Pod Insights This Podcast Will Kill You From the Vault - Hepatitis B: Hepatiti, Take 2 (Ep 89) About this episode This episode originally aired on January 25th, 2022.
In light of the recent changes by RFK jr’s Advisory Committee on Immunization Practices (ACIP) to eliminate the universal birth dose of the hepatitis B vaccine in the US, a decision which will result in preventable infections and deaths in this country every year, it seems timely to remind everyone of the global consequences of this incredibly prevalent pathogen.
This week, we’re dipping a toe back into the vast waters of hepatitis viruses, this time with a focus on hepatitis B. The hepatitis B virus, though second to be named, was first to be discovered, and effective vaccines and treatments have been available for decades. Yet the global prevalence of this virus remains staggering, with nearly 300 million people chronically infected and 1.5 million new infections annually. So what’s going on? In this episode, we weave our way through the complicated biology of this virus and its deadly potential, the strange history of its identification that shows that you don't have to be looking for something to find it, and the current status of this virus that underlines how safe, effective tools for disease prevention are only as good as our delivery infrastructure. We are also so excited to be joined by Dr. Su Wang, Medical Director for the Center for Asian Health https://www.rwjbh.org/saint-barnabas-medical-center/treatment-care/center-for-asian-health/ & Viral Hepatitis Programs at the Cooperman Barnabas Medical Center https://www.rwjbh.org/saint-barnabas-medical-center/ and outgoing President of the World Hepatitis Alliance https://www.worldhepatitisalliance.org/.
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Transcript 14,857 words · 10 speakers
0:01 Speaker 00 This is Exactly Right.
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0:38 Speaker 02 Hey, I'm Niall Rogers. This fall, I'll be driving across the country, meeting some of today's coolest and most fascinating artists. We'll explore the stories before the moments that changed everything. Because every musician remembers the moment where it all began. Experience Before the Moment, a Lincoln Original Series on the iHeartRadio app, YouTube, or wherever you get your podcasts.
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1:41 Speaker 04 My name is Sue Wong. I am a physician. I'm an MD, MPH. I'm the Medical Director for the Center for Asian Health and Viral Hepatitis Programs at the Cooperman Barnabas Medical Center in New Jersey. And I'm also just coming off a two-year presidency for the World Hepatitis Alliance, which is a nonprofit organization that represents patients living with viral hepatitis. And our goal is to harness the power of people living with viral hepatitis to achieve global elimination of viral hepatitis. I was diagnosed with hepatitis B in college.
2:22 Speaker 04 In my first year of college, I went to donate blood, right, to do a good thing, donate blood. And shortly after, I got a big fat envelope sent to my dorm and it said, "Don't be worried, you don't have HIV, but you do have hepatitis B." And I was a pre-med student, but honestly, I didn't know anything about Hep B. I called my sister, confided in her about this new diagnosis and she said, "Oh, didn't you know mom also has Hep B?" And then I just, I just remember thinking, "Oh, who do I need to tell?" And when I went back home, I did go see a doctor and talked to her about it. And I think she did blood work and basically said I was a carrier and there was nothing to worry about.
3:07 Speaker 04 So I honestly pushed it to the, you know, back burner, didn't want to think about it. So it didn't come up again until med school. Um, I filled in all my med school forms and a lot of our employment forms and our screenings for working at a hospital, you do have to indicate, you know, what your Hep B vaccination and statuses. And I had indicated that I was a carrier and didn't hear anything about it. I didn't think anything of it. And it's not till now that I've heard numerous people who are in med school, found out to have Hep B and actually they lose their acceptances to med school. Or they face quite a bit of what I would consider discrimination over their status. Uh, and it's happened to residents, it's happened to nurses, it's happened to dental students.
3:53 Speaker 04 So it is an issue of stigma and discrimination. But I was fortunate, it didn't happen to me. And it kind of was in the back of my mind and I remember kind of when we learned about hepatitis, just kind of listening a little bit more attentively. And when I got to residency after med school, um, I became really good friends with somebody. A friend of mine went into infectious disease and I had confided in her that I had hepatitis B. And um, she told me, "Oh, make sure you see a doctor for it." I hadn't seen a doctor in years at that point. So I went in to see somebody and um, They did my viral load and I did the ultrasound and everything was fine. It was very low. I didn't need medication. And at that point, I remember I was engaged, I think. And so my friend had said, oh, make sure your
4:38 Speaker 04 fiance also gets tested. And he ended up getting tested and needing to get vaccinated. And, you know, so that was kind of the extent of how it impacted my life. And I had told him about it and I was, you know, I was happy that he was, he didn't make a big deal out of it. And these are all points now, looking back, I realize, you know, I was fortunate. And so many people around the world are not so fortunate to have, you know, a career that's not affected by it, or a relationship that's not affected by it. You know, there are a lot of people who, you know, lose their partners. They end up, they may get divorced, they may get disowned by family, or unable to pursue the career they want to. So I didn't have any of that. And I got married and we got pregnant. I've had four kids and
5:22 Speaker 04 with each one of those kids, especially the first one, it did hit me that, oh, I know there's a chance that I could pass this infection on to my children. And that definitely weighed heavily on me, although I knew the research that because my viral load was low, there would be very low chance of the infant developing Hep B. But that's where I really all of a sudden felt like, oh, my gosh, you know, this could really impact me personally. And I'm happy to say that all four of my kids are Hep B free. And that they don't have to live with this chronic disease and worry about risk of liver cancer and other things that other kids have to go through, even now in this day and age. And so as a physician, I, I didn't particularly have a inkling that I was going to do hepatitis work at all. And it wasn't until I moved to New York City
6:07 Speaker 04 after I finished my residency and I took a job with a community health center in Chinatown. So I began serving the largely Chinese community in Chinatown and learned so much more about Hep B than I ever knew. That it's, you know, one of the most common infectious diseases around the world, up to like one in 10 of our patients had Hep B. It was as common as hypertension. And whereas I had seen specialists, you know, during residency, a lot of our patients could not afford to see a specialist and they weren't necessarily easily accessible. So many of us at the community health center learned to treat Hep B along with hypertension, diabetes and other chronic diseases. So during that time, I really saw, you know, a lot of the difficulties that people face in getting care.
6:52 Speaker 04 And so I began really advocating and creating programs that would help people living with hepatitis B to increase screening in the communities, linkage to care, all these things that can happen in a very complex medical system. We tried to create a program to kind of streamline and all of that. As I was getting more and more immersed in, you know, really providing the care that needs to happen, I really had the hat on, like, you know, the physician hat, like, this is what needs to be done. These are the interventions. This is the science behind it. I did not wear the patient hat at all in terms of what it meant for me. And I kind of didn't feel like that, that was my role. And it wasn't until somebody did an interview, actually, I did an interview for CDC, and it was the first time, like, on camera that I had, I said, you know, I'm actually living
7:37 Speaker 04 with hepatitis B myself. And at that point, I'd already occasionally mentioned it to patients. So if I was counseling a patient who had been newly diagnosed with Hep B and I could see they were really distraught or felt really overwhelmed, I would share with them that I also was living with Hep B. I was just like them. I had to go for blood tests. And I think that really helped them see that it's possible to live a happy, healthy life and it's not a death sentence. So I was using that more often, but I'd never spoken about it publicly. So it took me a while. And what I've seen as a physician, which I think as physicians, we don't quite get is just how powerful that personal experience is. And I have only learned this through other people. Somebody asked me to get involved with the World Hepatitis Alliance, which is led by patients.
8:22 Speaker 04 And through that, on the board, the board is all patients who represent each of the WHO regions. And I heard specifically from a good friend of mine who is now a good friend of mine, Dee Lee, who represented the Whippa region, the Western Pacific region. He told me all these stories of people who really had Hep B drastically impact their life in ways that us in medicine don't measure, right? We measure the outcomes we look at are morbidity, mortality, life expectancy, right? Cirrhosis, liver cancer. We don't look at outcomes in terms of somebody's quality of life. Um, you know, when I hear these stories of, of how people have, have suffered with the burden of the disease, even if they're, I mean, as, as a doctor, if you were to look
9:06 Speaker 04 at them, they would look healthy. You would tell them they're perfectly healthy. Their liver enzymes are normal, their viral load is low, like, you know, I only need to see you once a year, you're fine. You know, in our mind, we think it's, we think it's nothing. Like if you were to then delve into how they feel about themselves, and most patients won't even tell me that. So I, I know that what I see, what I glimpse in my exam room is just such a small part of what it means for them to live with a disease. And so, you know, it's beyond just like keeping them from getting cirrhosis and liver cancer. You know, us in medicine, if we're, if our mission is to improve quality of life and decrease burden of disease on people's lives, we have to think outside just, you know, our, our biochemical tests.
9:48 Speaker 04 Um, I think, you know, I've just learned that we can't afford to operate in our silos, right? The scientists cannot afford to operate in, you know, their silos, only like publishing to the scientific community and having meetings that are only for scientists and medical researchers. But we have to get out of the box. We have to combine, you know, the people living with the disease have to work in concert with the medical community if we're really going to make progress for elimination and for, uh, you know, really alleviating the suffering of Hep B on people's lives.
11:03 Speaker 05 Thank you so much, Dr. Wong, for sharing your story.
11:06 Speaker 01 Thank you.
11:08 Speaker 05 Hi, I'm Erin Welsh.
11:10 Speaker 01 And I'm Erin Allman Updike.
11:12 Speaker 05 And this is This Podcast Will Kill You.
11:15 Speaker 01 Welcome to another episode.
11:18 Speaker 05 Yes, welcome, welcome. As you have probably gathered, we are going to be talking about another hepatitis virus, our second in the podcast's history. Yes, this one hepatitis B.
11:33 Speaker 01 Yeah, we started with C, now we're going to B.
11:36 Speaker 05 What's next?
11:37 Speaker 01 Well, I am going to mention D.
11:40 Speaker 05 I figured.
11:43 Speaker 01 I think next will be A.
