Speaker 1: My name is su Wang. I am a physician. I'm
Speaker 1: an MD MPH. I'm the medical director for the Center
Speaker 1: for Asian Health and Viral Hepatitis Programs at the Cooperman
Speaker 1: Barnabas Medical Center in New Jersey. And I'm also just
Speaker 1: coming off a two year presidency for the World Hepatitis Alliance,
Speaker 1: which is a nonprofit organization that represents patients living with
Speaker 1: viral hepatitis. And our goal is to harness the power
Speaker 1: of people living with viral hepatitis to achieve global elimination
Speaker 1: of viral hepatitis. I was diagnosed with hepatitis B in college.
Speaker 1: In my first year of college, I went to donate blood,
Speaker 1: right to do a good thing, donate blood, and shortly
Speaker 1: after I got a big, fat envelope sent to my
Speaker 1: dorm and it said, don't be worried. You don't have HIV,
Speaker 1: but you do have hepatitis B. And I was a
Speaker 1: pre med student, but honestly I didn't know anything about
Speaker 1: hep BEE. I called my sister, confided in her about
Speaker 1: this new diagnosis, and she said, oh, didn't you know
Speaker 1: Mom also has hep BE. And then I just I
Speaker 1: just remember thinking, Oh, who do I need to tell
Speaker 1: and when I went back home, I did go see
Speaker 1: a doctor and talked to her about it, and I
Speaker 1: think she did blood work and basically said I was
Speaker 1: a carrier and there was nothing to worry about. So
Speaker 1: I honestly pushed it to the back burner. Didn't want
Speaker 1: to think about it, so it didn't come up again
Speaker 1: until med school. I filled in all my med school
Speaker 1: forms and a lot of our employment forms and our
Speaker 1: screenings for working at a hospital. You do have to
Speaker 1: indicate you know what your heppy vaccination and statuses. And
Speaker 1: I had indicated that I was a carrier and didn't
Speaker 1: hear anything about it. I didn't think anything of it.
Speaker 1: And it's not untill now that I've heard numerous people
Speaker 1: who are in med school found out to have happy
Speaker 1: and actually they lose their acceptances to med school or
Speaker 1: they faced quite a bit of what I would consider
Speaker 1: discrimination over their status.
Speaker 2: Uh.
Speaker 1: And it's happened to residents, it's happened to nurses, it's
Speaker 1: happened to dental students. So it is an issue of
Speaker 1: stigma and discrimination. But I was fortunate it didn't happen
Speaker 1: to me, and kind of was in the back of
Speaker 1: my mind and I remember kind of when we learned
Speaker 1: about hepatitis is kind of listening a little bit more attentively.
Speaker 1: And when I got to residency after med school, I
Speaker 1: became really good friends with somebody. A friend of mine
Speaker 1: went into infectious disease, and I had confided in her
Speaker 1: that I had happatitis B and she told me, oh,
Speaker 1: make sure you see a doctor for it. I hadn't
Speaker 1: seen a doctor in years at that point. So I
Speaker 1: went in to see somebody and they did my viral
Speaker 1: load and I did the ultrasound and everything was fine.
Speaker 1: It was very low. I didn't need medication. And at
Speaker 1: that point, I remember, I was engaged, I think, and
Speaker 1: so my friend had said, oh, make sure your fiance
Speaker 1: also gets to and he ended up getting tested and
Speaker 1: needing to get vaccinated, and you know, so that was
Speaker 1: kind of the extent of how it impacted my life.
Speaker 1: And I had told him about it, and I was,
Speaker 1: you know, I was happy that he was. He didn't
Speaker 1: make a big deal out of it, and these are
Speaker 1: all points Now looking back, I realized, you know, I
Speaker 1: was fortunate, and so many people around the world are
Speaker 1: not so fortunate to have, you know, a career that's
Speaker 1: not affected by it, or a relationship that's not affected
Speaker 1: by it. You know, there are a lot of people
Speaker 1: who you know, lose their partners, they end up, they
Speaker 1: may get divorced, they may get disowned by family or
Speaker 1: unable to pursue the career they went to.
Speaker 2: So I didn't have.
Speaker 1: Any of that, and I got married and we got pregnant.
Speaker 1: I've had four kids, and with each one of those kids,
Speaker 1: especially the first one, it did hit me that, oh,
Speaker 1: I know, there's a chance that I could pass this
Speaker 1: affection on to my children, and that definitely weighed heavily
Speaker 1: on me. Although I knew the research that because my
Speaker 1: viral load was low, there would be very low chants
Speaker 1: of the developing hep BE. But that's where I really
Speaker 1: all of a sudden felt like, oh my gosh, you know,
Speaker 1: this could really impact me personally. And I'm happy to
Speaker 1: say that all for my kids are heap BE free
Speaker 1: and that they don't have to live with this chronic
Speaker 1: disease and worry about risk of lover cancer and other
Speaker 1: things that other kids have to go through even now
Speaker 1: in this day and age. And so as a physician,
Speaker 1: I didn't particularly have an inkling that I was going
Speaker 1: to do hepatitis work at all, And it wasn't until
Speaker 1: I moved to New York City after I finished my
Speaker 1: residency and I took a job with a community health
Speaker 1: center in Chinatown. So I began serving the largely Chinese
Speaker 1: community in Chinatown and learned so much more about HEPBE
Speaker 1: than I ever knew. That it's, you know, one of
Speaker 1: the most common infectious diseases around the world. Up to
Speaker 1: like one in ten of our patients had heppy was
Speaker 1: as common as hypertension. And whereas I had seen specialists,
Speaker 1: you know, during residency, a lot of our patients could
Speaker 1: not afford to see a specialist and they weren't necessarily
Speaker 1: easily accessible. So many of us at the community health
Speaker 1: center learned to treat hep BEE along with hypertension, diabetes,
Speaker 1: and other chronic diseases. So during that time, I really saw,
Speaker 1: you know, a lot of the difficulties that people face
Speaker 1: and getting care, and so I began really advocating and
Speaker 1: creating programs that would help people living with hepatitis. Be
Speaker 1: to increase screening in the communities, linkage to care, all
Speaker 1: these things that can happen in a very complex medical system.
Speaker 1: We tried to create a program to kind of streamline
Speaker 1: all of that. As I was getting more and more
Speaker 1: immersed in, you know, really providing the care that needs
Speaker 1: to happen, I really had the hat on, like, you know,
Speaker 1: the physician hat, like this is what needs to be done,
Speaker 1: these are the interventions, this is the science behind it.
Speaker 1: I did not wear the patient hat at all in
Speaker 1: terms of what it meant for me, and I kind
Speaker 1: of didn't feel like that that was my role, and
Speaker 1: it wasn't until somebody did an interview. Actually, I did
Speaker 1: an interview for CDC, and it was the first time,
Speaker 1: like on camera that I had I said, you know,
Speaker 1: I'm actually living with hepatitis B myself. And at that
Speaker 1: point I had already occasionally mentioned it to patients. So
Speaker 1: if I was counseling a patient who had been newly
Speaker 1: diagnosed with HEPPY and I could see they were really
Speaker 1: distraught or felt really overwhelmed, I would share with them
Speaker 1: that I also was living with hep BEE. I was
Speaker 1: just like them. I had to go for blood tests,
Speaker 1: and I think that really helped them see that it's
Speaker 1: possible to live a happy, healthy life and it's not
Speaker 1: a death sentence. So I was using that more often,
Speaker 1: but I'd never spoken about it publicly, so it took
Speaker 1: me a while.
Speaker 2: And what I've seen.
Speaker 1: As a physician, which I think as physicians we don't
Speaker 1: quite get, is just how powerful that personal experience is.
Speaker 1: And I have only learned this through other people. Somebody
Speaker 1: asked me to get involved with the World Hepatitis Alliance,
Speaker 1: which is led by patients, and through that on the board.
Speaker 1: The board is all patients who represent each of the
Speaker 1: WHO regions. And I heard specifically from a good friend
Speaker 1: of mine who was now a good friend of my
Speaker 1: d lee, who represented the Whippo region, the Western Pacific region.
Speaker 1: He told me all these stories of people who really
Speaker 1: had happy drastically empire their life in ways that us
Speaker 1: in medicine don't measure, right. We measure the outcomes. We
Speaker 1: look at our morbidity, mortality, life expectancy right soorrhosis, lever cancer.
Speaker 1: We don't look at outcomes in terms of somebody's quality
Speaker 1: of life. You know, when I hear these stories of
Speaker 1: how people have suffered with the burden of the disease,
Speaker 1: even if they are I mean, as a doctor, if
Speaker 1: you were to look at them, they would look healthy.
Speaker 1: You would tell them they're perfectly healthy, their liver enzymes
Speaker 1: are normal, their viral load is low, like you know,
Speaker 1: I only need to see you once a year, You're fine.
Speaker 1: You know, in our mind we think it's we think
Speaker 1: it's nothing like if you were to then delve into
Speaker 1: how they feel about themselves, and most patients won't even
Speaker 1: tell me that. So I know that what I see,
Speaker 1: what I glimpse in my exam room is just such
Speaker 1: a small part of what it means for them to
Speaker 1: live with a disease. And so you know, it's beyond
Speaker 1: just like keeping them from getting sorosis and liver cancer.
