This Podcast Will Kill You - Ep 76 Chickenpox: There's always a 'but'

Episode Date: June 29, 2021

Ah, chickenpox, that pesky old childhood illness. And that’s all it is, right? Just a mild, routine infection that we all used to catch until the vaccine came around? Not quite. In this episode, we learn that, when it comes to the varicella-zoster virus, not everything is as it seems. We explore the complex nature of this virus, how it can make you kinda sick and then how it can make you really, really sick. After that, we dive into the evolutionary origins of this virus and the different infections it causes (spoiler alert: shingles as a viral survival strategy?!). And finally we trace its human history from discovery to vaccine to where we stand with chickenpox and shingles today. See omnystudio.com/listener for privacy information.

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and it just was like a not scratchable itch. It was all day, all day, all day. But I thought like at first I was like, oh, it's just hat day. Like I'm just not comfortable wearing this ridiculous Christmas tree hat at school. By the weekend, so that like started midweek. By that weekend, it had started to move down my forehead to like my eyebrow area. And that's when it just became this burning. itchy, couldn't really make it go away thing.

A few days went by, and so this was all at Christmas time. That's when we were driving from where we live in Buffalo down to my parents on Long Island. And that drive, my forehead felt like someone had a match to it. I think I kind of lucked out with shingles because it was a really small patch that I had. had, but it just feel like someone had a lighter on my forehead for as long as it did was just the craziest thing. I had no idea what it was, though. So I started doing like the WebMD thing. And I was searching for like, what's a large red spot, red spot with blisters? Because it started to get these really small spots over time. And that's kind of when I started to see.

other pictures of people who had this same thing and people were saying it shingles, it shingles, it shingles. So I finally called my doctor and I said, hey, I have all these symptoms, but like I don't know what this is. And they said, that sounds like shingles. You need to get to, you need to come see us right away. But we were traveling for Christmas. By the time I kind of got all that together, we were already en route from Long Island up to Rhode Island. the weekend. So that's when I ended up at a out of state urgent care. And I walked in, the receptionist looked at me and she's like, oh, look at that, you have shingles. And it was just as fast. And then as soon as they saw that they were able to prescribe medication and get it

under wraps. So by the time I got that, they were like, it's probably too late because it had been a week since I started showing the first symptom. But the really scary thing that they kept sounding the alarm on was, this is really close to your eye. This is really close to your eye. So when I came home, I had follow-ups with my eye doctors. I had to go back to my primary care just to continue watching it to make sure that whatever it was wasn't going to affect the optical nerves and all of those forehead things. But like I said, it was just the craziest thing because I didn't know anybody who had ever had it. I didn't know, like, was I going to pass this on to my mom? Was my sister going to get it? I think everybody here is you get shingles from chicken pox.

And of my generation, like, I think I was the end of like the chicken pox party. So I was just so afraid that like I was going to pass this on to all of my family members and they were just kind of like, no, you're, everything's going to be fine. Like, just kind of cover it up and, um, go about your day. So that was my, that was my shingles experience, I guess. Thank you so much for taking the time to chat with us and for being willing to share your story. Thanks. Hi, I'm Aaron Welsh. And I'm Aaron Olman Updike. And this is this podcast. will kill you. Welcome. Welcome. This is a fun one. I'm honestly thrilled. I don't know, I don't know exactly why, but I have been looking forward to covering this for a really long time.

I have too, and I've been kind of like daunted because I don't, I didn't know anything about the history. And it turns out there's like kind of not that much to it. So I hope you don't fall asleep. I'm sure. Or if you're listening to this podcast to fall asleep, I hope you do fall asleep. But yeah, I think it's like, it's one of, like, we all have experienced it or know someone that's experienced it. And I think, Aaron, you and I are part of the generation, like the last remnants that didn't get the vaccine. Exactly. We definitely are the last cohort that just got chickenpox, which is the subject of today's

episode. There we go. Plus shingles slash zoster, whatever you want to call it. Exactly. Yeah. Basically the varicel zoster virus. Yeah. Aaron, when did you get chickenpox? I don't remember exactly how old I was, but it had to have been after 1994 or five. And we all four got it in a row. It went boop, boop, boop, boom, boom, like down the row of older brother than me, then my younger brother, than the baby brother. We all got it in age order. And I have a very distinct memory of my first pock. Oh. I had my very first chicken pock was on my left side, like right on my ribs on my left side.

And obviously, like, my brother was already sick with it. So I knew this is chicken pox. And I showed my mom and I was like, mom, I found this is this chicken pox? And she was like, ugh, yes, it's chicken pox. And I was like, okay, but can I still go to gymnastics? Did you go? I did. As far as I can remember, maybe my memory is off, but my mom was like, you've already exposed everyone.

Just keep it covered. That's hilarious. She might dispute that memory of it. We'll see. Mom? Is that what happened? That's how I remember it. I have the scar that I know that was my first pot.

I really should have called my mom to ask her my chicken pox story because I don't remember, and I don't even know if I, I think I might have been too young, like, to actually remember, but I think it was my older sister and I at the same time got it. And then my two younger brothers got it. And then I honestly don't know about my younger sister, whether she got it or whether she got vaccine. Yeah. Yeah. Anyway, should we should we move on to like actual podcast? The actual business of our podcast, maybe. Is it quarantini time? I think it's definitely quarantine time. What are we drinking this week?

Erin, we're drinking chicken scratch. I love this. It works on so many levels. It's like people always complain about how doctors have chicken scratch handwriting. It's true. And also a few chicken pox, you're definitely going to be scratching. It's really itchy. Yeah.

And what's in a chicken scratch? There is tequila. There is kiwi. There is ginger and there is mint. Kind of just a fun summary bev. Yeah. We'll post the full recipe for that quarantini as well as our non-alcoholic plissy barita on our website. This podcast will kill you.com and our social media.

And on our website, you can find so many different things like transcripts, like alcohol-free episodes, like promo codes for all of the ads that we do, like the links to Bloodmobile, who does the music for all of our episodes. We've also got a Patreon. I mean, it's endless. Just go in there, explore it. And I'm sure you'll come up with something interesting. Definitely. All right. That was a longer intro than we usually do.