11:44 Speaker 05 Yeah, next will definitely be A. And then we'll have to do E. And then maybe by the time that comes out, there'll be a few more that we can cover all in one.
11:53 Speaker 01 Quite possible.
11:55 Speaker 05 Well, Erin, what time is it?
11:58 Speaker 01 It's Quarantini time, Erin.
12:00 Speaker 05 It is. And what are we drinking this week?
12:04 Speaker 01 We're drinking the bee sting.
12:06 Speaker 05 We are.
12:07 Speaker 01 Hepatitis B.
12:09 Speaker 05 Hepatitis B. And what is in the bee sting?
12:12 Speaker 01 Well, it's a lovely little bev, a ginger mint syrup, some lemon juice, club soda. If you're drinking alcohol, you could certainly put some gin in it.
12:24 Speaker 05 That will be the little sting. But otherwise, on its own, it is delicious.
12:30 Speaker 01 Very refreshing.
12:31 Speaker 05 I just, I love it. And we will post the full recipe for this Quarantini, as well as our non-alcoholic placebo-rita, on our website, thispodcastwillkillyou.com, as well as on all of our social media channels.
12:47 Speaker 01 On our website, thispodcastwillkillyou.com, you will find any and every of the things that you ever wanted to know about the podcast. You can find Bloodmobile, who does all of our music and the link to their Spotify. You can find merch, all of our merch. You can find transcripts for all of our episodes. You can find... Uh, bookshop.org affiliate account and a Goodreads list. You can find all the sources for all of our episodes. Thanks. I need the encouragement. And you can find our Patreon.
13:22 Speaker 05 Wow, that was impressive.
13:24 Speaker 01 Thank you. Thanks.
13:26 Speaker 05 I'm always relieved when I don't have to do it.
13:28 Speaker 01 I always get really nervous and then I just power through.
13:32 Speaker 05 I like it. It's like you get in the zone and then you're there.
13:37 Speaker 05 Well, before we get into the episode, I wanted to mention one thing because endometriosis, which was the last episode we released, is still on my mind, even though I've been reading a lot about hepatitis B. I still have these like little thoughts of endo that pop in. And I realized that there was like one more thing that I wanted to say. Also, like endometriosis, we've recorded it. It's not yet released. And so maybe people will have already said this by the time this comes out. It's sort of a weird time travel thing we're doing here.
14:11 Speaker 01 Yeah.
14:13 Speaker 05 But in the endometriosis episode, we talked about how often complete or partial hysterectomy is recommended as like a cure for endometriosis, which it isn't, and which that can also add another dimension of pain and anguish to an already difficult disease. But I also think that another aspect to that that we didn't really touch on, and I think is important to mention, is that there can also be a reluctance on the part of physicians to perform hysterectomies, or even just tubal ligations, like getting your tubes tied, for whatever reason, even if that reason is, I don't want to have any children or any more children. A lot of people are just told, oh, you're just too young. You might
14:58 Speaker 05 change your mind and want to have kids in the future. And so really, that's sort of another way in which many times physicians don't fulfill the very basic requirement of listening to their patient and how the social and gender role of someone can be held as like more important than what they want, than their wishes.
15:15 Speaker 01 Yeah.
15:16 Speaker 05 Anyway, that just kept like circulating in my head and I was like, oh, gosh, I need to say it.
15:22 Speaker 01 So, yeah. Okay, got it out. Yeah, that's an incredibly important point. Okay, should we, should we move on to the actual topic of today's episode? Today's topic, hepatitis B. Let's take a quick break and then get into the biology.
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16:40 Speaker 02 Hey, it's Niall Rogers, host of Before the Moment, a Lincoln original series. I'm driving across the country, meeting some of today's most fascinating artists. We're exploring the stories before the moment that changed everything. This week, I'm joined by my friend, John Legend. How does music actually enter your mind?
17:02 Speaker 06 I'm not sure why or how the music comes to me, but I think people who love music and write music, our brains are just filled with music.
17:11 Speaker 02 Right.
17:12 Speaker 06 Like, we have listened to so much music, we've been a part of so much music. I think of the story that I want to tell, the mood that I want to create with the music, start playing chords, see where they lead me.
17:23 Speaker 02 Sometimes I'm just not even thinking about music, right? And I hear this little thing and I go, oh, that could be this.
17:33 Speaker 06 You know, you just have to be ready for when the inspiration hits.
17:36 Speaker 02 It comes.
17:37 Speaker 06 Yeah.
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17:47 Speaker 07 Hello, hello. I'm Malcolm Gladwell, host of Smart Talks with IBM. Imagine your business depends on a system you didn't build and don't fully control. For years, it works perfectly. It's fast, reliable, affordable. So over time, more and more of your operations rely on it. Then one day, the terms change. What once felt flexible now feels difficult to leave. Moving to another provider or bringing those capabilities back under your own control could take years, cost millions, and disrupt the business in the process. That's the challenge of digital sovereignty. Businesses today rely on all sorts of third-party systems:
18:30 Speaker 07 cloud platforms, data pipelines, AI models, software tools. Most days, these systems operate quietly in the background. But when something changes, like costs go up or rules shift, organizations are forced to confront how much control and flexibility they actually have. So to understand the challenge up close, I traveled to Paris to speak with IBM's Annapola Assis and Acts as CIO, Giovanni Daniele, two people who think about these questions every day. Hear the full conversation at ibm.com/smarttalks or wherever you get your podcasts.
19:44 Speaker 01 So like you mentioned, Erin, this is our second hepatitis virus. And I know for sure that during our hepatitis C episode, we talked at least a little bit about how all the hepateeti, all the hepatitis viruses are named not for anything that links the particular viruses together, aside from the fact that they all predominantly affect the liver. Right. So there are five predominant viruses, which we kind of already named at the beginning, A, B, C, D, and E. And today, we're focusing on hepatitis B. And I will mention hepatitis D. And you'll understand why in a minute, if you don't already know the little interplay
20:29 Speaker 01 between hepatitis D and B. All right. Hepatitis B, it's in the family Hepatnaviridae, which essentially just means viruses that affect the liver. Like, no surprise. Straightforward. One thing that's, there's a lot of interesting things about the virology of hepatitis B, and I'm probably not even going to do them justice, but here we try. Hepatitis B virus is a partially double-stranded DNA virus, which is weird. Mm hmm. So it has a genome that it's like in a little circle, and part of it is double-stranded and part of it is single-stranded, which is very bizarre. Do you have a question already, Erin? I can see it on your face.
21:14 Speaker 01 I mean, yes, but I'm waiting. Okay. I'm being patient. Okay. We'll see if I have any answers. Hepatitis B virus has a lot of different genotypes that vary very widely in their overall geographic distribution. However, as we mentioned up top, and as we'll talk a lot about towards the end of this episode, this is a globally distributed, incredibly prevalent virus. Like incredibly prevalent. Incredibly prevalent. And it's still, as far as I can tell, a little bit up for debate whether these different genotypes really vary in their tendency to cause chronic infection or in their overall disease course. A lot of sources I read said that yes, different genotypes
21:57 Speaker 01 kind of have different tendencies or characteristics, and some said it's up for debate. So.
22:02 Speaker 05 Oy. Okay.
22:04 Speaker 01 But being a virus, this is, of course, a pathogen that has to find its way into our cells. And being a virus that infects the liver, it's unsurprising that the primary cell type that it infects is our hepatocytes, our actual liver cells, not the blood vessels in our liver, not any of the other things around there, but generally our liver cells.
22:28 Speaker 05 The things that make up the meat of the liver.
22:31 Speaker 01 Exactly. Also called the parenchyma of the liver.
22:35 Speaker 05 Mm hmm.
22:35 Speaker 01 It's the fancy word for the meat.
22:39 Speaker 01 So hepatitis B is transmitted in very similar ways to hepatitis C, as you may remember from several seasons ago now, but with a few important caveats. So hepatitis B can be a bloodborne virus. So anything that involves the sharing of blood, whether that's contaminated needles in the healthcare setting or in intravenous drug use settings, it can be transmitted via blood transfusions. And of course, it's something that we screen for to try and reduce the risk of that. But hepatitis B is also much more easily transmitted sexually compared to hepatitis C. It's present in so many bodily fluids.
23:24 Speaker 05 Why is that?
23:26 Speaker 01 It's a really good question. I imagine it is largely because hepatitis B is very, very infectious. As an example, according to WHO, it's 50 to 100 times more infectious than HIV.
23:43 Speaker 05 Whoa. So
23:44 Speaker 01 I know.
23:45 Speaker 05 Do we know the reasons for that increased infectivity?
23:50 Speaker 01 Oh, that's a very good question. I do not.
23:53 Speaker 05 Okay.
23:54 Speaker 01 Yeah. And I don't also have numbers on like the actual infectious dose. I couldn't find a solid answer on that either. I do know that it can persist in the environment for at least several days. So I think it's a pretty hardy virus. So that might be part of it. Yeah.
24:10 Speaker 05 Interesting.
24:12 Speaker 05 Okay, so going back real quick to the partially double stranded, what's, what's the implication of that in like a virology sense?
24:20 Speaker 01 So it's really interesting. Hepatitis B is one of the few viruses that's not an RNA virus, but uses a reverse transcriptase in order to replicate its genome. So HIV is an RNA virus that relies on an enzyme, reverse transcriptase, to make a form of DNA in order to then replicate. And Hep B also does, even though it's a DNA virus.
24:46 Speaker 05 That is so bizarre. And so I definitely came across some of that in the evolution papers, because it kind of throws a wrench in things as to like the mutation rates, the scale of the molecular clock, blah, blah, blah.
24:58 Speaker 01 Yeah, and it also, as I'll kind of talk a little bit more about later, it allows it to integrate into our genome in a way that then sets us up for both chronic infection and also potentially cancer, right? And cancer causing mutations.
25:14 Speaker 05 Ah ha.
25:15 Speaker 01 Spoilers.
25:17 Speaker 05 Do other viruses have this partially double stranded DNA thing as well?