Speaker 1: You know, us in medicine, if we're if our mission
Speaker 1: is to prove quality of life and decrease burden of
Speaker 1: disease on people's lives, we have to think outside just
Speaker 1: you know, our our biochemical tests. I think, you know,
Speaker 1: I've just learned that we can't afford to operate in
Speaker 1: our silos. Right the scientists cannot afford to operate in
Speaker 1: you know, their silos only like publishing to the scientific
Speaker 1: community and having meetings that are only for scientists and
Speaker 1: medical researchers. But we have to get out of the box.
Speaker 1: We have to combine, you know, the people living with
Speaker 1: the disease have to work in concert with the medical
Speaker 1: community if we're really going to make progress for elimination
Speaker 1: and for uh you know, really alleviating the suffering of
Speaker 1: be on people's lives.
Speaker 3: Thank you so much, doctor Wong for sharing your story.
Speaker 2: Thank you. Hi.
Speaker 4: I'm Aaron Welsh and.
Speaker 2: I'm Aaron Alman Updyke.
Speaker 3: And this is this podcast will Kill You.
Speaker 2: Welcome to another episode.
Speaker 4: Yes, welcome, Welcome.
Speaker 3: As you have probably gathered, we are going to be
Speaker 3: talking about another hepatitis virus, our second podcast history.
Speaker 2: Yes, this one hepatitis B. Yeah, we started with C.
Speaker 2: Now we're going to be what's next? Uh, well, I
Speaker 2: am going to mention D. I've figured I think next
Speaker 2: will be A.
Speaker 3: Yeah, next will definitely be A, and then we'll have
Speaker 3: to do E and then maybe by the time that
Speaker 3: comes out, there'll be a few.
Speaker 4: More and we can cover all in one quite possible. Well, Aaron,
Speaker 4: what time is it?
Speaker 2: It's quarantiny time, Aaron.
Speaker 4: It is. And what are we drinking this week?
Speaker 2: We're drinking the beasting.
Speaker 3: We are appatitis B, hepatitis B.
Speaker 4: And what is in the beasting?
Speaker 2: Well, It's a lovely little bev a ginger mint syrup,
Speaker 2: some lemon juice, club soda. If you're drinking alcohol, you
Speaker 2: could certainly put some gin in it.
Speaker 3: That will be the little sting, But otherwise on its own,
Speaker 3: it is delicious, very refreshing.
Speaker 4: I just I love it.
Speaker 3: And we will post the full recipe for this quarantini
Speaker 3: as well as our non alcoholic Placey Brita on our
Speaker 3: website This Podcast will Kill You dot com, as well
Speaker 3: as on all of our social media channels.
Speaker 2: On our website This Podcast will Kill You dot Com,
Speaker 2: you will find any and every of the things that
Speaker 2: you ever wanted to know about the podcast. You can
Speaker 2: find Bloodmobile, who does all of our music, and the
Speaker 2: link to their Spotify. You can find merch all of
Speaker 2: our merch. You can find transcripts for all of our episodes.
Speaker 2: You can find a bookshop dot org affiliate account, and
Speaker 2: a good Reads list. You can find all you're doing
Speaker 2: great things for all of our episodes. Thanks. I need
Speaker 2: the encouragement, and you can find our Patreon.
Speaker 3: Wow, that was impressive.
Speaker 2: Thank you. Thanks.
Speaker 4: I'm always relieved when I don't have to do it.
Speaker 2: I always get really nervous and then I just power through.
Speaker 4: I like it.
Speaker 3: It's like you get in the zone and then you're there.
Speaker 3: Well before we get into the episode, I wanted to
Speaker 3: mention one thing because Endometriosis, which was the last episode
Speaker 3: we released, is still on my mind. Even though I've
Speaker 3: been reading a lot about happatitis B, I still have
Speaker 3: these like little thoughts of endo that pop in, and
Speaker 3: I realized that there was like one more thing that
Speaker 3: I wanted to say. Also, like endometriosis, we've recorded it,
Speaker 3: it's not yet released, and so maybe people will have
Speaker 3: already said this by the time this comes out. It's
Speaker 3: sort of a weird time travel thing we're doing here. Yeah,
Speaker 3: But in the endometriosis episode, we talked about how often
Speaker 3: complete or partial hysterectomy is recommended as like a cure
Speaker 3: for endometriosis, which it isn't, and which that can also
Speaker 3: add another dimension of pain and anguish to an already
Speaker 3: difficult disease. But I also think that another aspect to
Speaker 3: that that we didn't really touch on, and I think
Speaker 3: is important to mention, is that there can also be
Speaker 3: a reluctance on the part of physicians to perform hysterectomies,
Speaker 3: or even just tubal ligations, like getting your tubes tied
Speaker 3: for whatever reason. Even if that reason is I don't
Speaker 3: want to have any children or any more children, a
Speaker 3: lot of people are just told, oh, you're just too young.
Speaker 3: You might change your mind and want to have kids
Speaker 3: in the future. And so really that's sort of another
Speaker 3: way in which many times physicians don't fulfill the very
Speaker 3: basic requirement of listening to their patient and how the
Speaker 3: social and gender role of someone can be held as
Speaker 3: more important than what they want than their wishes. Yeah, anyway,
Speaker 3: that just kept like circulating in my head and I
Speaker 3: was like, oh, gosh, I need to say it.
Speaker 4: So yeah, okay, got it out.
Speaker 2: Yeah, that's an incredibly important point.
Speaker 3: Okay, should we move on to the actual topic of
Speaker 3: today's episode.
Speaker 2: Today's topic hepatitis B. Let's take a quick break and
Speaker 2: then get into the biology. So, like you mentioned erin,
Speaker 2: this is our second hepatitis virus. And I know for
Speaker 2: sure that during our hepatitis C episode we talked at
Speaker 2: least a little bit about how all the hepatiti all
Speaker 2: the hepatitis viruses are named, not for anything that links
Speaker 2: the particular viruses together, aside from the fact that they
Speaker 2: all predominantly affect the liver. So there are five predominant
Speaker 2: viruses which we kind of already named at the beginning, A, B, C, D,
Speaker 2: and E. And today we're focusing on hepatitis B, and
Speaker 2: I will mention hepatitis D and you'll understand why in
Speaker 2: a minute if you don't already know the little interplay
Speaker 2: between hepatitis D and B. All right, hepatitis B. It's
Speaker 2: in the family Hepadnaviridae, which essentially just means viruses that
Speaker 2: affect the liver, like no surprise, straightforward. One thing that's
Speaker 2: there's a lot of interesting things about the virology of
Speaker 2: hepatitis B, and I'm probably not even going to do
Speaker 2: them justice, but here we try. Hepatitis B virus is
Speaker 2: a partially double stranded DNA virus, which is weird. So
Speaker 2: it has a genome that it's like in a little circle,
Speaker 2: and part of it is double stranded and part of
Speaker 2: it is single stranded, which is very bizarre. Do you
Speaker 2: have a question already? Erin, I can.
Speaker 3: See an I mean yes, but I'm waiting being patient.
Speaker 2: Okay, we'll see if I have any answers. Hepatitis B
Speaker 2: virus has a lot of different genotypes that vary vary
Speaker 2: widely in their overall geographic distribution. However, as we mentioned
Speaker 2: up top, and as we'll talk a lot about towards
Speaker 2: the end of this episode, this is a globally distributed,
Speaker 2: incredibly prevalent virus, like incredibly incredibly prevalent, and it's still,
Speaker 2: as far as I can tell a little bit up
Speaker 2: for debate whether these different genotypes really vary in their
Speaker 2: tendency to cause chronic infection or in their overall disease course.
Speaker 2: A lot of sources I read said that yes, different
Speaker 2: genotypes kind of have different tendencies or characteristics, and some
Speaker 2: said it's up for debate, so okay. But being a virus,
Speaker 2: this is of course a pathogen that has to find
Speaker 2: its way into our cells, and being a virus that
Speaker 2: infects the liver, it's unsurprising that the primary cell type
Speaker 2: that it infects is our hepatocites, our actual liver cells,
Speaker 2: not the blood vessels in our liver, not any of
Speaker 2: the other things around there, but generally our liver cells.
Speaker 3: The things that make up the meat of the liver.
Speaker 2: Exactly, also called the paranama of the liver, the fancy
Speaker 2: word for the meat. So hepatitis B is transmitted in
Speaker 2: very similar ways to hepatitis C, as you may remember
Speaker 2: from several seasons ago now, but with a few important caveats. So,
Speaker 2: hepatitis B can be a blood born virus, So anything
Speaker 2: that involves the sharing of blood, whether that's contaminated needles
Speaker 2: in the healthcare setting or in intravenous drug use settings,
Speaker 2: it can be transmitted via blood transfusions, and of course
Speaker 2: is something that we see screen for to try and
Speaker 2: reduce the.
Speaker 4: Risk of that.
Speaker 2: But hepatitis B is also much more easily transmitted sexually
Speaker 2: compared to hepatitis C. It's present in so many bodily fluids.