Yeah, it was. It was. It was fun, it was. It's fun getting to relive my chicken box story. Anyways. Should we dive into the biology of this thing? Let's do it. We'll take a quick break first. Dinner shows up every night, whether you're

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That's Q-U-I-N-C-E.com slash this podcast to get free shipping and 365-day returns. Quince.com slash this podcast. Veracela Zoster, or herpes zoster, or if you want to be very official, human alpha herpes virus three. So this virus that we're dealing with is a herpes virus, which I think, Some people might not realize because it's called chicken pox. People might think it's a pox virus. It's a herpes virus.

And in fact, it's very closely related to herpes simplex one, which is a common cause of oral herpes. Can also cause genital herpes. Check out our herpes virus episode for more on that. And so like all of the herpes viruses, this is a DNA virus. It has a double-stranded genome, blah, blah, blah. Like many of the human herpes viruses, this is a very human-specific virus. It doesn't infect any other animals, which, as we'll see, is part of why we don't have a lot of answers about some of the specifics of the diseases that this virus causes, because we don't have great animal models in which to study it. That makes sense, yeah.

Yeah. This particular virus doesn't have a lot of variability. There aren't a lot of different strains of varicella. There doesn't seem to be a lot of variation in the virulence across outbreaks or over time. It's a pretty stable virus. And, Erin, you asked me something before we started researching this, which is why is chickenpox often called varicella zoster and shingles is called herpes zoster? Yeah. Did you find an answer to that?

Well, so the only thing I can think of is the etymology of it. So varicella is another word for chicken pox, like that rash that happens for that initial infection. And in a lot of other languages, besides English, it tends to be not like the equivalent of chicken pox, but some sort of variation of varicela. And the word varicela might come from like the diminutive form of variola, which is the word for smallpox. And so, you know, So it might just be like, you know, it's analogous where chickenpox is to smallpox as varicella is to variola. Etymologically. Does that make sense? Yeah, it totally makes sense. No, I genuinely make sense. And then herpes zoster.

Herpes comes from, herpes is like the old, you know, word that was used by ancient Greeks, like Hippocrates and whatnot to describe those rashes. So it seems to just boil down to the fact that even though. we're talking about one single pathogen. We're talking about two completely different clinical diseases. Exactly. Yeah. So I think that that's something that's interesting. I feel like we've covered a lot of pathogens that just cause like one disease where we're like, here's the disease we're talking about and here's the pathogen that causes it. And then we've talked about some things like Staph aureas, for example, that can cause any number of diseases.

Yeah. Or strep pyogenes. Exactly, right? So, yeah, I don't know. I just feel like that's an interesting aspect of this, that there's this big distinction between the pathogen and the diseases or the illnesses that they might cause. Yeah. So let's get into the pathogen and both of these diseases, shall we? Let's do it. So I talked about how similar already this human herpes virus. to other herpes viruses. Let's start to talk about how it's a little different. Unlike many other

herpes viruses, varicella is transmitted primarily via the respiratory route. What? Yeah. Isn't that interesting? I want to know, and I didn't find the evolutionary history. Like, what about it? How did that happen? It's a really good question that I still don't fully understand. Aside from the fact that we've talked on this podcast a number of times about the tropism of different viruses, right? So viruses, because they are dependent on host cells to be able to replicate, oftentimes specific viruses can only infect a limited range of cell types. It seems like varicella can infect a pretty wide range of cell types. So is it just that that's a really easy route of transmission?

and it happens to be good at invading and replicating within not just our respiratory epithelium, but also it's very good at invading and replicating in our white blood cells in lymph nodes. And so a big thing where it replicates is in the lymph nodes in our chest and things like that. Oh, that's very interesting. Because I thought that like it also though does have a tropism towards nerves, or is that just later? Oh, certainly. Certainly. Let's get into all of this, shall we? Basically, I think the bottom line is that it can infect all of those cell types.

Interesting. Okay. Cool. Yeah. All right. But primarily, the way that people become exposed is via respiratory. So a kid, because it's usually kids who are infected, comes up and it's like, I don't feel good, and then breathes right on your face, and you inhale those viral particles. particles. They, you speak from experience. I guess I do. And they travel, those viral particles travel to those regional lymph nodes and they replicate. And what's really important about the fact that they can infect these white blood cells is from there they can travel anywhere and everywhere, right? So they travel throughout our body and they're able to continue replicating as they invade different cells. In general, the incubation period is about to,

weeks. It can be from 10 to 20 days after exposure to when you first start to show symptoms. But what's important, especially for a respiratory virus, is that you become infectious and able to infect others at least two days before those first symptoms start. Aha. And this is quite an infectious pathogen. It's pretty contagious. I've seen anywhere from 60 to 90% of susceptible household contacts are likely to become infected. What is the estimated R-Not? According to a lecture from Johns Hopkins School of Public Health, the R-Not for Chicken Pox is 9 to 10.

Oh. That's a lot higher than I realized. Goodness. So when you say respiratory transmission, is it respiratory droplets or is it like aerosol, like airborne? Good question. I didn't find the specific answer to that. They just say respiratory route.

So I don't know how long it can hang out in the air. I don't think that it's quite as bad as something like measles that can stay airborne for like hours at a time. But with an attack rate that's so high, I would guess that it's probably pretty well airborne. Like it's aerosolizing pretty well. Okay. So those chickenpox parties that people used to have, those are probably pretty effective at spreading disease. Oh, yes. Not a good idea. Let's talk about why. Shall we? Let's do it. So once this virus has disseminated throughout our body, one of the main cells that they tend to infect are our epidermal cells, our skin cells. Inside of our skin cells, it begins to replicate, and this is what causes the typical chickenpox rash that we all know and don't love. So what's really common is that one to two days, like 24 to 48 hours before this rash, kids, I say kids, of course this affects adults too, but most often kids will have, like they'll feel kind of cruddy for a day or so beforehand.

Maybe a headache, maybe a little tummy ache, maybe like a fever probably. But then comes the rash, which is very characteristic and kind of what we call chicken pox. The rash starts, for anyone who hasn't experienced this, starts as very, very itchy, red, flat patches. And then these patches become raised or get little bumps within them. And then those little bumps develop into small, fluid-filled vesicles, tiny little blisters. And these tiny little blisters are chock full of virus. So this is not only a respiratory pathogen, but it can also be transmitted by direct. contact. Okay. It's just covering all the bases. It's covering all the bases. Exactly.

