okay, but I have a question about these vaccines because
Speaker 2: usually when we talk about vaccines, we're talking about pathogens,
Speaker 2: and with these two vaccines, we're using disease these names,
Speaker 2: even though they're both against the same virus ver cells
Speaker 2: lost virus. Yeah, I don't get it.
Speaker 3: I quite honestly also don't get it.
Speaker 2: So if you like, for the shingles vaccine, right, if
Speaker 2: you gave that to someone who has never been exposed
Speaker 2: to varro cel's lostter virus period, what would happen?
Speaker 3: You would protect them against verisella and shingles. As far
Speaker 3: as I know, I think what you're getting at is, like,
Speaker 3: what is the real difference between especially the original shingles
Speaker 3: vaccine that was developed in two thousand and six, or
Speaker 3: that was licensed in two thousand and six, that was
Speaker 3: a live attenuated vaccine. What's the difference between that vaccine
Speaker 3: and the vericeella vaccine that we give to kids. Yeah,
Speaker 3: probably not much, right, It's just who do we give
Speaker 3: it to, Who was it tested on, and who do
Speaker 3: we give it to and why. The data that we
Speaker 3: have so far, what they tell us about these new,
Speaker 3: relatively new vericella vaccines, the ones that we give to kids.
Speaker 3: Somebody who gets vaccinated with this vericella vaccine is far
Speaker 3: less likely to develop shingles in their lifetime than someone
Speaker 3: who gets chicken pox naturally as a kid. So we've
Speaker 3: seen this in vaccinated cohorts compared to unvaccinated years previous,
Speaker 3: that the vercella vaccine strain is less likely to develop
Speaker 3: this latent infection and reactivate into shingles. So giving someone
Speaker 3: as a child the vercella vaccine is protective against both
Speaker 3: chicken pox and shingles. That much we know, and it
Speaker 3: does not appear. In the almost thirty years now twenty
Speaker 3: five plus years that this vaccine has been in use
Speaker 3: in the un giving this vaccine to children has not
Speaker 3: increased the incidence of shingles in the adult population, like
Speaker 3: the math models predicted.
Speaker 2: Right, So what are the recommendations like for shingles vaccination
Speaker 2: right now?
Speaker 3: In the US, the newer shingles vaccine has been shown
Speaker 3: to be a lot more effective than the older one.
Speaker 3: So the recommendation is that starting at age fifty. At
Speaker 3: age fifty is when you get it. It's a two
Speaker 3: dose series and I don't know if there's data on
Speaker 3: whether or not you need boosters after that. Right now,
Speaker 3: it's a two dose series starting at age fifty. Yeah,
Speaker 3: but that's just in the US. Vaccine uptake for veriicella
Speaker 3: across the world is pretty spotty, But there are a
Speaker 3: number of different papers that really highlight just how big
Speaker 3: of an impact vaccination campaigns child like adding vericella to
Speaker 3: the childhood vaccination campaigns can really have have on a population,
Speaker 3: and that is chicken pox and shingles.
Speaker 2: Wow, it was interesting.
Speaker 3: Good right, I think it's a good episode.
Speaker 2: I think so too. Well. Should we wrap up the
Speaker 2: way we.
Speaker 3: Usually do with our sources?
Speaker 2: Absolutely, So I'll shout out just a few papers I
Speaker 2: have more, but by Gross from twenty twelve, Pangaea and
Speaker 2: the out of Africa model of veri Cela's aster virus
Speaker 2: evolution and philogeography, and then also by Oaklander from nineteen
Speaker 2: ninety nine the pathology of shingles head in Campbell's nineteen
Speaker 2: hundred monograph, and another one Pontremoli at All from twenty
Speaker 2: twenty possible European origin of circulating Vericela's aster virus strains.
Speaker 2: And I have more and I will post more on
Speaker 2: our website This podcast will kill You dot Com.
Speaker 3: Yeah, I mentioned a couple of my sources already. I
Speaker 3: have a lot more as well as those two papers
Speaker 3: I already mentioned, one by dol and DaCosta in the
Speaker 3: American Journal of Bioethics and the other by Harpause that
Speaker 3: was about the epidemiology of herpexhauster. Check them out on
Speaker 3: our website This podcast will kill You dot Com.
Speaker 2: Thank you again so much for sharing your first hand
Speaker 2: account with us. We really appreciate it.
Speaker 3: Thank you. Thank you also to Bloodmobile for providing the
Speaker 3: music for this episode and every one of our episodes.
Speaker 2: And thank you to the Exactly Right Network, of whom
Speaker 2: we are a very proud member.
Speaker 3: Thank you to all of you listeners, and thank you
Speaker 3: especially to our patrons. We love all of you so
Speaker 3: very much. Yeah, thanks for listening.
Speaker 2: We hope you liked this episode. Well, until next time,
Speaker 2: wash your hands.
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Speaker 2: Oh ba.
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