Speaker 4: Why is that?
Speaker 2: It's a really good question. I imagine it is largely
Speaker 2: because hepatitis B is very, very infectious. As an example,
Speaker 2: according to WHO, it's fifty to one hundred times more
Speaker 2: infectious than HIV WHOA.
Speaker 3: So I know, do we know the reasons for that
Speaker 3: increased infectivity.
Speaker 2: Oh, that's a very good question. I do not, Okay, yeah,
Speaker 2: And I don't also have numbers on like the actual
Speaker 2: infectious dose. I couldn't find a solid answer on that. Either.
Speaker 2: I do know that it can persist in the environment
Speaker 2: for at least several days, so I think it's a
Speaker 2: pretty hardy virus, So that might be part of it.
Speaker 3: Yeah, Okay, So going back real quick, partially double stranded,
Speaker 3: what's the implication of that in like a virology sense.
Speaker 2: So it's really interesting. Hepatitis B is one of the
Speaker 2: few viruses that's not an RNA virus but uses a
Speaker 2: reverse transcriptase in order to replicate its genome. So HIV
Speaker 2: is an RNA virus that relies on an enzyme reverse
Speaker 2: transcriptase to make a form of DNA in order to
Speaker 2: then replicate, and B also does even though it's a
Speaker 2: DNA virus.
Speaker 3: That is so bizarre, and so I definitely came across
Speaker 3: some of that in the evolution behabers because it kind
Speaker 3: of throws a wrench in things as to like the
Speaker 3: mutation rates, the scale of the molecular clock, blah blah
Speaker 3: blahh Yeah.
Speaker 2: And it also, as I'll kind of talk a little
Speaker 2: bit more about later, it allows it to integrate into
Speaker 2: our genome in a way that then sets us up
Speaker 2: for both chronic infection and also potentially cancer right and
Speaker 2: cancer causing mutations. Ahah, spoilers.
Speaker 3: Do other viruses have this partially double stranded DNA thing
Speaker 3: as well?
Speaker 2: I don't know of any other human viruses, but I
Speaker 2: know that there are other animal hepatnaviruses that do.
Speaker 3: Right, Okay, those so that's like the unifying future of hepatnaviruses.
Speaker 2: Okay, yeah, yeah, wow?
Speaker 4: Cool?
Speaker 2: Okay. So hepatitis B is also transmitted back to that
Speaker 2: part of it vertically at much higher rates.
Speaker 3: This.
Speaker 2: Let me tell you some numbers. The estimates that I
Speaker 2: read ranged from forty to ninety percent of babies born
Speaker 2: to people living with hepatitis B, with chronic hepatitis B
Speaker 2: will become infected with hepatitis if they are not treated.
Speaker 4: Wow.
Speaker 2: And this is in comparison to only six percent of
Speaker 2: people with hepatitis C will then transmit hepatitis C to
Speaker 2: their offspring.
Speaker 3: What is the reason for that difference?
Speaker 2: Again, I think it's largely just how infectious hepatitis B is. Okay,
Speaker 2: but here's something that I think is very interesting and
Speaker 2: important about this vertical transmission of hepatitis B. First of all,
Speaker 2: a lot of times when we talk about vertical transmissions,
Speaker 2: so from parent to offspring, it's wind viruses or bacteria
Speaker 2: can cross the placenta and infective fetus during pregnancy. That
Speaker 2: is not what happens in hepatitis B. The transmission is
Speaker 2: not transplacental. In the vast, vast majority of cases, it's
Speaker 2: happening during the process of childbirth, and it's not happening
Speaker 2: during breastfeeding. It's not happening during pregnancy crossing the placenta.
Speaker 2: It's happening specifically during the period of childbirth, whether that
Speaker 2: birth happens vaginally or VC section. What there is some
Speaker 2: papers that suggest that C section delivery is a slightly
Speaker 2: lower risk, but it's not conclusive. And if you've ever
Speaker 2: seen a delivery of either kind, it kind of makes
Speaker 2: sense because neither one is really less bloody than the other,
Speaker 2: and so many bodily fluids are being exchanged no matter
Speaker 2: what exit root a baby takes.
Speaker 3: It's so it's just like the blood and bodily fluids.
Speaker 2: Blood bodily fluids. It's thought that cervical secretions, so if
Speaker 2: a baby comes out vaginally, and that's why maybe there's
Speaker 2: some thought that it's a slightly higher risk, but the
Speaker 2: data hasn't really borne that out necessarily.
Speaker 3: What that's very interesting, I know, because I didn't really
Speaker 3: realize that.
Speaker 2: I kind of thought that it was something that could
Speaker 2: be transmitted transpolacentally. Yet it's not, and that is really
Speaker 2: important when we talk about how to treat and prevent
Speaker 2: hepatitis B infection. So let me keep going, shall I?
Speaker 2: You shall The incubation period of infection, the time from
Speaker 2: when someone gets infected to when they show symptoms, can
Speaker 2: really range anywhere from thirty days to up to six months.
Speaker 2: And I think that this incubation period, even noting it
Speaker 2: incubation period, is interesting because hepatitis B is a virus
Speaker 2: that can be entirely asymptomatic, and chronic infection is generally
Speaker 2: defined as the persistence of a specific anigen being able
Speaker 2: to detect hepatitis B surface antigen for a period of
Speaker 2: at least six months. So it's interesting that you can
Speaker 2: also say the incubation period itself might be six months
Speaker 2: before you show symptoms, but you also might never show symptoms.
Speaker 4: Yeah.
Speaker 3: Yeah, that makes it really difficult to calculate an incubation exactly.
Speaker 3: It sure does.
Speaker 2: So let's talk briefly about what the symptoms can be
Speaker 2: if people do have kind of an acute infection or
Speaker 2: you know, symptoms with an initial infection. Most of the time,
Speaker 2: of course, it's completely asymptomatic or very minimally symptomatic. And
Speaker 2: it's important to note that some people can clear the
Speaker 2: virus entirely from their system after an acute infection, whether
Speaker 2: they show symptoms or not. But we'll talk about how
Speaker 2: that doesn't happen for a lot of people and who
Speaker 2: those people are and why. Okay, okay, But when symptoms
Speaker 2: do occur in the case of an acute infection, they
Speaker 2: really don't look any different from a lot of the
Speaker 2: other viruses and pathogens that affect our liver, including hepatitis C.
Speaker 2: So hepatitis B is less likely to cause acute liver
Speaker 2: failure completely, but it can cause things like jaundice where
Speaker 2: your skin can become yellow, or the whites of your
Speaker 2: eyes and your gums, things like that that become yellowish.
Speaker 2: And this occurs because our liver is what conjugates and
Speaker 2: helps eliminate bilirubin from our bodies, and so without that process, bilirubin,
Speaker 2: which is a breakdown product of our red blood cells,
Speaker 2: builds up in our skin and our eyes, and that's
Speaker 2: what turns us yellow. It then also causes a lot
Speaker 2: of nausea and vomiting from this buildup of not just bilirubin,
Speaker 2: but a lot of stuff in our system that our
Speaker 2: liver is supposed to filter out. It causes abdominal pain
Speaker 2: because your liver is inflamed, and even though your liver
Speaker 2: itself doesn't have sensory innervation, this inflammation can reach the
Speaker 2: lining of the liver, the lining of the abdominal cavity
Speaker 2: and cause pretty severe abdominal pain. And then all of
Speaker 2: these toxins that can accumulate in your bloodstream can cause
Speaker 2: severe fatigue. It can cause a darkening of your urine
Speaker 2: as the bilirubin tries to be excreted through your urine
Speaker 2: instead of your poop, and in very rare cases, it
Speaker 2: can cause actual acute onset liver failure, which can be fatal,
Speaker 2: but much more commonly, liver failure happens as a progressive
Speaker 2: process of long term inflammation, leading to cirrhosis and fibrosis
Speaker 2: and potentially hepatocellular carcinoma or cancer. So I want to
Speaker 2: focus on this, this chronic infection of hepatitis B, because
Speaker 2: it's not only very interesting but it's also the most
Speaker 2: important part of this virus. So, first of all, the
Speaker 2: likelihood of a chronic infection becoming established varies person to person,
Speaker 2: and it's inversely related to the age at which you
Speaker 2: become exposed and infected. So for infants, for neonates who
Speaker 2: get infected vertically during birth, the likelihood of a chronic
Speaker 2: infection is over ninety percent over ninety percent, So that
Speaker 2: means that almost all babies that become infected at birth
Speaker 2: or shortly thereafter go on to have a chronic lifelong
Speaker 2: infection with a very significant risk of progression to fibrosis
Speaker 2: and or liver cancer.
Speaker 3: So this inverse relationship, is it like a straight line
Speaker 3: or does it kind of have any sort of peaks
Speaker 3: and valleys?
Speaker 2: It's not a straight line. It's a it's a well,
Speaker 2: what do you call it? No, it's a what a zoop? Maybe?
Speaker 4: What do you call it? Sigmore a jay?