This rash can also be present on mucous membranes, like in the mouth or even the eyes. And there, the lesions can kind of ulcerate a bit more and be really quite painful, not unlike the lesions that we see with herpes simplex. These all cause a very similar looking lesion. And this rash spreads anywhere and everywhere. It's pretty cool. common that they might start on the head or face or like centrally on the trunk, but will pretty quickly spread across the entire body. And new lesions, this rash essentially continues to develop over the course of three to five days, although the range can be anywhere from one to seven days where you're continually getting more and more little pox. Oh, yeah. I mean, I don't remember

any of this, but sounds obnoxious. It's not great. And of course, they're incredibly itchy. If you don't scratch the heck out of them, then eventually, after a few days, these vesicles kind of cloud over, so it's not like a clear fluid anymore. And then they'll encrust. Usually, if you don't scratch them off, this will only take about a day or two per blister, kind of. And once every vesicle is crusted over, that's when someone is no longer infectious.

So you're able to spread this disease from about two days before you got that fever and headache, so up to four days potentially before the rash, until every blister is crusted over. Now, chickenpox is generally considered a very benign childhood disease. That's why people had things like chickenpox parties, because it was generally considered, you know, a pretty benign. yes, your kid is miserable for a week maybe, but they get over it. And most of the time, that's true. Chickenpox is an annoying but self-limited disease. But I knew there was a butt. There's always a butt. There are a number of potential complications associated with Veracella.

And that's before we're even going to talk about shingles. Okay. Let's just focus on this primary infection with varicella virus, aka chickenpox. So first of all, these lesions are itchy, itchy, itchy, itchy. And especially for kids, it's very difficult to not scratch at an itch. So this inevitably leads to open wounds all over the skin, which can lead to a very easy route for a secondary bacterial infection to establish. Yeah. Our bodies are covered in bacteria, especially all over our skin.

and bacteria like strep pyogenes and staphoreus can both invade deeper tissues and cause very serious and potentially fatal infections. So that's one, probably the most common complication. Number two, varicella, like we've talked a lot about, is this respiratory pathogen, right? Except that for most people who are infected, it doesn't actually cause any respiratory symptoms. However, it certainly can. And in kids who are immunocompromised especially, but also in older teens and adults who are exposed to varicella for the first time, infection tends to be more severe. And primary infection, this first time being exposed to varicella virus, can cause a viral pneumonia,

which can be very severe or even fatal. Wow. Yeah. So the numbers that I saw were that of otherwise healthy seeming people who were infected with varicella, up to 16% of those people had radiographic evidence. So if you took an x-ray of their chest, you saw that something was going on in their lungs. So even in people who maybe don't have respiratory symptoms, this virus is still doing stuff in their lungs. but only about a third of those would have any respiratory symptoms. Okay.

But before the advent of antivirals, so before we had any kind of antiviral therapy, mortality from varicella pneumonia was as high as 30%. And even today with treatment, it's still around 10%. So even though this is a small, a very small proportion of people who would go on to develop varicella pneumonia, it's pretty serious when it does occur. Right. I feel like I have heard, you know, a lot of people be like, chickenpox vaccine. Like, why do we need a chicken pox vaccine? Everyone gets it. It's totally fine. And I mean, I was kind of like, well, I had the chicken pox. Should I have gotten a vaccine somehow? But it totally makes sense. Yeah. So I think that's one

thing I hope that everyone can learn, especially in talking about all these complications of varicella, as well as shingles, which we'll get to in a little bit. Even though all of these complications are very, very rare, because varicella is such or was such a widespread pathogen, literally almost 100% of adults in the U.S., for example, and in most temperate regions across the world, were exposed and infected by the time they reached adulthood, almost like 99% of the population. And so when you have that large of a population that's exposed, even these small numbers like proportionally lead to pretty severe morbidity and mortality.

Yeah, right. Because again, it's not just death. There's other complications. So speaking of other complications, we haven't even really talked about it, but we'll talk about it in more detail, that this is a virus that is good at infiltrating our nervous system, right? all herpes viruses are good at kind of getting into our nervous system and lying latent. So it's not surprising then that neurologic complications are another potential serious complication of varicella infection. Overall, the incidence of neurologic complications is low.

It's estimated at about 1 to 3 per 10,000 cases have some kind of neurologic involvement, whether that's encephalitis, or inflammation of the cerebellum, which leads to ataxia, that kind of wobbly not being able to walk and move normally. And so it's low incidence, one to three per 10,000, but of all those neurologic cases, anywhere from 5 to 18% of those are fatal. Wow. Yeah. And these complications...

How? Usually from encephalitis. Okay. Yeah. And these complications are most common. in very, very young kids, like under five, and then adults over age 20. And then there's a lot of other things. This is a virus that can infect almost any one of our cells,

so it can infect the liver or the kidneys cause liver failure, kidney failure. It can infect your heart muscle and cause myocarditis or paracarditis if it infects the lining of your heart. It can lead to low platelet counts, which can lead to hemorrhage. And all of these complications are rare, but they happen, especially for children who are immunocompromised or adults who get infected for the first time who weren't exposed as children. And if that's not enough, varicella can also cross the placenta and infect a developing fetus. So infection during pregnancy is very bad and can result in congenital varicella syndrome if it happens early in pregnancy,

which can lead to neurologic development problems, limb development problems, scarring of the skin can be pretty serious. And infection later in pregnancy can result in pneumonia in the newborn that is often fatal. Oh my gosh. As well as leading to like premature delivery. It's, it's not as benign as I think people think it is. Yeah, definitely, definitely a lot worse than I thought it was. Yeah. And all of that is just chicken pox. What about shingles? What about shingles? Okay, shingles. Like other herpes viruses, like herpes simplex that we talked about, varicella zoster, is able to invade our nerve cells, hang out there, and chill. Just hang out in our little ganglia, not be detected by all the antibodies that we make against this virus.