25:25 Speaker 01 I don't know of any other human viruses, but I know that there are other animal hepatoviruses that do.
25:30 Speaker 05 Right. Okay, those, so that's like the unifying feature of hepatoviruses. Okay.
25:35 Speaker 01 Yeah.
25:35 Speaker 05 Yeah.
25:36 Speaker 01 Oh, wow, cool. Okay, so hepatitis B is also transmitted back to that part of it, vertically, at much higher rates. This, let me tell you some numbers. The estimates that I read ranged from 40 to 90% of babies born to people living with hepatitis B, with chronic hepatitis B, will become infected with hepatitis if they are not treated.
26:04 Speaker 05 Wow.
26:04 Speaker 01 And this is in comparison to only 6% of people with hepatitis C will then transmit hepatitis C to their offspring.
26:14 Speaker 05 What is the reason for that difference?
26:17 Speaker 01 Again, I think it's largely just how infectious hepatitis B is.
26:21 Speaker 05 Okay.
26:22 Speaker 01 But here's something that I think is very interesting and important about this vertical transmission of hepatitis B.
26:30 Speaker 01 First of all, a lot of times when we talk about vertical transmission, so from parent to offspring, it's when viruses or bacteria can cross the placenta and infect a fetus during pregnancy. That is not what happens in hepatitis B. The transmission is not transplacental. In the vast, vast majority of cases, it's happening during the process of childbirth. And it's not happening during breastfeeding. It's not happening during pregnancy crossing the placenta. It's happening specifically during the period of childbirth, whether that birth happens vaginally or via C-section.
27:11 Speaker 05 What?
27:12 Speaker 01 There is some papers that suggest that C-section delivery is a slightly lower risk, but it's not conclusive. And if you've ever seen a delivery of either kind, it kind of makes sense because neither one is really less bloody than the other. And so many bodily fluids are being exchanged, no matter what exit route a baby takes.
27:33 Speaker 05 So it's just like the blood and bodily fluids?
27:36 Speaker 01 Blood, bodily fluids. It's thought that cervical secretions, so if a baby comes out vaginally, and that's why maybe there's some thought that it's a slightly higher risk. But the data hasn't really borne that out necessarily.
27:48 Speaker 05 Hmm. What? That's very interesting.
27:51 Speaker 01 I know, because I didn't really realize that. I kind of thought that it was something that could be transmitted transplacently. But it's not. And that is really important when we talk about how to treat and prevent hepatitis B infection. So let me keep going, shall I?
28:09 Speaker 05 You shall.
28:10 Speaker 01 So the incubation period of infection, the time from when someone gets infected to when they show symptoms, can really range anywhere from 30 days to up to six months.
28:24 Speaker 01 And I think that this incubation period, even noting an incubation period is interesting because hepatitis B is a virus that can be entirely asymptomatic. And chronic infection is generally defined as the persistence of a specific antigen being able to detect hepatitis B's surface antigen for a period of at least six months. So it's interesting that you can also say the incubation period itself might be six months before you show symptoms, but you also might never show symptoms.
28:57 Speaker 05 Yeah.
28:58 Speaker 01 Yeah.
28:59 Speaker 05 That makes it really difficult to calculate an incubation.
29:03 Speaker 01 Exactly. It sure does. So let's talk briefly about what the symptoms can be if people do have kind of an acute infection or, you know, symptoms with an initial infection. Most of the time, of course, it's completely asymptomatic or very minimally symptomatic. And it's important to note that some people can clear the virus entirely from their system after an acute infection, whether they show symptoms or not. But we'll talk about how that doesn't happen for a lot of people and who those people are and why. Okay.
29:42 Speaker 05 Yeah.
29:43 Speaker 01 But when symptoms do occur, in the case of an acute infection, they really don't look any different from a lot of the other viruses and pathogens that affect our liver, including hepatitis C. So hepatitis B is less likely to cause acute liver failure completely, but it can cause things like jaundice, where your skin can become yellow, or the whites of your eyes and your gums, things like that, become yellowish. And this occurs because our liver is what conjugates and helps eliminate bilirubin from our bodies. And so without that process, bilirubin, which is a breakdown product of our red blood cells,
30:25 Speaker 01 builds up in our skin and our eyes, and that's what turns us yellow. It then also causes a lot of nausea and vomiting from this buildup of not just bilirubin, but a lot of stuff in our system that our liver is supposed to filter out. It causes abdominal pain because your liver is inflamed. And even though your liver itself doesn't have sensory innervation, this inflammation can reach the lining of the liver, the lining of the abdominal cavity, and cause pretty severe abdominal pain. And then, all of these toxins that can accumulate in your bloodstream can cause severe fatigue. It can cause a darkening of your urine as the bilirubin tries to be excreted through your urine instead of your poop.
31:10 Speaker 01 And in very rare cases, it can cause actual acute onset liver failure, which can be fatal. But much more commonly, liver failure happens as a progressive process of long-term inflammation, leading to cirrhosis and fibrosis, and potentially hepatocellular carcinoma or cancer. So I want to focus on this, this chronic infection of hepatitis B, because it's not only very interesting, but it's also the most important part of this virus.
31:50 Speaker 01 So first of all, the likelihood of a chronic infection becoming established varies person to person, and it's inversely related to the age at which you become exposed and infected. So for infants, for neonates who get infected vertically during birth, the likelihood of a chronic infection is over 90%. Over 90%. So that means that almost all babies that become infected at birth or shortly thereafter go on to have a chronic, lifelong infection with a very significant risk of progression
32:35 Speaker 01 to fibrosis and/or liver cancer.
32:38 Speaker 05 So this inverse relationship, is it like a straight line? Or does it kind of have any sort of peaks and valleys?
32:46 Speaker 01 It's not a straight line. It's a, it's a... What do you call it? No, it's a jupe, maybe?
32:55 Speaker 05 Sigmoi?
32:55 Speaker 01 A J. So let me just tell you numbers because I'm clearly not doing a good job swooping.
33:05 Speaker 01 So infant neonate, 90% chance. A child, if they get infected when they're young, like between ages one to five, the risk of chronic infection is like 30%. So it's a pretty big drop. And then it's a little lower for older children. And for adults, if you don't get infected until you are an adult, the risk of chronic infection is only about 2 to 5%. So substantially lower.
33:32 Speaker 05 Hmm. I mean, okay, I have to ask why.
33:35 Speaker 01 I'm glad you asked, Erin. Let's talk about it. But first, let me also say that even though the risk of chronic infection, if you get infected as an adult, is low, the chronic infection itself and the like prognosis of a chronic infection with hepatitis B in general is worse than, for example, the chronic infection of hepatitis C. And if you listened to our hepatitis C episode, then you remember hepatitis C is not a good virus. Right?
34:10 Speaker 01 But in hepatitis C, the likelihood of a chronic infection is much higher for adults across the board. But the rate of, for example, liver cancer is very low, like 2.5% for people who have chronic hepatitis C. Right? But much more people who get infected as adults with Hep C go on to get chronic Hep C.
34:33 Speaker 05 That makes sense.
34:35 Speaker 01 Yeah.
34:35 Speaker 05 Like, okay, in the numbers perspective.
34:38 Speaker 01 Right. But for hepatitis B, 15 to 40% of people who have chronic infection go on to have liver cancer, hepatocellular carcinoma. It's a huge percentage.
34:53 Speaker 05 Yeah.
34:54 Speaker 01 And again, 90% of infants who become infected go on to have chronic infection. So that's major.
35:03 Speaker 05 That's a really disturbingly large number.
35:07 Speaker 01 Right. Okay, so you asked why?
35:10 Speaker 05 Yeah, I did.
35:11 Speaker 01 In short,
35:14 Speaker 01 We don't fully know.
35:18 Speaker 01 That's always my answer.
35:20 Speaker 05 I'm going to cross stitch that onto a pillow for you.
35:23 Speaker 01 I would love that pillow. Oh, my gosh.
35:27 Speaker 01 Okay, but so the question of why are infants who get infected more likely than adults who get infected to go on to have a chronic infection? While we don't fully know the answer, it likely has to do with a few different factors that relate to the various phases of this chronic infection. So a chronic hepatitis B infection, which is defined just as the persistence of the virus and like detection of these viral antigens for at least six months in the bloodstream. After that point, like after that six months point, this isn't a static infection. It's very dynamic and it progresses through several different phases that can vary in their length and their severity.
36:13 Speaker 01 So the first phase is often known as immune tolerance. And that's essentially when our body doesn't really do much about this infection. The virus is there and one thing that it tends to do is integrate into our genome the way that, do you remember the other virus that does that, Erin?
36:31 Speaker 05 HPV?
36:32 Speaker 01 HPV, that's right.
36:35 Speaker 01 And as our cells replicate, so does this virus. But in the immune tolerance phase, it doesn't cause much in the way of damage. Then there is the immune active phase. And in some papers, they call this the immune clearance phase. And this is really the meat of chronic hepatitis B infection. This is when our bodies are recognizing this virus. We are mounting an immune response to it. And therefore, we ourselves are causing a lot of inflammation and damage to our own liver cells. It's not the virus itself.
37:09 Speaker 05 Okay, yeah.
37:10 Speaker 01 And this is the phase where people are more likely to be symptomatic, like maybe have jaundice. But this is the phase where that inflammation is causing fibrosis, which is damage to the liver due to that inflammation. That fibrosis can eventually lead to scarring or permanent damage, cirrhosis. And that can ultimately lead to liver cancer. And so this is the phase, the immune active phase, that the longer that somebody is in this phase, their immune system fighting the infection, the greater their risk of cancer.
37:44 Speaker 05 Okay.
37:45 Speaker 01 But there is another phase, just to make it more complicated. And that's a so-called inactive phase, wherein the virus is still there and we've maybe made some antibodies against that virus. So we're kind of at a standstill. But at any point, people could still revert back to a more immune active infection, like, say, if they became immunocompromised for some reason. And therefore, the virus is still there and still posing a risk of cancer development.