Speaker 2: So let me just tell you numbers, because I'm clearly
Speaker 2: not doing a good job swooping. So infant neonate ninety
Speaker 2: percent chance a child if they get in afected when
Speaker 2: they're young, like between ages one to five, the risk
Speaker 2: of chronic infection is like thirty percent, so it's a
Speaker 2: pretty big drop. And then it's a little lower for
Speaker 2: older children and for adults. If you don't get infected
Speaker 2: until you are an adult, the risk of chronic infection
Speaker 2: is only about two to five percent, so substantially lower.
Speaker 4: Hmm. I mean, okay, I have to ask why.
Speaker 2: I'm glad you asked Aaron, Let's talk about it. But
Speaker 2: first let me also say that even though the risk
Speaker 2: of chronic infection if you get infected as an adult
Speaker 2: is low, the chronic infection itself and the like prognosis
Speaker 2: of a chronic infection with hepatitis B in general is
Speaker 2: worse than, for example, the chronic infection of hepatitis C.
Speaker 2: And if you listened to our hepatitis C episode, then
Speaker 2: you remember hepatitis C is not a good virus, right,
Speaker 2: But in hepatitis C, the likelihood of a chronic infection
Speaker 2: is much higher for adults across the board. But the
Speaker 2: rate of for example, liver cancer is very low, like
Speaker 2: two point five percent for people who have chronic hepatitis C. Right,
Speaker 2: But much more people who get infected as adults with
Speaker 2: HEPSI go on to get chronic HEPSI.
Speaker 4: That makes sense.
Speaker 3: Yeah, like, okay, in the numbers perspective, right, But.
Speaker 2: For hepatitis B, fifteen to forty percent of people who
Speaker 2: have chronic infection go on to have liver cancer, hepatocellular carcinoma.
Speaker 2: It's a huge percentage.
Speaker 4: Yeah.
Speaker 2: And again, ninety percent of infants who become infected go
Speaker 2: on to have chronic infection. So that's major.
Speaker 4: That's a really disturbingly.
Speaker 3: Large number, right.
Speaker 2: Okay, So you asked why, Yeah, I did. In short,
Speaker 2: we don't fully know. It's always my answer.
Speaker 3: I'm going to cross stitch that onto a pillow for you.
Speaker 2: I would love that pillow.
Speaker 3: Oh my gosh.
Speaker 2: Okay. But so the question of why are infants who
Speaker 2: get infected more likely than adults who get infected to
Speaker 2: go on to have a chronic infection. While we don't
Speaker 2: fully know the answer, it likely has to do with
Speaker 2: a few different factors that relate to the various phases
Speaker 2: of this chronic infection. So, a chronic hepatitis B infection
Speaker 2: which is defined just as the persistence of the virus
Speaker 2: and like detection of these viral antigens for at least
Speaker 2: six months in the bloodstream after that point, like after
Speaker 2: that six months point. This isn't a static infection. It's
Speaker 2: very dynamic and it progresses through several different phases that
Speaker 2: can vary in their length and their severity. So the
Speaker 2: first phase is often known as immune tolerance, and that's
Speaker 2: essentially when our body doesn't really do much about this infection.
Speaker 2: The virus is there, and one thing that it tends
Speaker 2: to do is integrate into our genome the way that
Speaker 2: do you remember the other virus that does that er
Speaker 2: in HPV HPV That's right, And as our cells replicate,
Speaker 2: so does this virus. But in the immune tolerance phase,
Speaker 2: it doesn't cause much in the way of damage. Then
Speaker 2: there is the immune active phase, and in some papers
Speaker 2: they call this the immune clearance phase. And this is
Speaker 2: really the meat of chronic hepatitis B infection. This is
Speaker 2: when our bodies are recognizing this virus, we are mounting
Speaker 2: an immune response to it, and therefore we ourselves are
Speaker 2: causing a lot of inflammation and damage to our own
Speaker 2: liver cells. It's not the virus itself, Okay, Yeah, this
Speaker 2: is the phase where people are more likely to be symptomatic,
Speaker 2: like maybe have jaundice. But this is the phase where
Speaker 2: that inflammation is causing fibrosis, which is damage to the
Speaker 2: liver due to that inflammation. That fibrosis can eventually lead
Speaker 2: to scarring or permanent damage cirrhosis, and that can ultimately
Speaker 2: lead to liver cancer. And so this is the phase,
Speaker 2: the immune active phase that the longer that somebody is
Speaker 2: in this phase their immune system fighting the infection, the
Speaker 2: greater their risk of cancer. Okay, but there is another
Speaker 2: phase just get more complicated, and that's a so called
Speaker 2: inactive phase, wherein the virus is still there and we've
Speaker 2: maybe made some antibodies against that virus, so we're kind
Speaker 2: of at a standstill. But at any point, people could
Speaker 2: still revert back to a more immune active infection, like
Speaker 2: say if they became immuno compromised for some reason and
Speaker 2: therefore the virus is still there and still posing risk
Speaker 2: of cancer development.
Speaker 4: Gotcha that makes sense.
Speaker 2: Yeah, So I know that that was a lot and
Speaker 2: it was really just a drive by. The immunology of
Speaker 2: HEPBIE infection is a lot more complicated. There's a lot
Speaker 2: more detail. But one of the things that's different among
Speaker 2: adults who get infected versus infants is that infants tend
Speaker 2: to have a very long immune tolerant phase, whereas adults
Speaker 2: who have chronic hepatitis B, that is, they get infected
Speaker 2: and aren't able to clear that infection right away, they
Speaker 2: tend to not really have an immune tolerant phase, but
Speaker 2: rather progress directly to that active inflammatory chronic hepatitis infection. Right, Okay,
Speaker 2: So that's a really big difference. And it's thought that
Speaker 2: during pregnancy, viral particles or maternal antibodies or both are
Speaker 2: passing through to the fetus, and then when that infant
Speaker 2: is born and exposed to hepatitis B, while they're not
Speaker 2: able to fight off that virus entire the way most
Speaker 2: adults who are exposed can, they instead establish this relationship
Speaker 2: of tolerance that lends itself more easily to a chronic infection.
Speaker 3: Oh right, okay, so it's kind of like getting to
Speaker 3: know you and like, all right, I guess we'll just
Speaker 3: tolerate you know each other for a while.
Speaker 2: Right, but then eventually progress to the other phases of disease.
Speaker 4: Right, Okay, interesting.
Speaker 2: But that is generally hepatitis B virus.
Speaker 3: So I have a question, h you mentioned that. Okay,
Speaker 3: there are people who become infected and they clear the virus,
Speaker 3: they develop antibodies.
Speaker 2: Boom.
Speaker 3: They're in the category that you didn't discuss the later
Speaker 3: stages on for obvious reasons. And so these people now
Speaker 3: have a lifetime immunity to hepatitis B virus. What about
Speaker 3: different genotypes are is there any sort of like genotype
Speaker 3: dependent immunity where you can be infected with one genotype
Speaker 3: and then clear that and be exposed to another one
Speaker 3: and not clear that?
Speaker 2: Great question, Aaron. As far as everything that I have read,
Speaker 2: immunity to hepatitis B is immunity to hepatitis B across genotypes.
Speaker 2: That's great news exactly. It's really great news, Aaron, because
Speaker 2: we in fact have a vaccine for hepatitis B. It
Speaker 2: is a recombinant vaccine that contains only the surface antigen
Speaker 2: of hepatitis B, and that is what we make antibodies too.
Speaker 3: Have a follow up question, Okay, if someone is chronically
Speaker 3: infected with one genotype of hepatitis B, can they become
Speaker 3: infected with another genotype of hepatitis B?
Speaker 2: Not as far as I know, But do you know what?
Speaker 2: They can become infected.
Speaker 4: With hepatitis D.
Speaker 2: Hepatitis D. Thanks for the little intro there.
Speaker 4: You're welcome. You're welcome.
Speaker 2: I want to just very we briefly mention hepatitis D
Speaker 2: because I don't think that we would ever do a
Speaker 2: full episode on it. I don't know, maybe I'm wrong,
Speaker 2: but delta hepatitis virus or hepatitis delta HEPD, it's a
Speaker 2: fascinating virus. This virus belongs to its entire own viral
Speaker 2: genus that doesn't have an actual family that it falls within.
Speaker 2: And some people say it's not even really a virus,
Speaker 2: it's like something else entirely. It's a subviral agent.
Speaker 4: Whoa what it's like a virus of a virus.
Speaker 2: It's kind of so. Hepatitis D has an RNA genome,
Speaker 2: and it can replicate on its own inside of our
Speaker 2: cells and when it infects us, and it does infect
Speaker 2: our liver cells, but it can't actually infect our cells
Speaker 2: by itself. It relies on the surface pines of hepatitis
Speaker 2: B virus in order to get into our cells and
Speaker 2: in order to be released from our cells. So hepatitis
Speaker 2: D is a virus that can only infect someone who
Speaker 2: has a chronic or acute hepatitis B infection.
Speaker 3: I'm really regretting right now not reading more about the
Speaker 3: evolutionary origins of hepatitis D because.
Speaker 2: On Earth, maybe it does deserve its whole own episode. Yeah,
Speaker 2: that's that's literally all I have to say about it.
Speaker 2: But it is very very interesting.
Speaker 3: Okay, So what about besides the vaccine? What about treatments?