We make a lot of antibodies. Yeah. I want to make that clear. It's not like the people who get shingles didn't develop antibodies. They totally did. But this virus just hangs out in their nerve cell bodies. And eventually, when the time is right, this virus can travel back out again along those nerves, back up to the skin surface, and cause a similar but different disease. that is shingles. So shingles starts out as a pain most often, a pain or like a burning sensation,

a tingling sensation. And this nerve pain usually is along one nerve route. This is what we call a dermatome, which is the fancy word for the area of skin that your sensory nerve innervates. Like each one of your sensory nerves only innervates like one like triangle or one section of your skin, right? Mm-hmm. Yeah. And so this virus, you can think of it as traveling along that nerve and irritating just the skin, just where that nerve is. Gotcha. Okay.

That makes sense based on the spread. Interesting. And then following this pain or this burning sensation, usually a few days later, blisters start to appear. these blisters look a lot like the initial blisters of chicken pox. They have like irregular red borders, these raised fluid-filled vesicles. And they can be itchy, but they're often just super painful. And they're often in that same dermatome where that pain is. Yeah, I feel like if there's one word to describe chickenpox, it's itchy. And if there's one word to describe shingles, it's painful. painful. Absolutely. I agree 100%. And it is possible to get lesions like away from just this one

dermatome or you could even have like multiple dermatomes involved. But most of the time it's just like one. So for example, T-11, so like your 10th and 11th thoracic vertebrae, T-10 and 11, that dermatome goes kind of right around your belly button. And you've got one nerve on the left and one nerve on the right. So it's usually just one or the other. So you'll get pain and a rash on one side going wrapping around your belly, wrapping around your back to your belly and stopping at the midline. Interesting. Isn't it?

I feel like that then does that make diagnosis like fairly straightforward? Yeah. If it looks like kind of classic shingles, it's a pretty classic shingles presentation. The other very classic area besides the trunk. And of course, this can happen anywhere. You have nerves everywhere. But very classically, it happens on the trunk or on your head because the other place that they like to hang out is the trigeminal ganglia.

So that's your nerve that innervates all of the sensory of your face. And there it'll just be in like one section. So let's say it's V1. That's like just the head, forehead, and nose, but not probably like your cheeks and ears and most likely just on the right side or the left side but not both sides. And as uncomfortable as that probably sounds, shingles can be a lot more debilitating than just an uncomfortable, painful rash. Especially in those who are immunocompromised or the very elderly, this rash can become quite widespread so you can have involvement of a number of different nerves. Or this

reactivation can spread beyond just these nerves and cause a disseminated disease just like primary infection, just like the first time you got exposed to varicella. It can leave those nerves and go anywhere. And even in folks who aren't immunocompromised, there's a phenomenon called post-herpetic neuralgia. This is when this pain, this numbness, this pain, this tingling can persist long after the rash has come and gone and result in chronic, sometimes lifelong pain. So this is like reason 500 why the vaccine is so crucial. Yeah. So overall, of people who get shingles, I think it's about 10% of people might go on to develop post-trapetic neuralgia, but in people over 60, the risk can be as high as 40 to 50%. Now, what proportion of people get shingles? About 30% of people will go on

to develop shingles. Okay. If you've been naturally infected, not... If you've been, if you've gotten chicken pox. Right. Yeah. And is there something like, is it sort of like a stress type thing that triggers it or is it kind of question mark? Such a good question because my next thing I have written is like the question is how does this virus do this? And I can't really answer that, Aaron. Dang. Yeah. You know, this virus like many other herpes viruses can have these long latent periods. But exactly how it gets into our nerves in the first place, how it's so good at evading our immune system, what causes it to come back out and who is going to get shingles and who isn't going to get shingles and when and why? We don't fully know. Fascinating. And like I said

earlier, a lot of the reason we don't is because we don't have super great animal models. So there are a number of different sort of theories and ideas out there, but we just don't fully understand these exact mechanisms. Yeah. The good news is that there is treatment. It's the same kind of treatment that we use for herpes simplex virus. So it's acyclovir or vali cyclovier. It's a specific drug for treating these herpes viruses.

Yeah. Yeah. It reduces the severity of symptoms and can prevent severe complications like varicella pneumonia, but it doesn't rid your body of the virus just like if you use it to treat herpesy simplex. Right. Right. Right. So that's the biology, Aaron. Ooh. There's a vaccine, but I'm not going to talk about it yet because I've already talked enough. So tell me what's up with this virus, where did it come from, and what's going on? I can't wait to try to answer those. We'll take a quick break first. Anyone who works long hours knows the routine. Wash, sanitize, repeat. By the end of the day, your hands feel like they've been through something. That's why O'Keeffe's working hands hand cream is such a relief. It's a concentrated hand cream that is specifically designed to relieve extremely

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I always want to know. Well, it turns out that we've actually been down this road before with our Herpes Symplex one and two episode that we did last season, which was Erin, that was less than a year ago. No-uh, that was six years ago. I know. I know. It was before we started podcasting. Yeah.

But just like with every other episode, I end up forgetting so much of what we talk about. like as soon as the editing is done and the episode is released and it's just like gone from my brain. Yeah. And so then I like come across things that I've read or I've learned before and I'm like, oh yeah, that's right. Which was absolutely the case for this episode. I hate to admit, but it's the truth. So maybe you remember from the herpes episode, but in case you don't, the group Herpes Veriday, which the varicella zoster virus is part of, is very old.

like millions and millions of years old group. And this group of viruses in general tends to be, like you mentioned, super species specific, meaning that a lot of the diversification events where like a new species of herpes virus emerges, those happen right alongside their host diversifying as well. So that might all be a bit of a review, but I did learn one new, very fascinating thing. So in the biology section, you talked about how varicels ostra virus, it's a herpes virus, and like all herpes viruses, they tend to infect nervous tissue or nerves. And it turns out that that characteristic, the neurotropism, dates back almost 500 million years. What?

Uh-huh. Which kind of like, so that's based on how the abalone herpes virus infects nervous. tissue leading to ganglionuritis and eventual necrosis of the nervous tissue and ultimately death. I'm sorry. Uh-huh. Oh my goodness. I know. I know.