38:12 Speaker 05 Gotcha. That makes sense.
38:14 Speaker 01 Yeah. So I know that that was a lot, and it was really just a drive-by. The immunology of Hep B infection is a lot more complicated. There's a lot more detail. But one of the things that's different among adults who get infected versus infants is that infants tend to have a very long immune tolerant phase. Whereas adults who have chronic hepatitis B, that is, they get infected and aren't able to clear that infection right away, they tend to not really have an immune tolerant phase, but rather progress directly to that active inflammatory chronic hepatitis infection.
38:52 Speaker 05 Right, okay.
38:53 Speaker 01 So that's a really big difference. And it's thought that during pregnancy, viral particles, or maternal antibodies, or both, are passing through to the fetus. And then when that infant is born and exposed to hepatitis B, while they're not able to fight off that virus entirely the way most adults who are exposed can, they instead establish this relationship of tolerance that lends itself more easily to a chronic infection.
39:21 Speaker 05 Oh.
39:22 Speaker 01 Right?
39:23 Speaker 05 Okay, so it's kind of like getting to know you and like, all right, I guess we'll just tolerate, you know, each other for a while.
39:30 Speaker 01 Right, but then eventually progress to the other phases of disease.
39:34 Speaker 05 Right, okay. Interesting.
39:37 Speaker 01 But that is generally hepatitis B virus.
39:41 Speaker 05 So I have a question.
39:42 Speaker 01 Mm hmm.
39:43 Speaker 05 You mentioned that, okay, there are people who become infected and they clear the virus, they develop antibodies, boom, they're in the category that you didn't discuss the later stages on for obvious reasons.
39:53 Speaker 01 Mm hmm.
39:54 Speaker 05 And so these people now have a lifetime immunity to hepatitis B virus. What about different genotypes? Is there any sort of like genotype dependent immunity where you can be infected with one genotype and then clear that and be exposed to another one and not clear that?
40:14 Speaker 01 Great question, Erin. As far as everything that I have read, immunity to hepatitis B is immunity to hepatitis B across genotypes.
40:25 Speaker 05 That's great news.
40:26 Speaker 01 Exactly. It's really great news, Erin, because we in fact have a vaccine for hepatitis B. It is a recombinant vaccine that contains only the surface antigen of hepatitis B. And that is what we make antibodies to.
40:43 Speaker 05 I have a follow up question.
40:44 Speaker 01 Okay.
40:46 Speaker 05 If someone is chronically infected with one genotype of hepatitis B, can they become infected with another genotype of hepatitis B?
40:56 Speaker 01 Not as far as I know, but do you know what they can become infected with?
41:01 Speaker 05 Hepatitis D.
41:03 Speaker 01 Hepatitis D. Thanks for the little intro there.
41:08 Speaker 05 You're welcome, you're welcome.
41:09 Speaker 01 I want to just very briefly mention hepatitis D because I don't think that we would ever do a full episode on it. I don't know, maybe I'm wrong. But Delta hepatitis virus, or hepatitis Delta, hep D, it's a fascinating virus. This virus belongs to its entire own viral genus that doesn't have an actual family that it falls within. And some people say it's not even really a virus. It's like something else entirely. It's a sub viral agent.
41:43 Speaker 05 Whoa.
41:43 Speaker 01 What?
41:44 Speaker 05 It's like a virus of a virus?
41:47 Speaker 01 It's kind of. So hepatitis D has an RNA genome, and it can replicate on its own inside of our cells and when it infects us, and it does infect our liver cells. But it can't actually infect our cells by itself. It relies on the surface proteins of hepatitis B virus in order to get into our cells and in order to be released from our cells. So hepatitis D is a virus that can only infect someone who has a chronic or acute hepatitis B infection.
42:31 Speaker 05 I am really regretting right now not reading more about the evolutionary origins of hepatitis D. Because what on earth?
42:38 Speaker 01 Maybe it does deserve its whole own episode.
42:41 Speaker 05 Yeah.
42:43 Speaker 01 That's, that's literally all I have to say about it, but it is very, very interesting.
42:48 Speaker 05 Okay, so what about, besides the vaccine, what about treatments? Are there antiviral treatments for hepatitis B virus? Or maybe Hep B and Hep D combined?
42:58 Speaker 01 Yes, for hepatitis B, there are. So there's a number of different treatments that we have, actually. None of them can cure hepatitis B. They're all used to sort of manage it and to try and reduce the rate of inflammation and complications. But pegylated interferon, which I think we talked about in our Hep C episode, possibly. But that's basically like an immune modulator, you can think of it as. That can be used and has been used to treat hepatitis B. But there are also a number of antivirals that, in many cases, are used to treat HIV or were used to treat HIV and are now used to treat Hep B.
43:42 Speaker 01 So yes, there are. Again, none of them actually clear the infection, but they all just sort of help to manage it.
43:48 Speaker 05 Okay.
43:49 Speaker 01 And what's really important about all of these is that Because all of those different states, immune tolerance, immune active, inactive, these different phases of infection really vary person to person and how severe someone's symptoms might be, like, it really varies. So just because someone has an infection with chronic hepatitis B doesn't necessarily mean that they have to be on treatment if they're in a phase that isn't directly causing damage. Does that make sense?
44:22 Speaker 05 Yeah, that's interesting.
44:23 Speaker 01 At least as of now, because the treatments that we do have are not without side effects, and in a lot of cases, they have quite a lot of side effects. So it requires a lot of careful monitoring and everything, which makes it a lot harder to do, quite honestly.
44:37 Speaker 05 There's so much here about this virus that...
44:40 Speaker 01 I know. So, speaking of so much about this virus, Erin,
44:46 Speaker 01 like, what? Where did it come from? What the heck?
44:49 Speaker 05 I will do my best to answer those questions, but let's take a quick break first.
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45:53 Speaker 02 Hey, it's Niall Rogers, host of Before the Moment, a Lincoln original series. I'm driving across the country, meeting some of today's most fascinating artists. We're exploring the stories before the moment that changed everything. This week, I'm joined by rising star Sienna Spiral. What is so fascinating to you about impermanence?
46:15 Speaker 00 Everything about us, everything we do is temporary. And I just got terrified of that. You know, what we do with our time and how I feel like the way the world is today and how fast paced it is and how much we don't even acknowledge anything around us. How I felt temporary to the people around me and how that made me scared and how much I wanted to last and make an impact on people. And I guess to change the way I looked at things and to change myself and to change how I guess I approached everything in my life. It's important that things are impermanent because nothing would feel special. And enjoying, you know, learning to love with knowing it's not going to last.
46:49 Speaker 02 Experience Before the Moment, a Lincoln original series on the iHeartRadio app, YouTube, or wherever you get your podcasts.
46:59 Speaker 07 Hello, hello, I'm Malcolm Gladwell, host of Smart Talks with IBM. Imagine your business depends on a system you didn't build and don't fully control. For years, it works perfectly. It's fast, reliable, affordable. So over time, more and more of your operations rely on it. Then one day, the terms change. What once felt flexible now feels difficult to leave. Moving to another provider or bringing those capabilities back under your own control could take years, cost millions, and disrupt the business in the process. That's the challenge of digital sovereignty. Businesses today rely on all sorts of third-party systems: cloud platforms, data pipelines,
47:44 Speaker 07 AI models, software tools. Most days, these systems operate quietly in the background. But when something changes, like costs go up or rules shift, organizations are forced to confront how much control and flexibility they actually have. So to understand the challenge up close, I traveled to Paris to speak with IBM's Annapola Assis and Access CIO, Giovanni Doniello, two people who think about these questions every day.
48:15 Speaker 07 Hear the full conversation at ibm.com/smarttalks or wherever you get your podcasts.
48:56 Speaker 05 All right, the story of hepatitis B. I feel like in the last couple of episodes, I've maybe deviated a bit from the normal history overview that I usually give. But don't worry, I'm going back to my roots for this one.
49:15 Speaker 05 I'm going to start with a bit of evolutionary history, mix in some early accounts of infectious hepatitis, then the fascinating story of its identification, and then finally getting us to where we are today. The usual.
49:28 Speaker 01 The usual, I love it.
49:29 Speaker 05 But usual doesn't mean boring or straightforward, especially in the case of hepatitis B. So, beginning at the beginning, where does the hepatitis B virus come from? It turns out that the answer to that question has been a moving target for a number of years, with new hypotheses introduced or old hypotheses overturned or tweaked to fit new findings as more about the evolutionary history of this virus has come to light. And this should come as no surprise, really, considering how widespread this virus is, how many genotypes there seem to be. How the virus can undergo recombination,
50:13 Speaker 05 the confusion about its partially double stranded DNA, and how we don't really know exactly, maybe, the rate of evolution or mutation. There's been a lot of work on this, I was happily surprised to find, especially recently. And so I'm going to try to bring us up to speed on what the current consensus is, relying mostly on two papers that came out in 2021 about the origins and evolution of the hepatitis B virus, one by Locornini et al. and the other by Kocher et al. Like you said, Erin, the hepatitis B virus belongs to the Hepatoviridae family. And in the years after the hepatitis B virus was first identified,
50:57 Speaker 05 researchers found viruses belonging to that family that infected birds, fish, reptiles and amphibians, other mammals, non-human primates, et cetera. Basically, this is a lot bigger and a lot older of a virus family than we thought. With, and there are some estimates that it originated around 82 million years ago.
51:19 Speaker 01 Whoa.
51:20 Speaker 05 So like, this thing was infecting birds.
51:23 Speaker 01 Dinosaurs.
51:24 Speaker 05 Essentially, yeah. Back when birds and dinosaurs were the same thing.
51:28 Speaker 01 Yeah.
51:30 Speaker 05 We're, I hope that that's probably not accurate. But you know what I mean. Eighty-two million years, let's stick with that.
51:37 Speaker 01 Yeah.