Speaker 3: Are there anti viral treatments for hepatitis B virus or
Speaker 3: maybe B and hept combined.
Speaker 2: Yes, for hepatitis B there are. So there's a number
Speaker 2: of different treatments that we have. Actually none of them
Speaker 2: can cure hepatitis B. They're all used to sort of
Speaker 2: man and to try and reduce the rate of inflammation
Speaker 2: and complications. But pigilated interferon, which I think we talked
Speaker 2: about in our hepsy episode. Possibly, but that's basically like
Speaker 2: an immune modulator you can think of it as that
Speaker 2: can be used and has been used to treat hepatitis B.
Speaker 2: But there are also a number of anti virals that
Speaker 2: in many cases are used to treat HIV or we're
Speaker 2: used to treat HIV and are now used to treat
Speaker 2: he B. So yes, there are Again, none of them
Speaker 2: actually clear the infection, but they all just sort of
Speaker 2: help to manage it. Okay, And what's really important about
Speaker 2: all of these is that because all of those different
Speaker 2: states immune tolerance, immune active, inactive, these different phases of
Speaker 2: infection really very person to person and how severe someone's
Speaker 2: symptoms might be, like it really varies. So just because
Speaker 2: someone has an infection with chronic hepatitis B doesn't necessarily
Speaker 2: mean that they have to be on treatment if they're
Speaker 2: in a phase that isn't directly causing damage. Does that?
Speaker 4: Okay? Yeah, that's interesting.
Speaker 2: At least as of now, because the treatments that we
Speaker 2: do have are not without side effects, and in a
Speaker 2: lot of cases they have quite a lot of side effects,
Speaker 2: so it requires a lot of careful monitoring and everything,
Speaker 2: which makes it a lot harder to do. Quite honestly,
Speaker 2: there's so much here about this virus that I know,
Speaker 2: so speaking of so much about this virus arin like,
Speaker 2: what where did it come from? What the heck?
Speaker 3: I will do my best to answer those questions, But
Speaker 3: let's take a quick break first, all right, the story
Speaker 3: of hepatitis B. I feel like in the last couple
Speaker 3: of episodes, I've maybe deviated a bit from the normal
Speaker 3: history overview that I usually give. But don't worry, I'm
Speaker 3: going back to my roots for this one. I'm going
Speaker 3: to start with a bit of evolutionary history, mix in
Speaker 3: some early accounts of infectious hepatitis, then the fascinating story
Speaker 3: of its identification, and then finally getting us to where
Speaker 3: we are today.
Speaker 2: The usual, the usually, I love it, but usual.
Speaker 3: Doesn't mean boring or straightforward, especially in the case of
Speaker 3: hepatitis B. So beginning at the beginning, where does the
Speaker 3: hepatitis B virus come from? It turns out that the
Speaker 3: answer to that question has been a moving target for
Speaker 3: a number of years, with new hypotheses introduced or old
Speaker 3: hypotheses overturned or tweaked to fit new findings. As more
Speaker 3: about the evolutionary history of this virus has come to light,
Speaker 3: and this should come as no surprise really, considering how
Speaker 3: widespread this virus is, how many genotypes there seem to be,
Speaker 3: how the virus can undergo recombination, the confusion about its
Speaker 3: partially double stranded DNA, and how we don't really know
Speaker 3: exactly maybe the rate.
Speaker 4: Of evolution or mutation.
Speaker 3: There's been a lot of work on this I was
Speaker 3: happily surprised to find, especially recently, and so I'm going
Speaker 3: to try to bring us up to speed on what
Speaker 3: the current consensus is relying mostly on two papers that
Speaker 3: came out in twenty twenty one about the origins evolution
Speaker 3: of the hepatitis B virus, one by Lochernini at all
Speaker 3: and the other Bycolture at All. Like you said, Erin,
Speaker 3: the hepatitis B virus belongs to the Hepadinaviidae family, and
Speaker 3: in the years after the hepatitis B virus was first identified,
Speaker 3: researchers found viruses belonging to that family that infected birds, fish, reptiles,
Speaker 3: and amphibians, other mammals, non human primates.
Speaker 4: Et cetera.
Speaker 3: Basically, this is a lot bigger and a lot older
Speaker 3: of a virus family than we thought with there. And
Speaker 3: there are some estimates that it originated around eighty two
Speaker 3: million years ago.
Speaker 4: WHOA, So, like this thing.
Speaker 3: Was infecting birds essentially, Yeah, back when birds and dinosaurs
Speaker 3: were the same thing. Yeah, I hope that that's probably
Speaker 3: not accurate, but you know what I mean, eighty two
Speaker 3: million years let's stick with that. Yeah, So from eighty
Speaker 3: two million years years ago, how did it get into
Speaker 3: modern humans? And on that there seems to be some
Speaker 3: debate surprise surprise for a long time, it was thought
Speaker 3: that hepatitis B virus originated in Africa, or for a
Speaker 3: while it was thought maybe the Americas, and then it
Speaker 3: spilled over into humans, possibly from like a non human primate,
Speaker 3: and then dispersed. Maybe it was dispersing out of Africa
Speaker 3: following prehistoric patterns of human migrations. But more recently that
Speaker 3: assumption has been questioned. So one of the studies published
Speaker 3: in twenty twenty one used hepatitis B virus detected in
Speaker 3: skeletal remains of one hundred and thirty seven individuals found
Speaker 3: in Eurasia and the Americas and dating between ten thousand,
Speaker 3: five hundred years ago and four hundred years ago. What
Speaker 3: that's some old viral DNA.
Speaker 2: I just love it when you find things like this, Aaron,
Speaker 2: I know.
Speaker 3: It's This paper was really interesting. It also had the
Speaker 3: most authors of any paper I've ever seen. I think
Speaker 3: it was one hundred and seventy something.
Speaker 2: Oh my goodness, that's more than like the whole human
Speaker 2: genome paper.
Speaker 3: But I mean it makes sense because I'm assuming that
Speaker 3: there was a lot of collaboration across many different universities
Speaker 3: with all of these remains, skeletal remains so okay.
Speaker 4: Anyway, So what this.
Speaker 3: Paper, using all of these old skeletal remains with hepatitis
Speaker 3: B virus did is that they wanted to reconstruct the
Speaker 3: evolutionary history and dispersion of the virus. And what they
Speaker 3: propose is that the most recent common ancestor of the
Speaker 3: hepatitis B virus dates back to around twelve thousand to
Speaker 3: sixteen thousand years ago, which is more recent actually than
Speaker 3: was previously thought. And it places that most recent common
Speaker 3: ancestor in your Asia, where over the next hundreds and
Speaker 3: thousands of years it spread across Eurasia, into Africa, through
Speaker 3: Europe and to the Americas. It seems like the emergence
Speaker 3: of the hepatitis B virus and some of it spread
Speaker 3: happened to before the Neolithic Revolution, which is when people
Speaker 3: began settling in larger groups and farming and so on.
Speaker 3: And if you think about it, this completely makes sense
Speaker 3: because what are some of the transmission characteristics that hepatitis
Speaker 3: BEE has. Right, People can be carriers. It can be
Speaker 3: transmitted to a baby at birth. It can be spread
Speaker 3: during sexual contact or through blood so like violent interactions
Speaker 3: or tattooing. Even there are many different ways that this
Speaker 3: virus can be transmitted, and the fact that there are
Speaker 3: people who can carry it for long periods of time
Speaker 3: means that it doesn't need this critical population size in
Speaker 3: order to spread or persist in a pupeat.
Speaker 2: So in that way, it's a lot like a couple of.
Speaker 3: The other viruses that we've talked about before, like the
Speaker 3: herpee simplex virus or chicken pox virus. But once people
Speaker 3: began settling in larger groups around seven thousand to eight
Speaker 3: thousand years ago, that meant, of course, more opportunities for transmission,
Speaker 3: which led to an increase in the diversity of hepatitis
Speaker 3: B virus strains and the emergence of multiple genotypes or lineages.
Speaker 4: I'm not going to go.
Speaker 3: Into a ton of detail about this, but the paper
Speaker 3: that I keep mentioning by Kosher at all actually trace
Speaker 3: the kind of like rise and fall of different hepatitis
Speaker 3: B virus lineages. So one, for instance, seemed to be
Speaker 3: the prevailing lineage in western Eurasia for like four thousand years,
Speaker 3: but then it disappeared around thirty three hundred years ago.
Speaker 3: It just went almost extinct. No idea why, Maybe sampling bias,
Speaker 3: maybe a reduction in human population that kind of like
Speaker 3: bottlenecked or eliminated it, or maybe it was like inter
Speaker 3: genotype dynamics.
Speaker 2: Who knows, so interesting.