It is, it's amazing. And I think that that kind of also goes a little bit towards explaining why we, like, why this is so good at evading our immune system. Yeah, it's been doing it for literally ever. Forever. Yeah. And so that also gives you a sense of just how old. old these are. And to underline that point, I read that the alpha herpes virus group, which

includes herpes simplex 1, HSV2, and varicellusoster virus, as well as other mammalian and avian viruses, that dates back to around 180 to 210 million years ago. Stop. Very old. Wow. And so like herpes simplex 1 and 2 viruses, it seems reasonable then to assume that the chickenpox virus, varisal zoster virus, I'm going to use those interchangeably, also evolved with humans, like alongside humans. Right. And that is what was thought for a while that the varicel zoster virus originated in Africa where modern humans evolved. This wasn't just like a passing thought, though. It wasn't just an assumption. This origin story is backed up by several pieces of evidence. First is that this would follow the trend of like all herpes viruses co-evolving or co-speciating with their hosts.

Second, the closest relative of varicellososter virus is the simian varicellavirus, which infects old world monkeys. And so the VZV, varisselzoster virus and the simian varissel virus, they share about 70% identity, which is like pretty similar. and it turns out that immunization of monkeys with human varisole azoster virus prevents later infections with simian varissel virus. All right, all right. So that's like kind of, I think, suggestive, right? And the third piece of evidence is that some genetic dating analyses put the evolutionary origin of varissela zoster virus at about 110,000 years ago, although I also saw like older numbers,

mentioned a few times, like in the millions of years. In either case, it was before humans started moving out of Africa, which happened around 60,000 years ago. All right. Seems pretty straightforward, right? Yeah. Maybe not so much. A recent paper from 2020 seems to question this assumption that the varicelidoster virus, like other herpes viruses, evolved with humans in this out-of-Africa way. Instead, they present some evidence. that places the emergence of varisela's oster virus in Europe and also like much more recently. Huh. But their estimates were a little bit all over the place.

So within varissel's astrobiirus, there are several clades with virus strains in one clade more similar to each other than to strains in other clades, right? And these clades follow some pretty strong geographic distribution patterns. So, for instance, clade five is found pretty much. only in Africa. Claytooth is found mostly in Eastern Asia and so on. And the authors of this paper then compare these different clades and then the strains within them to try to trace, okay, when did they diverge from one another and what is like the oldest one? Like what do we think the oldest one was? Which led them to conclude that it was actually the clades found in Europe

that seemed to be the oldest. I think there are though, I really want to point out a couple of important caveats to this. One is that they had very few strains from Africa that they included in the analysis. Just like not great sampling. No, it was like from a very limited geographic range, but they had tons of North American and European strains included, which of course would have biased those results. And the second thing, and the authors noted this one as well, is that it's totally possible that of all the clades of varisol'soster virus that are present, today that they did originate in Europe, but that even older clades from Africa just went extinct. Which is, I think, like, really fascinating to think about. We don't talk a lot about, like,

extinction, accidental extinction of, we talk about eradication, but we don't really talk about extinction of pathogens just like happenstance. Yeah, just happening, which it totally makes sense that it could happen. It totally does. And I remember, when I was doing my PhD, there are like sloth ticks, and there are also like ticks that are very specific to certain animals. And they're, you know, like one of the things is, well, if this endangered animal goes extinct, then the ticks and everything else and the sloth moths and everything will go extinct too. That happened with California condors. Right. When they rehabilitated California condors from a very small population, they lost, I think it was, I don't know if it was more than one

species of louse, bird louse that was specific to the California condor, but at least one. Yeah. It's so, it's so interesting. But yeah, so going back to varicel's ostracurvirus, like there's really only, I think this kind of just shows how there's really only so much we can tell about viral or bacterial evolution, because so much of it is based on, you know, the currently circulating strains and the samples that you collect. Right. And in the case of Ferris cell as oster virus, things might get trickier as the vaccine strain continues to become more widespread and as recombination events might happen. That's kind of a question mark. I don't know. All right. So I don't know if I like gave a satisfactory answer for your where did this come from

question. It's a lot of murky origins. But I think I can at least try to answer how did we get here, right? So regardless of where precisely it came from, the varicella zoster virus is now globally distributed and probably has been so for a long time, like thousands of years. And this type of widespread distribution is something we've seen for a lot of the typical childhood illnesses or what we would think of as childhood illnesses, things like measles, rubella, etc. And in many ways, it follows the same epidemic pattern too, right? You get a critical mass of susceptible individuals in a population, and then boom, like one exposure, the virus just races through, especially with an R-not of 9 to 10. Oh, my gosh.

Oh, m-G. Yeah. But there's one key difference between chickenpox and these other childhood diseases, and that is that unlike measles, for instance, which needs a certain population size in order to, in order for it not to go extinct, which is why, like, measles and these other crowd diseases took off after the agricultural revolution, chickenpox doesn't need that because, Erin? Because shingles.

Because shingles. Yes. So because this virus, like herpes simplex virus one and two, it hangs out in us forever and it can pop up later in life as shingles slash zoster, it has this amazing survival strategy that allows it to persist in even small nomadic populations rather than needing the agricultural revolution to take hold. Because if we didn't say this already and if listeners you didn't realize this, shingles rash is absolutely contagious by contact. Yes. So the virus can persist in a population even decades later. Mm-hmm. Mm-hmm. But, but,

where varicellosostrovirus is like other human herpes viruses in this way, in this sort of like latent period and then reactivation, in another sense, it's kind of an outlier, alongside herpes simplex, too, I guess, because of its transmission. So many herpes viruses, like HSV-1, cytomegalovirus, human herpes virus six, and Epstein-Barr virus, these are often or mostly transmitted vertically within the first few years of life, often through saliva transmission, like, for instance, pre-mastication of solid food or through breast milk. But like you said, the varicelzeal-osloster virus doesn't follow this pattern. And it's, you know, it's respiratory transmitted, which I just thought is so fascinating, because instead of being vertically transmitted like so many other herpes viruses,

this is still a horizontally transmitted pathogen. So from like an unrelated adult with Zoster to some kid to then give them chickenpox. Yeah. And then from that kid to like 10 other kids. Yeah. Yeah. Literally. So with seemingly no minimum population size and this incredibly high transmissibility,

it seems like the Veracellosolosostovirus would have made itself pretty well known among humans for as long as it's been around. I mean, I could see it going one of two ways here, Aaron. Okay, well, what did people say about it? It's kind of like not much, to be honest. Yeah, that was going to be my fear. Yeah, yeah, it was my fear too, and then it was realized. I was like, oh, boy, where's the history?