51:37 Speaker 05 So from 82 million years ago, how did it get into modern humans? And on that, there seems to be some debate. Surprise, surprise. For a long time, it was thought that hepatitis B virus originated in Africa, or for a while, it was thought maybe the Americas. And then it spilled over into humans, possibly from like a non-human primate, and then dispersed. Maybe it was dispersing out of Africa following prehistoric patterns of human migrations. But more recently, that assumption has been questioned. So one of the studies published in 2021 used hepatitis B virus detected in skeletal remains
52:22 Speaker 05 of 137 individuals found in Eurasia and the Americas and dating between 10,500 years ago and 400 years ago.
52:33 Speaker 01 What?
52:34 Speaker 05 That's some old viral DNA.
52:38 Speaker 01 I just love it when you find things like this, Erin.
52:41 Speaker 05 I know. It's, this paper was really interesting. It also had the most authors of any paper I've ever seen. I think it was 170 something.
52:50 Speaker 01 Oh, my goodness.
52:51 Speaker 05 Uh huh, uh huh.
52:52 Speaker 01 That's more than like the whole human genome paper.
52:57 Speaker 05 But I mean, it makes sense because I'm assuming that there was a lot of collaboration across many different universities with all of these remains, skeletal remains. So, okay, anyway, so what this paper, using all of these old skeletal remains with hepatitis B virus, did is that they wanted to reconstruct the evolutionary history and dispersion of the virus. And what they propose is that the most recent common ancestor of the hepatitis B virus dates back to around 12,000 to 16,000 years ago, which is more recent, actually, than was previously thought. And it places that most recent common ancestor in Eurasia,
53:40 Speaker 05 where over the next hundreds and thousands of years, it spread across Eurasia into Africa, through Europe, and to the Americas. It seems like the emergence of the hepatitis B virus and some of its spread happened before the Neolithic Revolution, which is when people began settling in larger groups and farming and so on. And if you think about it, this completely makes sense. Because what are some of the transmission characteristics that hepatitis B has, right? People can be carriers, it can be transmitted to a baby at birth, it can be spread during sexual contact or through blood, so like violent interactions
54:21 Speaker 05 or tattooing even. There are many different ways that this virus can be transmitted. And the fact that there are people who can carry it for long periods of time
54:32 Speaker 01 Right.
54:32 Speaker 05 means that it doesn't need this critical population size
54:36 Speaker 01 Mm hmm.
54:36 Speaker 05 to, in order to spread or persist in a population.
54:40 Speaker 01 Yeah.
54:41 Speaker 05 So in that way, it's a lot like a couple of the other viruses that we've talked about before, like the herpes simplex virus.
54:47 Speaker 01 Right.
54:48 Speaker 05 Or chickenpox virus. But once people began settling in larger groups around 7,000 to 8,000 years ago, that meant, of course, more opportunities for transmission, which led to an increase in the diversity of hepatitis B virus strains and the emergence of multiple genotypes or lineages. I'm not going to go into a ton of detail about this, but the paper that I keep mentioning by Kocher et al. actually traced the kind of like rise and fall of different hepatitis B virus lineages. So one, for instance, seemed to be the prevailing lineage in Western Eurasia for like 4,000
55:29 Speaker 05 years, but then it disappeared around 3,300 years ago. It just went almost extinct. No idea why, maybe sampling bias, maybe a reduction in human population that kind of like bottlenecked it or eliminated it, or maybe it was like intergenotype dynamics? Who knows?
55:48 Speaker 01 So interesting, Erin.
55:50 Speaker 05 It's, I, I find this so fascinating. And this pattern of genotypes going extinct and shifts in the predominant genotype, it still happens today. And we don't know for sure, but maybe it's partially due to the fact that some genotypes may be associated with certain transmission routes I've seen. And maybe some of the genotypes vary in their ability to cause severe disease or in their ability to cause this persistent carrier state. And so that's, I think, why it's really important to understand the origins and the evolutionary history of a virus like the hepatitis B virus. It can tell us in part why we see some of the epidemiological patterns that we see
56:33 Speaker 05 today, and it might be helpful for predicting what we could expect to see in the future.
56:40 Speaker 05 Okay, so we have this virus that has ancient roots and that had reached a global distribution a long time before the present day. And I already mentioned that evidence of hepatitis B infection has been found in ancient human remains dating back thousands and thousands of years, as well as just a couple thousand years, as well as more recent. So basically, it's kind of like persisted in human populations.
57:07 Speaker 01 Right.
57:07 Speaker 05 For all of that time.
57:09 Speaker 01 Yeah.
57:10 Speaker 05 But were the people who were around back then aware of this? Like, did they have any idea?
57:16 Speaker 01 Were they? Did they?
57:19 Speaker 05 Well, probably, in a sense. So jaundice, which can be caused by many different things, including the hepatitis B virus, has long been recognized and described in ancient medical texts. I'll toss in the Hippocratic texts from around 400 BCE because it's an episode of this podcast will kill you.
57:39 Speaker 01 We must do that.
57:41 Speaker 05 And outbreaks of jaundice were also written about. So one paper I read suggested that there was a description of what was likely infectious hepatitis dating back to the 8th century CE. And it was sometimes called campaign jaundice because it seemed prevalent during times of war. Surprise, surprise. But switching from talking about the evolutionary history of the hepatitis B virus to the written human history part, it's tricky because of the existence of other hepatitis viruses. Hepatitis.
58:16 Speaker 01 Hepatitis.
58:18 Speaker 05 We can test human remains for hepatitis B virus specifically, but we can't always know which hepatitis virus was causing whatever outbreak that was being described.
58:28 Speaker 01 Right.
58:29 Speaker 05 How likely was it that it was hepatitis B? In terms of outbreaks, I would guess actually that the hepatitis A virus, which is transmitted fecal orally, may have been the culprit more often than not, especially in crowded or unsanitary conditions like, you know, war.
58:48 Speaker 01 Yeah. And especially in any that were like acute infections.
58:54 Speaker 05 Yes.
58:54 Speaker 01 Right?
58:54 Speaker 05 Like, mm-hmm, exactly.
58:56 Speaker 01 Yeah.
58:57 Speaker 05 But it's certainly possible that hepatitis B and other hepatitis viruses transmitted through blood or bodily fluids caused outbreaks, especially as the use and reuse of needles became more popular.
59:12 Speaker 01 Yeah.
59:12 Speaker 05 Around the middle of the 19th century.
59:16 Speaker 05 So let's fast forward to then, the last decades of the 1800s.
59:20 Speaker 01 Let's.
59:21 Speaker 05 So this is like after the development of germ theory and after the introduction of some injectable vaccines.
59:29 Speaker 05 In 1885, an epidemic of jaundice followed a smallpox vaccination campaign among shipworkers in Bremen, Germany, which led to what seems like an early indication that hepatitis outbreaks could be caused by the reuse of needles or because this particular vaccine used like human serum as a stabilizing agent through like blood products.
59:54 Speaker 01 Right.
59:54 Speaker 05 But the link between the administration of this vaccine and the resulting hepatitis outbreak, it wasn't recognized for decades, possibly obscured by this longstanding recognition that epidemics of hepatitis or jaundice were also known to frequently happen in overcrowded unsanitary areas. So it was more difficult to pinpoint the vaccine itself as the cause, rather than like, oh, well, maybe they all went to the same
1:00:22 Speaker 01 watering hole.
1:00:24 Speaker 05 To the same, to the same watering hole where they all got hepatitis.
1:00:29 Speaker 01 Yeah.
1:00:30 Speaker 05 Yeah, but as blood transfusions increased and the practice of reusing needles persisted, there was this growing suspicion that an infectious hepatitis might also be carried in the blood or blood products. See our hepatitis C episode for more on the history of blood transfusions and the blood typing system and so on.
1:00:53 Speaker 01 Yeah.
1:00:54 Speaker 05 The differentiation of two different hepatitises, one called transfusion hepatitis and the other one being called infectious or food or waterborne hepatitis, this was finally made in the early 1940s. During World War II, hundreds of thousands of US Army personnel received the yellow fever vaccine, which, like the 1885 smallpox vaccine, had human serum as an ingredient. Obviously, that's no longer done for safety reasons. Needed to maybe clarify that. But after receiving this vaccine, 50,000 people came down with hepatitis, although those were just the clinically recognized cases.
1:01:39 Speaker 05 Later estimates put the total figure of hepatitis infections resulting from this vaccination campaign at around 330,000.
1:01:49 Speaker 01 Oh, dear. Okay. Oh, gosh. Oh, dear. Okay.
1:01:55 Speaker 05 It's a lot. It's a lot. And there was a British doctor named F. O. McCallum, who had been involved in the development and administration of this vaccine. And he hypothesized that it might have been transmitted by reusing syringes or carried in the vaccine itself. And he thought that this hepatitis represented a bloodborne infection, separate from the previously recognized food and waterborne hepatitis. He proposed that they be called hepatitis A and B, and that they may represent different viruses.
1:02:29 Speaker 01 So this is how it begins.
1:02:32 Speaker 05 This is how it begins. Because at the time, it was like not known whether it was the same virus or different viruses. And so it was more in like the clinical picture of it in a way. Because after this designation, after this recognition that like, hey, this might be transmitted through blood products and not just through like food and water or whatever. Other researchers began to describe differences in the way that these two hepatitis looked clinically. And to kind of keep an eye out more on the different routes of transmission.
1:03:08 Speaker 01 Right. Once you have it more like, hey, there are two different things here, then you start to notice more of the differences.
1:03:15 Speaker 05 Right. Once you create those like columns, then it becomes much easier to add to the list.
1:03:22 Speaker 01 Yeah.
1:03:22 Speaker 05 Mm hmm. But just because people now knew that hepatitis could be transmitted by reusing needles or via blood products, that didn't mean they could stop it from happening. Like I talked about in our hepatitis C episode, blood transfusion or blood product technology vastly outpaced our ability to identify many bloodborne pathogens, especially viruses, which led to blood products that were unknowingly contaminated. And often it was seen as this kind of situation where, you know, it was like, well, we don't know whether or not this batch of blood has hepatitis virus in it, but you can either receive the blood and possibly get hepatitis down the line,
1:04:07 Speaker 05 or not take the blood and die of blood loss immediately. So there was like no choice sometimes. There was no option.