Speaker 3: Eron, I find this so fascinating, and this pattern of
Speaker 3: genotypes going extinct and shifts in the predominant genotype, it
Speaker 3: still happens today, and we don't know for sure, but
Speaker 3: maybe it's partially due to the fact that some genotypes
Speaker 3: may be associated with certain transmission routes I've seen, and
Speaker 3: maybe some of the genotypes vary in their ability to
Speaker 3: cause severe disease or in their ability to cause this
Speaker 3: persistent carrier state. And so that's I think why it's
Speaker 3: really important to understand the origins and the evolutionary history
Speaker 3: of a virus like the hepatitis B virus. It can
Speaker 3: tell us, in part why we see some of the
Speaker 3: epidemiological patterns that we see today, and it might be
Speaker 3: helpful for predicting what we could expect to see in
Speaker 3: the future. Okay, so we have this virus that has
Speaker 3: ancient roots and that had reached a global distribution a
Speaker 3: long time before the present day. And I already mentioned
Speaker 3: that evidence of hepatitis B infection has been found in
Speaker 3: ancient human remains dating back thousands of thousands of years
Speaker 3: as well as just a couple thousand years as well
Speaker 3: as more recent So basically it's kind of like persisted
Speaker 3: in human populations for all of that time. But were
Speaker 3: the people who were around back then aware of this?
Speaker 4: Did they have any idea?
Speaker 2: Were they did?
Speaker 4: They?
Speaker 3: Well, probably in a sense. So jaundice, which can be
Speaker 3: caused by many different things, including the hepatitis B virus,
Speaker 3: has long been recognized and described an ancient medical text.
Speaker 3: I'll toss in the Hippocratic texts from around four hundred
Speaker 3: BCE because it's an episode of this podcast Will.
Speaker 4: Kill You.
Speaker 3: And and outbreaks of jaundice were also written about. So
Speaker 3: one paper I read suggested that there was a description
Speaker 3: of what was likely infectious hepatitis dating back to the
Speaker 3: eighth century CE, and it was sometimes called campaign jaundice
Speaker 3: because it seemed prevalent during times of war. Surprise, surprise,
Speaker 3: But switching from talking about the evolutionary history of the
Speaker 3: hepatitis B virus to the written human history part, it's
Speaker 3: tricky because of the existence of other hepatitis viruses hepatiti hepatid.
Speaker 3: We can test human remains for hepatitis B virus specifically,
Speaker 3: but we can't always know which hepatitis virus was causing
Speaker 3: whatever outbreak that was being described. How likely was it
Speaker 3: that it was hepatitis B in terms of outbreaks, I
Speaker 3: would guess actually that the hepatitis A virus which is
Speaker 3: transmitted f may have been the culprit more often than not,
Speaker 3: especially in crowded or unsanitary conditions like you know, war.
Speaker 2: Yeah, and especially in any that were like acute infections.
Speaker 3: Yes, like mm hm exactly, yeah. But it's certainly possible
Speaker 3: that hepatitis BE and other hepatitis viruses transmitted through blood
Speaker 3: or bodily fluids caused outbreaks, especially as the use and
Speaker 3: reuse of needles became more popular around the middle of
Speaker 3: the nineteenth century. So let's fast forward to then the
Speaker 3: last decades of the eighteen hundreds, So this is like
Speaker 3: after the development of germ theory and after the introduction
Speaker 3: of some injectable vaccines. In eighteen eighty five, an epidemic
Speaker 3: of jaundice followed a smallpox vaccination campaign among shipworkers in Bremen, Germany,
Speaker 3: which led to what seems like an early indication that
Speaker 3: hepatitis outbreaks could be caused by the reuse of needles,
Speaker 3: or because this particular vaccine used like human serum as
Speaker 3: a stabilizing agent through like blood products.
Speaker 4: But the link between the.
Speaker 3: Administration of this vaccine and the resulting hepatitis outbreak it
Speaker 3: wasn't recognized for decades, possibly obscured by this long standing
Speaker 3: recognition that epidemics of hepatitis or jaundice were also known
Speaker 3: to frequently happen in overcrowded, unsanitary areas, so it was
Speaker 3: more difficult to pinpoint the vaccine itself as the cause,
Speaker 3: rather than like, oh, well, maybe they all went to
Speaker 3: the same watering hole, to the same to the same
Speaker 3: watering hole where they all got hepatitis.
Speaker 2: Yeah.
Speaker 4: Yeah.
Speaker 3: But as blood transfusions increased and the practice of reusing
Speaker 3: needles persisted, there was this growing suspicion that an in
Speaker 3: infectious hepatitis might also be carried in the blood or
Speaker 3: blood products. See our hepatitis c episode for more on
Speaker 3: the history of blood transfusions and the blood typing system
Speaker 3: and so on. The differentiation of two different hepatitises, one
Speaker 3: called transfusion hepatitis and the other one being called infectious
Speaker 3: or food or waterborne hepatitis. This was finally made in
Speaker 3: the early nineteen forties. During World War Two, hundreds of
Speaker 3: thousands of US Army personnel received the yellow fever vaccine, which,
Speaker 3: like the eighteen eighty five smallpox vaccine, had human serum
Speaker 3: as an ingredient.
Speaker 4: Obviously that's no longer.
Speaker 3: Done for safety reasons needed to maybe clarify that. But
Speaker 3: after receiving this vaccine, fifty thousand people came down with hepatitis,
Speaker 3: although those were just the clinically recognized cases.
Speaker 4: Later estimates put the.
Speaker 3: Total figure of hepatitis infections resulting from this vaccination campaign
Speaker 3: at around three hundred and thirty thousand.
Speaker 2: Oh dear, okay, oh gosh, oh dear, okay.
Speaker 4: It's a lot, it's a lot.
Speaker 2: Yeah.
Speaker 3: And there was a British doctor named F. O. Mcallum
Speaker 3: who had been involved in the development and administration of
Speaker 3: this vaccine, and he hypothesized that it might have been
Speaker 3: transmitted by reusing syringes or carried in the vaccine itself.
Speaker 3: And he thought that this hepatitis represented a blood born infection,
Speaker 3: separate from the previously recognized food and waterborn hepatitis. He
Speaker 3: proposed that they be called hepatitis A and B and
Speaker 3: that they may represent different viruses.
Speaker 2: So this is how it begins.
Speaker 3: This is how it begins, because at the time it
Speaker 3: was like not known whether it was the virus or
Speaker 3: different viruses, and so it was more in like the
Speaker 3: clinical picture of.
Speaker 4: It in a way. Because after this.
Speaker 3: Designation, after this recognition that like, hey, this might be
Speaker 3: transmitted through blood products and not just through like food
Speaker 3: and water or whatever, other researchers began to describe differences
Speaker 3: in the way that these two hepatida looked clinically and
Speaker 3: to kind of keep an eye out more on the
Speaker 3: different roots of transmission.
Speaker 2: Once you have it more like, hey, there are two
Speaker 2: different things here, then you start to notice more of
Speaker 2: the differences.
Speaker 4: Right.
Speaker 3: Once you create those like columns, then it's then it
Speaker 3: becomes much easier to add to the listen. But just
Speaker 3: because people now knew that hepatitis could be transmitted by
Speaker 3: reusing needles or via blood products, that didn't mean they
Speaker 3: could stop it from happening. Liked I talked about in
Speaker 3: our hepatitis see episode. Blood transfusion or blood product technology
Speaker 3: vastly outpaced our ability to identify many blood borne pathogens,
Speaker 3: especially viruses, which led to blood products that were unknowingly contaminated,
Speaker 3: and often it was seen as this kind of situation
Speaker 3: where it was like, well, we don't know whether or
Speaker 3: not this batch of blood has hepatitis virus in it,
Speaker 3: but you can either receive the blood and possibly get
Speaker 3: hepatitis down the line, or not take the blood and
Speaker 3: die of blood loss immediately. So there was like no choice.
Speaker 3: Sometimes there was no option. That's not to say that
Speaker 3: people weren't working on finding a way to test the
Speaker 3: blood supply and identify what was causing the hepatitis. If anything,
Speaker 3: it was that feeling of being powerless to protect people
Speaker 3: from this disease that created a sense of urgency in
Speaker 3: finding out what the hepatitis bee agent was so that
Speaker 3: they could detect it in blood products. But despite a
Speaker 3: ton of people work looking on this, progress kind of
Speaker 3: stalled in the nineteen fifties and early nineteen sixties. And
Speaker 3: I think it stalled partially because this was a time
Speaker 3: when virology was kind of in its infancy as a field,
Speaker 3: and the technology that would allow for genetic testing or
Speaker 3: sequencing was still decades away.
Speaker 2: I'm sorry, I just I had I don't know how
Speaker 2: I didn't know that it was so recent I know,
Speaker 2: like nineteen fifties, nineteen sixties, that's not a long time ago.
Speaker 4: It is.
Speaker 3: All of the hepatitis viruses are like have very recent
Speaker 3: identification dates, but have been recognized for decades before that.
Speaker 3: And it's just sort of this like constantly unfolding tragedy
Speaker 3: where you're just like you see it, and you're like
Speaker 3: and they know, Like the people who were there at
Speaker 3: the time are like, I can't, Like, this might have
Speaker 3: hepatitis virus in it, but I can't do anything about it.
Speaker 2: Right, But I don't but I don't know it.
Speaker 3: I am like, I know it, but I.
Speaker 2: Can't know it.