So the link between chickenpox and shingles wasn't really known, or at least it wasn't widely suspected until the late 1800s, and I'll get to that later, but both diseases had been recognized long before that. So we get the first mention of chickenpox, or rather Veracella, as it was first called, in the 1550s, when an Italian physician named Giovanni Felipe engracia differentiated it from scarlet fever. The first thorough description, though, came from English physician William Heberts, than in 1785, and at the same time, he distinguished it from smallpox. And I already went through

like the etymology, so varicella is this diminutive form of the word variola. But why do we call it chicken pox? I didn't go through that etymology. Yeah, can you tell me? I mean, no one really knows for sure, but there are plenty of guesses. One popular guess is that the bumps resemble chickpeas. And so it was called chicken pox? That was like not very well supported. Yeah. But another like more popular one is that chicken pox kind of resemble smallpox but is way less deadly and horrible. And so it was called chicken pox as like the lesser version, the small fry version of the big bad smallpox.

Like you're just a chicken. Yeah. Yeah. I mean chicken chickens are cool though. Like I don't know why they get such a like I wonder why the negative connotation of chicken. began. It's a good question. It's a good question. Anyway, let us know if you know. But shingles goes even further back than chicken pox in terms of its name. So herpes zoster, the reactivation of the virus was named by Hippocrates from the words for to creep and girdle, zoster meaning girdle.

And shingles, which is the other name for this reactivation, is from the Latin word singulus for belt. where it typically happened. Yeah, along the girdle. Yeah. Very common. But I also want to mention that in Norway, they had a bit more colorful or evocative description for the rash. The Belt of Roses from Hell.

Which I love. I love that. That's great. So I'm not sure exactly when the first, like, description of shingles was, but by the 1860s, its neural qualities were recognized, and its focus in the dorsal root ganglion was identified. Wow. That's impressive. I know.

I was very surprised by that, too. It was sort of like, you know, autopsies were still, if you remember from our people fever episode. It's just so interesting that they were able to find, like, I mean, they didn't know virus, right? No, they didn't know virus. But I think it was like actually physical changes. Right. Yeah. Like the inflammation and things that you would see starting there.

So they were like, well, this is obviously the root of the root. Yeah. The root. Yeah. Wow. That's pretty cool. It is. And this period, like so from the 1860s on, sort of kicked off a growth in the interest of

Zoster and chicken pox, which, you know, probably was just sort of alongside the growth of interest in all diseases that appear. to be infectious, right? And so it makes sense then, given this high interest, that it was around 1875 that the transmissibility of chickenpox was first demonstrated through inoculation of human quote, volunteers. Quote, quote, volunteers. We all know what that means. And then in 1892, the link between chickenpox and Zoster was first suggested after the Viennese physician Yanos von Bocke, noticed that chickenpox tended to pop up in susceptible children in a household where there happened to be a zoster case.

Oh, okay. I was wondering how they finally made that connection. Yeah. I mean, it makes sense. But it was still at that point a hypothesis, right? Okay. Yeah. And it did gain a bit more support when the next year the antigens for the two diseases were

shown to be similar. But it wasn't until the 1940s that it was finally shown. chickenpox and zoster were caused by the same virus. Wow. So I talk a lot on this podcast about germ theory and how that reshaped, you know, our concept of disease, really altering the way that people saw the world and themselves. But what I haven't really given much time to, unless I'm forgetting that I've talked about it, which is entirely possible, is where viruses fit into all of this. because microscopes and microbiology labs in the 1800s, when germ theory first really gained traction, those allowed researchers to grow cultures primarily of like bacteria or fungi and visualize them

under either the scope or in the dish in colonies. And parasites, which are another big contributor to disease, were also pretty easily seen. But where does that leave viruses? Very difficult. Very difficult. And so there's this whole chunk of diseases, measles, smallpox, polio, yellow fever, influenza, chickenpox, diseases that were super prevalent, but they still lacked a tangible causative agent. You couldn't see it.

What was causing it? The infectiousness of these diseases could be demonstrated, again, mostly through these human, quote, volunteers. But what exactly was being transmitted remained a mystery for decades after the rise of germ theory. in part because human beings and other animals and plants are riddled with bacteria, and so it was really easy to culture bacteria from someone's sputum who was sick with, like, influenza, and assume that the bacteria you cultured were the responsible ones. Right, right. And also in part because we lacked a technology that would let researchers actually visualize

these causative agents of disease, these viruses. But that didn't stop some people from digging deeper when they're proposed. bacterial species failed to meet all four of coax postulates, which is what happened in the late 1800s when a disease was sweeping through tobacco farms in the Netherlands, leaving plants withered with patches of dead and living tissue. The farmers were understandably distraught about this, and so they enlisted the help of a scientist named Adolf Meyer, and Meyer couldn't find any bacteria or fungi or parasites on the disease plants that weren't on the healthy ones, but he knew there had to be something. So he injected sap from diseased plants into healthy ones, which then also grow diseased.

But the bacteria he isolated from the sap wasn't the culprit, and so he grew frustrated and dropped the project, which was then picked up a few years later by a couple of other scientists, who decided to grind up the plants and pass them through a filter that would block plant. cells and bacteria and fungi and parasites. So like what was even left, right? They then injected that fluid into healthy plants and voila, disease. So they called this contagious living fluid a virus or transmissible, filterable agent, which is what the term was for a lot of these viral diseases later on. Filtered transmissible agent. I love it. I love it. And then they're like that is when the field of virology was born, basically.

What? It just really was the first time doing this episode where I actually thought, wait a second, like, we just assume we lump viruses in with bacteria and parasites and fungi as like, you know, human pathogens of disease. Right. But it took a lot longer than these other ones in terms of like germ theory. It's just so fascinating that they thought to do that. I know.

You know, they thought, let's use a filter that we know is going to keep back all of the plant tissue, all of the bacteria even, and just see what's left. Mm-hmm. What an idea. I know. I know. It's amazing. It is amazing.