1:04:16 Speaker 05 That's not to say that people weren't working on finding a way to test the blood supply and identify what was causing the hepatitis. If anything, it was that feeling of being powerless to protect people from this disease that created a sense of urgency in finding out what the hepatitis B agent was so that they could detect it in blood products. But despite a ton of people working on this, progress kind of stalled in the 1950s and early 1960s. And I think it stalled partially because this was a time when virology was kind of in its infancy as a field and the technology that would allow for genetic testing or sequencing was still decades away.
1:05:00 Speaker 01 I'm sorry, I just, I had, I don't know how I didn't know that it was so recent.
1:05:09 Speaker 05 I know.
1:05:10 Speaker 01 Like 1950s, 1960s, that's not a long time ago.
1:05:15 Speaker 05 It is, all of the hepatitis viruses are, like, have very recent identification dates, but have been recognized for decades before that. And it's just sort of this, like, constantly unfolding tragedy where you're just like, you see it and you're like, and they know, like, the people who were there at the time are like, I can't, like, this might have hepatitis virus in it, but I can't do anything about it.
1:05:42 Speaker 01 Right, but I don't, but I don't know it. I, like, I know it, but I can't know it.
1:05:49 Speaker 05 Mm-hmm. And we can also blame the virus itself because this isn't to say that virology research on all fields, on all viruses, had stopped or stalled by the early 1950s or 60s because some were easier to work with in a lab setting than others.
1:06:05 Speaker 01 Yeah.
1:06:06 Speaker 05 And hepatitis B virus doesn't really lend itself very well to culturing in a lab setting. And so it was just more difficult. And especially if you don't know even what you're looking for, how do you know that you're on the right track at all?
1:06:19 Speaker 01 Yeah, and it's a weird virus. We already said that.
1:06:22 Speaker 05 Yeah, it's a weird one.
1:06:23 Speaker 01 It's very weird.
1:06:25 Speaker 05 And at the time, it wasn't, people were using the term virus, but it wasn't known for sure whether it was a virus or something else. It was, like, known to be a virus in concept, but without physical proof. But by the end of the 1960s, that would change. And the team that led to the breakthrough identification of the hepatitis B virus would not have been on anyone's short or even long list of people that were likely to have done the job.
1:06:57 Speaker 01 Why? Who was it?
1:07:00 Speaker 05 Okay, I'll get there. But before we get into the unlikely story of the discovery of the Hep B virus, I want to quickly mention the Willowbrook State School hepatitis studies, which were these unethical experiments that are sometimes referred to as the pediatric Tuskegee.
1:07:19 Speaker 01 Oh, dear.
1:07:20 Speaker 05 Yeah, I'm going to be brief because these studies are mostly about hepatitis A. And so when we do a hep A episode, I'll go into more depth on them. But I wanted to bring them up here because these studies mark one of the major points in the history of medical ethics. And also hepatitis B was a part of these studies. So Willowbrook State School was a state-funded institution established in 1947 on Staten Island, New York, for children who were intellectually or developmentally disabled.
1:07:51 Speaker 01 Ugh, I hate this already, Erin.
1:07:53 Speaker 05 I know, I know, I know. In 1958, infectious disease physician Dr. Saul Krugman from New York University and Bellevue Hospital, he was asked to join Willowbrook to help figure out why there were such high rates of hepatitis among the children there. With something like 30 to 50% admitted there would end up getting hepatitis. And they also asked him to help bring those rates down. And so he agreed and set out to not only bring down the rates of hepatitis, but also to, quote, "describe the circumstances under which the disease occurred and the effect of gamma globulin in reducing its occurrence,
1:08:32 Speaker 05 and an attempt to induce passive-active immunity by feeding virus to persons protected by gamma globulin, and to describe the excretion of virus during the incubation period of the disease."
1:08:45 Speaker 01 Oh, dear.
1:08:46 Speaker 05 Your face tells me you've picked up on some of the
1:08:49 Speaker 01 Yeah.
1:08:50 Speaker 05 Yeah, problems with these studies intentionally infecting children.
1:08:55 Speaker 01 Yeah.
1:08:56 Speaker 05 So Krugman justified the research by saying that the children would inevitably get hepatitis anyway because it was so prevalent in the school, and that this way, with his experiments, a vaccine could be developed and tested. Parental consent was obtained, but it's not clear the extent to which parents were told of the risks to their children and what exactly was involved. By his own estimation, Krugman's studies reduced the incidence of hepatitis by 85%. Again, it's not entirely clear which hepatitis, but his study did demonstrate that there were two different types of hepatitis transmitted in different ways, which, like I said, was already kind of known, and also tested a prototype of a Hep B vaccine, which did seem
1:09:41 Speaker 05 to be somewhat effective. The legacy of the Willibrach hepatitis studies is that the resulting outrage led to very strict regulations placed on including children in clinical trials and medical studies and a more revamping of what could be considered medical consent. There's a lot more, of course, like I said, to these studies and their place in the history of medical ethics. And so if you're interested in learning more and don't want to wait for our hepatitis A episode, I will list some sources for this on our website. And there's also a paper that Krugman wrote and published in 1986 in which he defends himself in the research.
1:10:24 Speaker 05 So that's kind of an interesting read. There's like a lot of discussion about this and I didn't do it justice, so let me just say that. Wow. Yeah. Okay. Okay. Back to strictly hepatitis B. So by the 1960s, the hepatitis B virus had still not been identified, despite the fact that tons of people were working on this problem. And when it was finally discovered, it wasn't by one of those researchers who had dedicated their lives to hepatitis. Oh, no. But by a team who had not even been looking for hepatitis B or any other virus. What were they looking for?
1:11:09 Speaker 05 I feel like this story is such a good example of how science like rarely proceeds in an orderly fashion. It's not A to B to C.
1:11:20 Speaker 01 Yep.
1:11:22 Speaker 05 It's especially because B happens to be the first hepatitis virus discovered.
1:11:26 Speaker 01 Yeah, okay, I saw that on a timeline and I was like, whoa, whoa, whoa, hold on, hold on, hold on.
1:11:30 Speaker 05 I know.
1:11:31 Speaker 01 What?
1:11:31 Speaker 05 I was like, why is it called B then?
1:11:33 Speaker 01 Yeah, it doesn't make any sense.
1:11:37 Speaker 05 Yep, everything's just arbitrary.
1:11:39 Speaker 01 Okay, cool, cool, cool, cool.
1:11:40 Speaker 05 Yep.
1:11:42 Speaker 05 But yeah, it's like, we often tell, like, I'm including myself in that, these stories of scientific discovery in a very linear way, in a very like, here's this nice little pretty narrative packaged. And that neat narrative does serve a purpose because it kind of is like, well, let's find the important things, let's find the compelling things.
1:12:03 Speaker 01 Yeah.
1:12:03 Speaker 05 But that's not the way things happen. It's just simply not. And so this, I think, really illustrates that. Sometimes you're looking for one thing and you end up stumbling upon something that never even crossed your mind.
1:12:19 Speaker 01 Mm hmm.
1:12:20 Speaker 05 So, let's meet Dr. Baruch Bloomberg.
1:12:24 Speaker 01 Okay, hi.
1:12:26 Speaker 05 Since early in his career, Bloomberg became interested in why some people get sick and others don't. How genetics interacts with human behavior and the environment to lead to disease, basically.
1:12:41 Speaker 05 And he became interested specifically in polymorphisms. So these are genetic traits for which there are multiple forms. So things like tongue twisting. Can you twist your tongue?
1:12:52 Speaker 01 Yes.
1:12:53 Speaker 05 Me too.
1:12:54 Speaker 01 Cool.
1:12:56 Speaker 05 Blood types, what, what blood type are you?
1:12:57 Speaker 01 I'm O positive.
1:12:59 Speaker 05 I'm AB positive.
1:13:00 Speaker 01 I knew that about you.
1:13:02 Speaker 05 I knew that about you. So these are examples of polymorphisms, right? Like, there are different forms of these, and there are different distributions in human populations. And so he wanted to see whether there were any of these polymorphisms that were associated with susceptibility to certain diseases. So kind of like asking the question, do people with type A blood have a greater chance of developing heart disease? And if they do, why? But instead of blood types, which at this point had already been pretty well established, Bloomberg was interested in finding new blood plasma protein polymorphisms that could be associated with variation in disease susceptibility. So that's what he was looking for.
1:13:46 Speaker 01 He wasn't even looking for a virus?
1:13:49 Speaker 05 No, he was looking for blood plasma protein polymorphisms.
1:13:52 Speaker 01 Wow. I bet he found some proteins, all right.
1:13:56 Speaker 05 He certainly did. But how did he find these proteins?
1:14:02 Speaker 01 Yeah.
1:14:03 Speaker 05 Well, he began his search by collecting blood samples from people all over the world, and then testing them to see whether certain antigens appeared and in what frequency. Basically, you use the blood of someone who had received multiple transfusions to find antibodies against a protein antigen that was new to them. And then you test those antibodies against other blood samples to see how frequently it reacts, meaning how often that protein antigen is present.
1:14:35 Speaker 01 Yeah.
1:14:36 Speaker 05 And this might seem like a very crude approach today, in the days of like, you know, super inexpensive genomic sequencing.
1:14:44 Speaker 01 Yeah.
1:14:45 Speaker 05 But back then, these were the early, early years of genetics.
1:14:49 Speaker 01 I mean, we still do that to do like regular blood typing.
1:14:52 Speaker 05 Yeah.
1:14:53 Speaker 01 So it's like, still very useful.
1:14:56 Speaker 05 It is. So it is, it is super useful, but the approach, like the technology that he used, which was agar gel diffusion, it was basically like one of the only ones available at the time. Immunology was in its infancy.