Speaker 3: Mm hmm. And we can also blame the virus itself,
Speaker 3: because this isn't to say that virology research on all fields,
Speaker 3: on all viruses had stopped or stalled by the early
Speaker 3: nineteen fifties or sixties, because some were easier to work
Speaker 3: with in a lab setting than others. Yeah, and hepatitis
Speaker 3: B virus doesn't really lend itself very well to culturing
Speaker 3: in a lab setting, and so it was just more difficult.
Speaker 4: And especially if you don't know even.
Speaker 3: What you're looking for, how do you know that you're
Speaker 3: on the right track?
Speaker 1: At all.
Speaker 2: Yeah, and it's a weird virus. We already said that, Yeah,
Speaker 2: it's a weird, very weird. And at the time it
Speaker 2: wasn't People were using the term virus, but it wasn't
Speaker 2: known for sure whether it was a virus or something else.
Speaker 2: It was like known to be a virus in concept,
Speaker 2: but without physical proof. But by the end of the
Speaker 2: nineteen sixties that would change, and the team that led
Speaker 2: to the breakthrough identification of the hepatitis B virus would
Speaker 2: not have been on anyone's short or even long list
Speaker 2: of people that were likely to have done the job.
Speaker 2: Why who was it?
Speaker 3: Okay, I'll get there, But before we get into the
Speaker 3: unlikely story of the discovery of the HEPB virus, I
Speaker 3: want to quickly mention the Willowbrook State School hepatitis studies,
Speaker 3: which were these unethical experiments that are sometimes referred to
Speaker 3: as the pediatric Tuskegee.
Speaker 2: Oh dear.
Speaker 4: Yeah.
Speaker 3: I'm going to be brief because these studies are mostly
Speaker 3: about hepatitis A, and so when we do a HEPA episode,
Speaker 3: I'll go into more depth on them. But I wanted
Speaker 3: to bring them up here because these studies mark one
Speaker 3: of the major points in the history of medical ethics,
Speaker 3: and also hepatitis B was a part of these studies.
Speaker 3: So Willowbrook State School was a state funded institution established
Speaker 3: in nineteen forty seven on Staten Island, New York, for
Speaker 3: children who were intellectually or developmentally disabled.
Speaker 2: I hate this already, erin, I know, I know, I know.
Speaker 3: In nineteen fifty eight, infectious disease physician doctor Saul Krugman
Speaker 3: from New York University in Bellevue Hospital, he was asked
Speaker 3: to join Willowbrook to help figure out why there were
Speaker 3: such high rates of hepatitis among the children there, with
Speaker 3: something like thirty to fifty percent admitted there would end
Speaker 3: up getting hepatitis, and they also asked him to help
Speaker 3: bring those rates down, and so he agreed and set
Speaker 3: out to not only bring down the rates of hepatitis,
Speaker 3: but also to quote describe the circumstances under which the
Speaker 3: disease occurred and the effect of gamma globulin in reducing
Speaker 3: its occurrence, and an attempt to induce passive active immunity
Speaker 3: by feeding virus to persons protected by gamma globulin, and
Speaker 3: to describe the excretion of virus during the incubation period
Speaker 3: of the disease. Dear your face tells me you've picked
Speaker 3: up on some of the yeah problems with these studies
Speaker 3: intentionally infecting children. So Krugman justified the research by saying
Speaker 3: that the children would inevitably get hepatitis anyway because it
Speaker 3: was so prevalent in the school, and that this way,
Speaker 3: with his experiments, a vaccine could be developed and tested.
Speaker 3: Parental consent was obtained, but it's not clear the extent
Speaker 3: to which parents were told of the risks to their
Speaker 3: children and what exactly was involved. By his own estimation,
Speaker 3: Krugman's studies reduced the incidence of hepatitis by eighty five percent. Again,
Speaker 3: it's not entirely clear which hepatitis, but his study did
Speaker 3: demonstrate that there were two different types of hepatitis transmitted
Speaker 3: in different ways, which like I said, was already kind
Speaker 3: of known, and also tested a prototype of a HEPB
Speaker 3: vaccine which did seem to be somewhat effective. The legacy
Speaker 3: of the Wiliberg hepatitis studies is that the resulting outrage
Speaker 3: led to very strict regulations placed on including children in
Speaker 3: clinical trials and medical studies, and a more revamping of
Speaker 3: what could be considered medical consent. There's a lot more,
Speaker 3: of course, like I said, to these studies and their
Speaker 3: place in the history of medical ethics. And so if
Speaker 3: you're interested in learning more and don't want to wait
Speaker 3: for our Hepatitis A episode, I will list some sources
Speaker 3: for this on our website. And there's also a paper
Speaker 3: that Krugman wrote and published in nineteen eighty six in
Speaker 3: which he defends himself in the research. So that's kind
Speaker 3: of an interesting read. There's like a lot of discussion
Speaker 3: about this, and I didn't do it justice, so let
Speaker 3: me just say that.
Speaker 2: Wow.
Speaker 3: Yeah, okay, okay, back to strictly hepatitis B. So, by
Speaker 3: the nineteen sixties, the hepatitis B virus had still not
Speaker 3: been identified, despite the fact that tons of people were
Speaker 3: working on this problem. And when it was finally discovered,
Speaker 3: it wasn't by one of those researchers who had dedicated
Speaker 3: their lives to hepatitis, but by a team who had
Speaker 3: not even been looking for hepatitis B or any other virus.
Speaker 2: What were they looking for?
Speaker 3: I feel like this story is such a good example
Speaker 3: of how science like rarely proceeds in an orderly fashion.
Speaker 4: It's not a to B two C.
Speaker 3: It's especially because B happens to be the first hepatitis
Speaker 3: virus discovered.
Speaker 2: Yeah, Okay, I saw that on a timeline and I
Speaker 2: was like, well, well we'll hold on, hold on, hold on.
Speaker 4: I don't know. It was like, why is it called B?
Speaker 2: Then yeah, it doesn't make any sense.
Speaker 3: Yep, everything's just arbitrary.
Speaker 2: Cool cool, cool, yep.
Speaker 3: But yeah, it's like we often tell, like I'm including
Speaker 3: myself in that these stories of scientific discovery in a
Speaker 3: very linear way, in a very like here's this nice little,
Speaker 3: pretty narrative packaged, and that neat narrative does serve a
Speaker 3: purpose because it kind of is like, well, let's find
Speaker 3: the important things, let's find the compelling things. Yeah, but
Speaker 3: that's not the way things happen. It's just simply not.
Speaker 3: And so this, I think really illustrates that sometimes you're
Speaker 3: looking for one thing and you end up stumbling upon
Speaker 3: something that never even crossed your mind.
Speaker 4: So let's meet doctor Baruch Bloomberg.
Speaker 2: Okay, Hi.
Speaker 3: Since early in his career, Bloomberg became interested in why
Speaker 3: some people get sick and others don't, how genetics interacts
Speaker 3: with human behavior and the environment to lead to disease basic,
Speaker 3: and he became interested specifically in polymorphisms. So these are
Speaker 3: genetic traits for which there are multiple forms. So things
Speaker 3: like tongue twisting. Can you twist your tongue?
Speaker 2: Yes?
Speaker 4: Can you too?
Speaker 2: Cool?
Speaker 4: Blood types? What blood type are you?
Speaker 3: I'm oh positive, I'm ab positive.
Speaker 2: I knew that about you.
Speaker 4: I knew that about you.
Speaker 3: So these are examples of polymorphisms, right, Like, there are
Speaker 3: different forms of these, and there are different distributions in
Speaker 3: human populations, and so he wanted to see whether there
Speaker 3: were any of these polymorphisms that were associated with susceptibility
Speaker 3: to certain diseases. So kind of like asking the question
Speaker 3: do people with type A blood have a greater chance
Speaker 3: of developing heart disease? And if they do, why, But
Speaker 3: instead of blood types, which at this point had already
Speaker 3: been pretty well established, Bloomberg was interested in finding new
Speaker 3: blood plasma pro teen polymorphisms that could be associated with
Speaker 3: variation in disease susceptibility.
Speaker 4: So that's what he was looking for.
Speaker 2: He wasn't even looking for virus.
Speaker 3: No, he was looking for blood plasma protein polymorphisms.
Speaker 2: Wow, I bet he found some proteins, all right.
Speaker 3: He certainly did but how did he find these proteins. Yeah, well,
Speaker 3: he began his search by collecting blood samples from people
Speaker 3: all over the world and then testing them to see
Speaker 3: whether certain antigens appeared and in what frequency. Basically, you
Speaker 3: use the blood of someone who had received multiple transfusions
Speaker 3: to find antibodies against a protein antigen that was new
Speaker 3: to them, and then you test those antibodies against other
Speaker 3: blood samples to see how frequently it reacts, meaning how
Speaker 3: often that protein antigen is present. Yeah, and this might
Speaker 3: seem like a very crude protein today in the days
Speaker 3: of like you know, super inexpensive genomic sequencing, but back then,
Speaker 3: these were the early early years of genetics.
Speaker 2: I mean we still do that to do like regular
Speaker 2: blood typing. Yeah, so it was like still very useful.