And so, you know, at this time, though, like when virology was first started as a field, scientists, virologists still lacked the tools to actually see what they were working with. Right. But it didn't stop them from writing papers or books about these viral diseases. But in 1931, the invention of the electron microscope by Ernst Ruska and Max Knoll would change all of that. And also I have to shout out X-ray crystallography, one of my favorite things still, go and listen to our radiation episode. episode. That also helped in terms of like somewhat of the structure of viruses or their composition. Okay. But anyway, so Ernst Ruska employed his brother Helmut, who was a medical

doctor in his lab and had him look at some various samples under this new electron microscope. Among these samples was tobacco mosaic virus. Okay. And vesicle fluid from chicken pox and Zoster rashes. Ooh. And so Helmut Ruska became the first person to see the varicel azoster virus and to definitively link the two diseases together. That is so cool. It's very cool to think about, like, the first time seeing that.

Yeah. Oh, my goodness. And the development of the electron microscope would reveal that viruses in general were not just, like, particles of protein, which is what had been thought, but that they had complex and varied structures, which was an enormous step forward in virology and molecular biology, and it earned the two inventors the Nobel Prize in 1986, like a long time after. Yeah, wow. Yeah.

And this Nobel Prize would not be the last one associated with varicelis-Oster virus. It was very surprised to learn. The development of the electron microscope was a pretty incredible new tool for this already rapidly growing field of virology, and other molecular biology techniques like tissue culture made it just a matter of time, really, before various viruses were isolated and then characterized. And one of these, of course, was the varicel zoster virus in 1952, which was given its name by the virologist Thomas Weller, who Nobel Prize number two was given a Nobel Prize along with John Enders and Frederick Robbins for their viral discoveries, primarily poliovirus.

Oh, that's why that name is familiar. Yeah, from our vaccines episodes way back in the day. And while the varicelosa's oster virus may not have been as, like, sexy of a thing to research as something like measles or smallpox, it still did attract a fair bit of attention. A researcher named Edgar Hope Thompson spent 15 years, so from 1947 to 1962, studying this virus in a small, isolated community. And from this, like, amazing data set, I imagine, made a ton of really important observations about its incidence rate, its pathogenesis, the reactivation of latent virus leading to Zoster and the role of the immune system in infection. And then Nobel Prize number three, our last Nobel Prize, in 1977, Gertrude Elion discovered a cyclovir as an effective treatment for herpes viruses, which that Nobel Prize was awarded in 1988. Wow.

Okay. Yeah. So that's like three Nobel Prizes linked in some way to this virus, which doesn't have like much of a big, oh, and then it caused this pandemic and this. epidemic, but still, I think it's really cool because it shows just how many different fields of research are involved in understanding, like gaining an understanding about a disease. Yeah, absolutely. But we still have one more major development in the history of varisal's ostracivirus before I turn it back over to you, which is the vaccine.

The vaccine. In the early 1970s, a Japanese researcher named Michiaki Takahashi, and, you know, Mishiaki Takahashi, isolated a strain of the varicelzeal-a-soster virus from a three-year-old boy and developed a live attenuated vaccine, aka the Oka vaccine, which was after the last name of the boy. Within a few years, Maurice Hilliman, if you remember that name from our vaccines episode. Maurice, let's hear it for Maurice. Let's hear it for Maurice. Maurice and colleagues worked on one in the U.S. based off of this Oka strain. And in 19, 1984, the first varicella vaccines became commercially available. But this was a pretty controversial

vaccine at the start with many scientists in disagreement about the duration of immunity, whether the virus was attenuated enough, and the modeling showing that there might be an increase in shingles, which, Erin, I know you'll go into. I'm so excited to talk about it. But ultimately, study after study show that the vaccine was safe and was. was effective. And so the vaccine was introduced to Korea and Japan in 1988 and eventually became available in the U.S. as of 1995. And I think it's really cool that we're doing this episode now 26 years after it became routine in the U.S. because it's probably only now that we're getting a true sense of the impact that it's had. So, Erin, tell me about that that.

impact. Where do we stand with chickenpox and shingles today? I am literally so excited. We'll take a quick break and then talk all about it. Okay, so let's just talk about vaccines, all right? Because it turns out, like you kind of mentioned, Darren, there's a lot of nuance to this discussion. And I'm excited about it. I am too. So the vaccine that we use, again, varicella in the U.S., like you mentioned, Aaron, it was licensed in 1995. Since 2006, 2005, 2006, the recommendations in the U.S. are for two doses, the first at age 12 to 15 months, and the second dose at age 4 to 6. When they first started giving this, they found it was pretty effective, but there were still a good number of like breakthrough infections. And so that is

why about 10 years later they added that second dose. And it's much more effective after two doses. Okay. And like you mentioned, Aaron, this vaccine is a live attenuated virus vaccine. That means it's a live, whole real virus. But even though vera cell, like wild type varicella is benign. This virus is even more benign. It doesn't cause disease, but it does provide you with the antibodies that protect against wild type veracela. At this point, like you said, Aaron, we have pretty good long-term data that shows that in a lot of populations, immunity actually is quite good, up to 20 years. That's amazing.

It's very good immunity, and that's awesome. But the biggest question that I... There's always a but. That's the title. The biggest question that I hear from people is if you get the varicella vaccine, instead of getting chickenpox as a kid, are you more susceptible to shingles later on in life because you only got the vaccine? and I think that that idea itself is a little bit off base, and I'll talk about why.

But I think that this idea came about because of these math models that you mentioned, Aaron. So when this Veracella vaccine was first introduced, and even before it was introduced in the U.S., but after it was shown to be quite effective, there were a lot of math models that suggested that by introducing this vaccine, what would happen is that we would see a huge increase, a very rapid increase in shingles in adults because the prevailing thought is that part of what protects you against the development of shingles is repeat exposure to varicella in the population. Oh my gosh, that makes sense. Right.