1:15:09 Speaker 01 Uh huh.
1:15:11 Speaker 05 And so with this approach, Bloomberg and his team identified a new protein that they called the Ag protein, A-G for antigen. This protein, which they found to have an uneven global distribution, turned out to be a serum lipoprotein, so serum protein combined with fats, that may play a role in serum cholesterol and triglyceride levels. Maybe not a strong marker for disease susceptibility, but it was an encouraging finding. It showed that their technique, even though it was, you know, maybe a little bit kind of rough-handed, could be used to find new serum proteins. So they kept looking. For the next hunt, Bloomberg teamed up with a blood researcher named Harvey Alter,
1:15:55 Speaker 05 whose name you should recognize from our hepatitis C episode. Except, when I looked through my notes for his name, I didn't mention that he was the person who identified the hepatitis C virus, and I am so embarrassed. Like, that's kind of a fundamental, important person for the history of hepatitis C.
1:16:18 Speaker 01 I bet you talked about a lot of important things, Erin.
1:16:21 Speaker 05 I'm just, I'm ashamed.
1:16:23 Speaker 01 You know?
1:16:24 Speaker 05 But I am, I'm mentioning him here. And I also want to shout out that in 2020, he was awarded the Nobel Prize for his role in hepatitis C research.
1:16:35 Speaker 01 Oh.
1:16:35 Speaker 05 Pretty cool.
1:16:36 Speaker 01 Wow.
1:16:37 Speaker 05 Yeah. So anyway, Alter, who was in the beginning of his career in the early 1960s, he was interested in why some people developed an immune response, like a fever, chills, rash, et cetera, after receiving a transfusion.
1:16:53 Speaker 01 Ooh.
1:16:54 Speaker 05 Yeah, interesting stuff. And it took a little bit of time, a little trial and error, but Alter and Bloomberg found another polymorphism. And this, they named "Australia antigen", because it was first found in the blood serum of a First Nations person from Australia. And we've talked about the problem with place names to describe a disease loads of times before. However, I want to point out that at the time, this Australia antigen was just thought to be a human protein, not necessarily an actual pathogen, which, surprise, spoilers, it turned out to be. But in any case, the name "Australia antigen", it didn't stick around for very long,
1:17:37 Speaker 05 because it was soon shown that the Australia antigen was actually the hepatitis B virus.
1:17:43 Speaker 01 I love this story.
1:17:45 Speaker 05 I know. I know. It's, I just think it's so amazing. It's like, I don't know. It's just such a fun story. So how did they make this connection? Well, first, after finding this new protein, they decided to look at its geographic patterns of prevalence, just like they had for their earlier ag protein, which, you know, was it more common in some areas or in some populations than others? And they did find variation in the global distribution. They found that the Australia antigen seemed to be somewhat rare in the US blood samples that they had, but it was a little bit more common in parts of Asia, in the Pacific, Africa, and Eastern and Southern
1:18:27 Speaker 05 Europe. They also showed that the antigen seemed to cluster in families, which at first glance suggested that it was an inherited trait, but as more data came in, that assumption kind of broke down.
1:18:42 Speaker 01 Ugh, yeah.
1:18:44 Speaker 05 Uh huh. Bloomberg and his team began getting suspicious that it might not be a human protein after all, but rather an infectious agent, one that was possibly bloodborne, as they had found it in several people who had at first tested negative for the antigen, but later tested positive shortly after receiving a blood transfusion.
1:19:05 Speaker 01 Oh, no.
1:19:08 Speaker 05 And then the connection to hepatitis B fell into place when they began to find the antigen at high rates in people who had hepatitis.
1:19:17 Speaker 01 Hmm, okay.
1:19:19 Speaker 05 Especially those with a history of transfusion.
1:19:21 Speaker 01 Mm-hmm.
1:19:23 Speaker 05 By 1965 or so, they had become convinced that they had finally found the long sought after hepatitis B virus, almost by accident.
1:19:32 Speaker 01 Wow.
1:19:32 Speaker 05 Truly by accident, really.
1:19:34 Speaker 01 Yeah.
1:19:35 Speaker 05 And they sent off a couple of papers to be published. One was outright rejected with a reviewer commenting that there simply wasn't enough evidence in support of their hypothesis. And now we look back on this and go, that's absurd. How could this monumental finding be rejected? But if you consider this in the larger context of the time, it does seem like it was kind of like a boy who cried wolf scenario. People were always submitting articles saying, I have found the hepatitis B virus. I have found it. It's this. It's this. Kind of like how I feel like every few months nowadays, there's an article saying the Zodiac Killer has finally been identified.
1:20:18 Speaker 05 It's like, okay, let's if we dig a little deeper, like, is it true? Or is it not so close to the truth? But another reason for the rejection, and this one is much more unfair, is that Bloomberg and his group were in no way part of the hepatitis B scene. They had no background in studying hepatitis. None of them had been trained as epidemiologists, let alone virologists. So what did they know about hepatitis?
1:20:48 Speaker 01 Yeah.
1:20:48 Speaker 05 But despite this initial rejection, and the resentment from some prominent hepatitis researchers, they managed to get a paper published in 1967 that awakened the world to the possibility that the virus causing transfusion hepatitis, the hepatitis B virus, had finally been found.
1:21:08 Speaker 01 1967.
1:21:11 Speaker 05 Mm hmm.
1:21:12 Speaker 01 Wow.
1:21:13 Speaker 05 Yeah. And this seems like an understatement, but this was huge news.
1:21:19 Speaker 01 Yeah.
1:21:19 Speaker 05 At the time, post-transfusion hepatitis rates reached 30%.
1:21:24 Speaker 01 Oh, my.
1:21:26 Speaker 05 Mm hmm. The beginnings of the incredible prevalence of global hepatitis that we have today really does have its roots during this time, during this time when there was a lot of blood transfusion happening, a lot of blood products being used, a lot of needles being reused without knowing what the virus was, how to test for it, how to how to prevent it. So it's, yeah.
1:21:51 Speaker 05 But there was still another step, and that was confirmation from other researchers. Boom, easily done, check. Here's hepatitis B.
1:22:01 Speaker 01 The end.
1:22:03 Speaker 05 Almost the end, actually. The discovery of the hepatitis B virus, this allowed not only for the testing of hepatitis B virus in blood products, but also the identification of carriers of the virus and the eventual development of a vaccine.
1:22:22 Speaker 05 This isn't to say that it was all smooth sailing after the link between the Australia antigen and the hepatitis B virus was made. For instance, the virus was still not able to be maintained in conventional tissue cultures, which made fulfilling coxposetolus difficult. And the test for determining whether or not the virus was present were pretty insensitive at the time. Like, I've seen estimates of 15 to 20%
1:22:49 Speaker 01 Oh.
1:22:49 Speaker 05 of the time it would detect hepatitis B virus. Yeah.
1:22:53 Speaker 01 That's pretty bad.
1:22:54 Speaker 05 It's gotten a lot better, we should point out.
1:22:57 Speaker 01 Yes.
1:22:57 Speaker 05 A lot, lot better. Like, very good. Like, excellent.
1:23:01 Speaker 01 Yep.
1:23:03 Speaker 05 And as I always talk about, there's typically this delay from when something new is discovered to when there is wide enough acceptance for that knowledge to be applied, especially in like a medical setting. So screening the blood supply for hepatitis B, even with this, you know, pretty poor test, didn't start for a few years after the virus was discovered. So in 1970, the hepatitis B virus test became official in the US. And in 1972, the American Association of Blood Banks had begun to require the testing of donors. And even though the test desperately needed to be improved, that was a good start.
1:23:44 Speaker 05 But being able to test for hepatitis B virus also meant that it could identify people who were carriers or infected with hepatitis B, which then led to widespread discrimination and ostracization for people who were positive for hepatitis B. People were fired from jobs. They were not allowed in classrooms. Children were taken off adoption lists. People were being denied health care from shared machines like dialysis machines. They were being denied admittance to medical school or kicked out of their jobs as doctors or dentists. I mean, the list goes on and on. It was just like, oh, great. We have this test. We can help prevent hepatitis. And also, we can put the scarlet letter of hepatitis
1:24:29 Speaker 05 on every single person that we test.
1:24:32 Speaker 01 I feel like that part of hepatitis B especially is so overlooked today.
1:24:39 Speaker 05 Mm hmm.
1:24:40 Speaker 01 Like,
1:24:40 Speaker 05 Yeah.
1:24:42 Speaker 01 Yeah.
1:24:43 Speaker 05 And yeah, a lot of these, many or most of these restrictions or regulations have been overturned. But the stigma and isolation faced by many people with hepatitis B continues today and has a huge detrimental impact on their quality of life. Right after the hepatitis B virus was identified, many people began working on a hepatitis B vaccine, including Bloomberg and his colleague, Dr. Irving Millman, who came out with one in 1969. And over the next decade, people would work on refining the vaccine and incorporating it into routine vaccine schedules. And I think since then, it's kind of faced like continuous like tweaking. And we've gotten a pretty solid, from my understanding, hepatitis B
1:25:28 Speaker 05 vaccine.
1:25:29 Speaker 01 Yeah, since 1981 was when the hepatitis B vaccine was licensed, like, in the US, widespread by the FDA. And then 1986, it was updated to not have any, like, human
1:25:43 Speaker 05 Mm hmm.
1:25:44 Speaker 01 parts in it, essentially.
1:25:46 Speaker 05 Right.
1:25:47 Speaker 01 It's, it's made in a yeast, and it's a recombinant vaccine. And as far as I know, it's the same vaccine since 1986.
1:25:54 Speaker 05 Do you know who helped work on the yeast aspect of it?
1:25:58 Speaker 01 Tell me who, Erin.
1:26:00 Speaker 05 Maurice Hilleman, our friend.
1:26:02 Speaker 01 Oh, let's hear it for Maurice.
1:26:04 Speaker 05 Let's hear it for Maurice. And I already mentioned one person in this story who was the recipient of a Nobel Prize for their work on hepatitis viruses, and that was in 2020. But in 1976, Dr. Baruch Bloomberg was awarded the Nobel Prize in Physiology or Medicine for his work in identifying the hepatitis B virus.
1:26:26 Speaker 01 Love it.
1:26:27 Speaker 05 Also, that same year, it was co-awarded to two different people just to, you know, that didn't have any work together. The other person awarded was Carlton Gadzasek. Do you remember him from "Prions," the bad, the bad guy?
1:26:42 Speaker 01 Oh, yes, I do. Uh huh.
1:26:48 Speaker 05 Over the decades since the discovery of the hepatitis B virus, there's been a great deal of research on understanding transmission dynamics, genotype differences, the cancer-causing potential of the hepatitis B virus, new hepatitis viruses like hepatitis D, like hepatitis C, like hepatitis E, better blood tests, improved vaccines, harm reduction programs, and a growing recognition of the tremendous global burden that this virus has in a physical, economic, and emotional sense. And despite all of the advancements made in the field of hepatitis B research, the virus is still extraordinarily prevalent,
1:27:31 Speaker 05 and transmission continues today. So Erin, that was kind of a quick wrap-up to the future, but I want to hear where we stand with hepatitis B today. So can you fill me in?
1:27:48 Speaker 01 Oh, I can't wait to, right after this break.
1:28:24 Speaker 01 Unlike our first three episodes, I have some, a lot of statistics for this section aired.
1:28:34 Speaker 01 First three episodes of the season, I mean. But they're pretty sobering.
1:28:39 Speaker 05 Okay.
1:28:40 Speaker 01 Globally, it is estimated that close to 4% of the entire world's population is living with chronic hepatitis B infection.
1:28:55 Speaker 01 That is close to 300 million human beings.
1:29:03 Speaker 01 And believe it or not, that's an improvement because the very first paper I read was a bit older from 2004. And that started off by saying over 400 million people. So we're down.
1:29:15 Speaker 05 So those are people chronically infected.
1:29:18 Speaker 01 Right, living with chronic hepatitis B.
1:29:20 Speaker 05 And how many people are infected newly every year? What's the incidence?
1:29:24 Speaker 01 The World Health Organization estimates 1.5 million people are newly infected every year.
1:29:32 Speaker 05 Wow, that's...
1:29:33 Speaker 01 Yes.
1:29:36 Speaker 01 It's horrific. If we look at the entire spectrum, or the whole alphabet of hepatitis, or viral hepatitis is. Viral hepatitis caused an estimated 1.34 million deaths in 2015 alone, which is more than HIV. It is substantially more than malaria, and it's nearly as much as tuberculosis.
1:30:05 Speaker 05 So why does it feel like it's not talked about?
1:30:09 Speaker 01 Why, Erin, I don't know. Okay. And that's all of the viral hepatitis, hepatitis.
1:30:16 Speaker 05 Okay.
1:30:17 Speaker 01 Of all of those deaths, 96% are estimated to be from chronic hepatitis. And of that 96%, 66% of those are from hepatitis B. So if we do some Erin math, just kidding, just kidding, the World Health Organization did this math. That is 820,000 humans
1:30:43 Speaker 05 Wow.
1:30:43 Speaker 01 that are dying from chronic hepatitis B infection every single year.
1:30:54 Speaker 01 Now, you asked why we're not talking about it.
1:30:57 Speaker 05 Yeah.
1:30:57 Speaker 01 Here's probably a large part of it. That burden is not borne equally across the globe.
1:31:03 Speaker 05 Of course not.
1:31:04 Speaker 01 The World Health Organization, you know, divides the globe into different regions. The Western Pacific region by far has the highest incidence and prevalence of hepatitis B, followed by the World Health Organization African region. And in these areas, the prevalence can be as high as 6% or greater in some cases.
1:31:26 Speaker 05 Wow. Oh, my gosh.
1:31:27 Speaker 01 Whereas in some parts of the world, like in Europe or in North America, the prevalence may be less than 1%. And so I think that huge global discrepancy can lead for some countries to not think a lot or talk a lot about hepatitis B.
1:31:44 Speaker 05 Yeah, it's, oh, well, it's not a problem here, so.
1:31:49 Speaker 01 Exactly, Erin. I think I wrote those exact words later on. Yeah. And it gets more sobering because it's also estimated that only 10%, 10 and 1/2% of people that are living with hepatitis B know their status.
1:32:11 Speaker 01 And it's also estimated that only 22% of those that are diagnosed that know their status are on treatment for chronic hepatitis B. That statistic I want you to take with a grain of salt because not everyone who is diagnosed with chronic hepatitis B necessarily needs treatment, at least not right away. So that statistic at least might not be quite as bad as it sounds, but 10% of people knowing their status is pretty bad.
1:32:39 Speaker 05 Yeah, that's, I mean, that's, yeah.
1:32:43 Speaker 01 Yeah. It's also, I have more numbers, this is a number heavy one. And these numbers are from a modeling study from 2016 data. But of this, almost 4% of the global population that is infected with chronic hepatitis B, between 1.6 to 2.2 million are children under the age of five.
1:33:10 Speaker 05 Mm hmm.
1:33:12 Speaker 01 And the World Health Organization's most recent data does suggest that it's now finally just under 1% of all children worldwide, under age five, that are chronically infected. That's down from around 5% of all children in the pre-vaccine era.
1:33:29 Speaker 05 Oh, my gosh.
1:33:30 Speaker 01 I know. And still, like, just under 1%, essentially 1% of all kids under age five globally, living with this chronic infection, that I can't emphasize enough, is entirely preventable at this point. We have had a vaccine for hepatitis B that is 98 to 100% effective for 17 to 30 years. Like, not a lot of waning immunity, incredibly effective vaccine for 40 years.
1:34:09 Speaker 05 So I have a question about that. So is it part of every single routine vaccine schedule?
1:34:17 Speaker 01 Over 180 countries have hepatitis B as part of their universal vaccine program. And it's estimated that 87% of infants worldwide received the three-dose Hep B vaccine series in their first year of life, which is great. But only 46% likely had a timely birth vaccination, that critical 12 to 24 hour window. And even less, the study estimated about 13% got both the hepatitis B vaccine and if needed, that IVIG to actually treat and provide more passive immunity.
1:34:58 Speaker 05 Right.
1:34:59 Speaker 01 But with IVIG and the vaccine within 12 to 24 hours of birth, it's still about 91% effective to prevent Hep B infection in those babies. But it's even more effective if you can treat the pregnant person to lower their viral load.
1:35:19 Speaker 05 Okay.
1:35:21 Speaker 01 And it's estimated that only about 1% of pregnant people are actually getting that testing and then treatment.
1:35:27 Speaker 05 1%?
1:35:29 Speaker 01 Yeah, 1% or less. And so that contributes a lot to the overall burden and why we still have such high infection rates.
1:35:40 Speaker 05 Mm hmm. We have the tools, just not the delivery.
1:35:43 Speaker 01 Yeah. So we have a lot of improvements to still be made.
1:35:49 Speaker 05 Yeah.
1:35:50 Speaker 01 Overall, like this is a massive, massive disease. I honestly didn't even realize how massive it was before researching for this episode. And because it's such an enormous global problem, I'm glad that we were able to highlight so many different parts of this really important disease. But there are still several aspects that we didn't fully cover in this episode, especially the substantial stigma and discrimination faced by so many people living with hepatitis B around the world.
1:36:21 Speaker 05 Right. And because this is such an important part of the hepatitis B story, I am so excited to be able to take a deeper dive into it in a bonus episode coming out next week.
1:36:34 Speaker 01 Woo woo, you heard that right, bonus episode.
1:36:38 Speaker 05 So I enlisted the help of the amazing Dr. Sherri Cohen, who is Senior Vice President of the Hepatitis B Foundation, to discuss some of the drivers of stigma and discrimination in hepatitis B and what's being done about it. I also got to pick Dr. Cohen's brain about what it's like to work in the public health nonprofit world, what the difference is between a doctor of public health and a PhD is, and some fantastic advice for people who might be interested in pursuing a career in public health.
1:37:08 Speaker 01 And we know there's a lot of you out there.
1:37:10 Speaker 05 There's a lot of you out there, yes. It was so much fun chatting with Dr. Cohen, and you should definitely mark your calendars so you don't miss the EP. It comes out next Tuesday, February 1st. Okay, but should we maybe wrap up this episode for now?
1:37:26 Speaker 01 I think we should. Time for sources?
1:37:29 Speaker 05 It is, all right. So I have a lot of papers for this, and I'll post them all on our website. But I do want to shout out one book in particular, and that is, of course, Hepatitis B: The Hunt for a Killer Virus by Dr. Brueck Blumberg.
1:37:47 Speaker 01 I have a few papers, not as many for this as some episodes, but a few really nice review papers. Most of them are from The Lancet, and they've just been like updates on each other. So the most recent one that I read was published in 2018 and called Chronic Hepatitis B Virus Infection. Has a lot more detail about the different phases of chronic infection. And we'll post the sources for this episode and every one of our episodes on our website, thispodcastwillkillyou.com.
1:38:15 Speaker 05 We sure will. A big thank you again to Dr. Wong for taking the time to chat with us and being willing to share your experiences with hepatitis B. And also, thanks for all the awesome work you do.
1:38:28 Speaker 01 Yeah, thank you so much. Thank you also to Blood Mobile for providing the music for this episode and all of our episodes.
1:38:36 Speaker 05 And thank you too, exactly right, of whom we are a very proud member.
1:38:40 Speaker 01 And thank you, of course, to you, listeners. We love making this podcast, and we couldn't do it if you didn't listen to it.
1:38:48 Speaker 05 That's very true. And also, an extra big thank you, as always, to our wonderful patrons. We love you. You're amazing.
1:38:57 Speaker 01 We love it.
1:38:58 Speaker 05 Okay, well, until next time, wash your hands.
1:39:02 Speaker 01 You filthy animals.
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