So it's like a natural booster that like you're an adult, you're exposed. to kids coming home with chickenpox and you're a body's like, hey, I remember that chickenpox because the kid just breathed in your face. And then your body's like, well, I'm going to make sure to just re-up my immunity and then you're less likely to get shingles. But is that, is that how it works? So there is data that suggests that people who have frequent or have higher numbers of exposures to varicella are less likely to get shingles. And so that was the data that these math modelers used to predict this increase in shingles. And these math models had such strong data that that's part of the reason that it took quite a long time before this vaccine was introduced into

childhood vaccination campaigns well after it had been shown to be safe and effective against preventing varicella disease. So now that this vaccine has been introduced for so long, What has happened with shingles? That's the question, right? Yeah. Let's talk about it. Big picture. Since the introduction, and I'm focusing on the U.S.

because, first of all, I have good data. There was a lot of studies published on the U.S., but also not every country. Like, there's not a ton of countries that have had this as part of their regular childhood vaccine campaign for as long. So anyways, that's why a lot of this data is from the U.S. since the introduction of the vaccine in the U.S. The cases of chickenpox varicella have declined by like 95 to 97%. And these declines have even been seen in adults over the age of 20 as well as in infants. And what that tells us is that not only have we prevented illness in the people who have been vaccinated,

but we have in fact done what these math models predicted, which is, decrease the potential for community exposure because infants under age one and anyone over 20 something likely was never vaccinated. So what's going on with shingles? Well, shingles rates have been increasing, but age-specific rates of shingles were increasing before we even started any vaccination campaigns, before any of these vaccines were used widespread in the U.S. Well, that is fascinating. Isn't it? And we don't know why. Since the introduction of these vaccines,

there haven't been any additional increases in this already increasing incidence. Like there's no acceleration of shingles since the introduction of the vaccines. What kind of increase are we talking about? Oh, gosh, I don't have good numbers on it. And the truth is, we just don't have good numbers for sure. shingles overall because not everyone who gets shingles is going to go to the hospital. It's not necessarily a reportable disease, et cetera, et cetera. Okay. But it's like a, is it a mild slope or like a, you know, cliff? It's a, it's a relatively mild slope. Okay. I will link to the paper, which was

published in 2019 called do Veracella vaccination programs change the epidemiology of herpes oster. It was a really comprehensive review. Okay. It was great. So, to, to, make things even a little bit more complicated. We don't just have one vaccine. We also have vaccines against shingles. Yeah, how does that work? Yeah. So we have two different vaccines against shingles. The first came out in 2006, and this one, like the varicella vaccine, was a live attenuated vaccine. But there's been a newer one that has come out in 2017. And this one is a recombinant vaccine. So it's just, I think just one of the surface proteins of varicella. And so it's not a live virus. It doesn't replicate in you. Okay. And that one came out in 2017, but the rollout in the U.S., especially,

has been very slow. There's been a lot of, like, backlog where people just couldn't get vaccines because there just wasn't enough supply. But in the last, like, five years or so, there has actually been a slight decline in the incidence of shingles. But we don't know why that is either, and it's probably not just because of these shingles vaccines. Okay, but I have a question about these vaccines because usually when we talk about vaccines, we're talking about pathogens. And with these two vaccines, we're using disease names, even though they're both against the same virus. Varzile's Loster virus. Yeah, I don't get it. I quite honestly also don't get it.

So if you, like for the shingles vaccine, right? If you gave that to someone who has never been exposed to varisal's ostracurvirus, period, what would happen? You would protect them against varicella and shingles, as far as I know. I think what you're getting at is like what is the real difference between, especially the the original shingles vaccine that was developed in 2006 or that was licensed in 2006. That was a live attenuated vaccine. What's the difference between that vaccine and the varicella vaccine that we give to kids? Yeah. Probably not much, right? It's just who do we give it to? Who is it tested on and who do we give it to? And why? All of the data that we have so far,

what they tell us about these new, relatively new, varicella vaccines, the ones that we give to kids. Somebody who gets vaccinated with this varicella vaccine is far less likely to develop shingles in their lifetime than someone who gets chickenpox naturally as a kid. So we've seen this in vaccinated cohorts compared to unvaccinated years previous. That the varicella vaccine strain is less likely to develop this latent infection and reactivate into shaming. So giving someone as a child the varicella vaccine is protective against both chickenpox and shingles. That much we know. And it does not appear in the almost 30 years now, 25 plus years that this vaccine has been in use in the U.S., giving this vaccine to children has not increased the incidence of shingles in the adult population. like the math model is predicted.

Right. So what are the recommendations like for shingles vaccination? Right now in the U.S., the newer shingles vaccine has been shown to be a lot more effective than the older one. So the recommendation is that starting at age 50, at age 50 is when you get it. It's a two-dose series. And I don't know if there's data on whether or not you need boosters after that. But right now it's a two-dose series starting at age 50. Mm-hmm. Yeah.

But that's just in the U.S. Vaccine uptake for Veracela across the world is pretty spotty. But there are a number of different papers that really highlight just how big of an impact vaccination campaigns, like adding Veracela to the childhood vaccination campaigns can really have on a population. Mm-hmm. And that is chickenpox and shank. angles. Wow. It was interesting. Good, right? I think it's a good episode. I think so too. Well, should we wrap up the way we usually do? With our sources? Absolutely.

So I'll shout out just a few papers. I have more, but by Gross from 2012, Pangaea and the Out of Africa model of Veracel's Ostervirus Evolution and Phylogyography, and then also by Oaklander from 1999, the Pathology of Shingles, Head in Campbell's 1900 monograph, and another one, Pontremoli at all from 2020, possible European origin of circulating varicelzeal's oster virus strains. And I have more, and I will post more on our website. This podcast We'll Kill You.com. Yeah, I mentioned a couple of my sources already. I have a lot more, as well as those two papers I already mentioned, one by Dahl and DeCoster in the American Journal of Bioethics and the other by Harpaws that was about the epidemiology of herpesoster. Check them out on our website. This podcast will kill you.com.

Thank you again so much for sharing your first-hand account with us. We really appreciate it. Thank you. Thank you also to Bloodmobile for providing the music for this episode and every one of our episodes. And thank you to the exactly right network of whom we are a very proud member. Thank you to all of you listeners. And thank you especially to our patrons. We love all of you so very much. Yeah, we do. Thanks for listening. We hope you liked this episode. Well, until next time, wash your hands. You filthy animals. Truck month is going on now at your local ram dealer. Hurry in for great deals and exceptional offers on a powerful selection of ram trucks. And right now Purchase and get 0% financing for 60 months on 2026 RAM-500 Big Horn and Laramie models.

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