Speaker 3: It so it is, it is super useful. But the approach,
Speaker 3: like the technology that he used, which was Agargell diffusion,
Speaker 3: it was basically like one of the only ones available
Speaker 3: at the time immunology was in its infancy, and so
Speaker 3: with this approach, Bloomberg and his team identified a new
Speaker 3: protein that they called the AG protein AG for antigen.
Speaker 3: This protein, which they found to have an uneven global
Speaker 3: distribution turned out to be a serum lipoprotein, so serum
Speaker 3: protein combined with fats that may play a role in
Speaker 3: serum cholesterol and triglyceride levels. Maybe not a strong marker
Speaker 3: for disease susceptibility.
Speaker 4: But it was an encouraging finding.
Speaker 3: It showed that their technique, even though it was, you know,
Speaker 3: maybe a little bit kind of rough handed, could be
Speaker 3: used to find new serum proteins. So they kept looking
Speaker 3: for the next hunt. Bloomberg teamed up with a blood
Speaker 3: researcher named Harvey Alter, whose name you should recognize former
Speaker 3: hepatitis C episode. Except when I looked through my notes
Speaker 3: for his name, I didn't mention that he was the
Speaker 3: person who identified the hepatitis C virus. And I am
Speaker 3: so embarrassed, Like, that's kind of a fundamental, important person
Speaker 3: for the history of hepatitis C.
Speaker 2: I bet you talked about a lot of important things, Karen.
Speaker 3: I'm just I'm ashamed, you know, but I am. I'm
Speaker 3: mentioning him here, And I also want to shout out
Speaker 3: that in twenty twenty he was awarded the Nobel Prize
Speaker 3: for his role in hepatitis C research.
Speaker 4: Ohty cool?
Speaker 2: WHOA Yeah?
Speaker 3: So anyway, Alter, who was in the beginning of his
Speaker 3: career in the early nineteen sixties. He was interested in
Speaker 3: why some people developed an immune response like a fever, chills, rash, etc.
Speaker 3: After receiving a transfusion. Yeah, interesting, sef And it took
Speaker 3: a little bit of time, little trial and error, but
Speaker 3: Alter in Bloomberg found another polymorphism, and this they named
Speaker 3: Australia antigen because it was first found in the blood
Speaker 3: serum of a First Nations person from Australia.
Speaker 4: And we've talked about the.
Speaker 3: Problem with place names to describe a disease loads of
Speaker 3: times before.
Speaker 4: However, I want to.
Speaker 3: Point out that at the time, this Australia antigen was
Speaker 3: just thought to be a human protein, not necessarily an
Speaker 3: actual pathogen, which surprised spoilers it turned out to be.
Speaker 3: But in any case, the name Australia antigen it didn't
Speaker 3: stick around for very long because it was soon shown
Speaker 3: that the Australia antigen was actually the hepatitis B virus.
Speaker 2: I love this story.
Speaker 3: I know it's I just think it's so amazing. It's like,
Speaker 3: I don't know, it's just such a fun story. So
Speaker 3: how did they make this connection? Well, first, after finding
Speaker 3: this new protein, they decided to look at its geographic
Speaker 3: patterns of prevalence, just like they had for their earlier
Speaker 3: AGG protein, which you know, was it more common in
Speaker 3: some areas or in some populations than others, and they
Speaker 3: did find variation in the global distribution. They found that
Speaker 3: the Australia antigen seemed to be somewhat rare in the
Speaker 3: US blood samples that they had, but it was a
Speaker 3: little bit more common in parts of Asia, in the
Speaker 3: Pacific Africa, and Eastern and southern Europe. They also showed
Speaker 3: that the antigen seemed to cluster in families, which at
Speaker 3: first glance suggested that it was an inherited tree, but
Speaker 3: as more data came in, that assumption kind of broke down.
Speaker 4: Yeah, uh huh.
Speaker 3: Bloomberg and his team began getting suspicious that it might
Speaker 3: not be a human protein after all, but rather an
Speaker 3: infectious agent, one that was possibly bloodborn, as they had
Speaker 3: found it in several people who had at first tested
Speaker 3: negative for the antigen but later tested positive shortly after
Speaker 3: receiving a blood transfusion. Oh no, And then the connection
Speaker 3: to hepatitis B fell into place when they began to
Speaker 3: find the antigen at high rates and people who had
Speaker 3: hepatitis okay, especially those with a history of transfusion. By
Speaker 3: nineteen sixty five or so, they had become convinced that
Speaker 3: they had finally found the long sought after hepatitis B
Speaker 3: virus almost by accident, I mean truly by accident, really,
Speaker 3: and they sent off a couple of papers to be published.
Speaker 3: One was outright rejected, with a reviewer commenting that there
Speaker 3: simply wasn't enough evidence in support of their hypothesis. And
Speaker 3: now we look back on this and go, that's absurd.
Speaker 3: How could this monumental finding be rejected? But if you
Speaker 3: consider this in the larger context of the time, it
Speaker 3: does seem like it was kind of like a boy
Speaker 3: who Cried Wolf scenario. People were always submitting articles saying,
Speaker 3: I've found the hepatitis B virus.
Speaker 4: I have found it.
Speaker 3: It's this, It's this kind of like how I feel
Speaker 3: like every few months nowadays, there's an article saying the
Speaker 3: Zodiac killer has finally been identified.
Speaker 4: It's like, okay, let's.
Speaker 3: If we dig a little deeper, like is it true
Speaker 3: or is it not so close to the truth. But
Speaker 3: another reason for the rejection, and this one is much
Speaker 3: more unfair is that Bloomberg and his group were in
Speaker 3: no way part of the hepatitis be seen. They had
Speaker 3: no background and studying hepatitis. None of them had been
Speaker 3: trained as epidemiologists, let alone virologists, so what do they
Speaker 3: know about hepatitis? But despite this initial rejection and the
Speaker 3: resentment from some prominent hepatitis researchers, they managed to get
Speaker 3: a paper published in nineteen sixty seven that awakened the
Speaker 3: world to the possibility that the virus causing transfusion hepatitis,
Speaker 3: the hepatitis B virus, had finally been found.
Speaker 2: Nineteen sixty seven.
Speaker 1: Hm.
Speaker 3: Wow, Yeah, and this seems like an understatement, but this
Speaker 3: was huge news at the time. Post transfusion hepatitis rates
Speaker 3: reached thirty percent.
Speaker 2: Oh my m.
Speaker 3: The beginnings of the incredible prevalence of global hepatitis that
Speaker 3: we have today really does have its roots during this time.
Speaker 3: During this time when there was a lot of blood
Speaker 3: transfusion happening, a lot of blood products being used, a
Speaker 3: lot of needles being reused, without knowing what the virus was,
Speaker 3: how to test for it, how to prevent it. So
Speaker 3: it's yeah, but there was still another step, and that
Speaker 3: was confirmation from other researchers.
Speaker 4: Boom, easily done.
Speaker 3: Check, here's hepatitis be the end almost the end actually,
Speaker 3: the discovery of the hepatitis B virus. This allowed not
Speaker 3: only for the testing of hepatitis B virus and blood products,
Speaker 3: but also the identification of carriers of the virus and
Speaker 3: the eventual development of a vaccine. This isn't to say
Speaker 3: that it was all smooth sailing after the link between
Speaker 3: the Australia antigen and the hepatitis B virus was made.
Speaker 3: For instance, the virus was still not able to be
Speaker 3: maintained in conventional tissue cultures, which made fulfilling Cook's postulates difficult,
Speaker 3: and the test for determining whether or not the virus
Speaker 3: was present pretty insensitive.
Speaker 4: At the time.
Speaker 3: Like I've seen estimates of fifteen to twenty percent of
Speaker 3: the time it would detect hepatitis B virus.
Speaker 2: Yeah, that's pretty bad.
Speaker 3: It's gotten a lot better, we should point out a
Speaker 3: lot yet better, like very good, like excellent. And as
Speaker 3: I always talk about, there's typically this delay from when
Speaker 3: something new is discovered to when there is wide enough
Speaker 3: acceptance for that knowledge to be applied, especially in like
Speaker 3: a medical setting. So screening the blood supply for hepatitis B.
Speaker 3: Even with this you know, pretty poor test didn't start
Speaker 3: for a few years after the virus was discovered, So
Speaker 3: in nineteen seventy the hepatitis B virus tests became official
Speaker 3: in the US, and in nineteen seventy two the American
Speaker 3: Association of Blood Banks had begun to require the testing
Speaker 3: of donors, though the test desperately needed to be improved.
Speaker 3: That was a good start, but being able to test
Speaker 3: for hepatitis B virus also meant that it could identify
Speaker 3: people who were carriers or infected with hepatitis B, which
Speaker 3: then led to widespread discrimination and ostracization for people who
Speaker 3: were positive for appatitis B. People were fired from jobs,
Speaker 3: they were not allowed in classrooms, children were taken off
Speaker 3: adoption lists. People were being denied healthcare from shared machines
Speaker 3: like dialysis machines.
Speaker 4: They were being.
Speaker 3: Denied admittance to medical school or kicked out of their
Speaker 3: jobs as doctors or dentists. I mean, the list goes
Speaker 3: on and on. It was just like, oh, great, we
Speaker 3: have this test, we can help prevent hepatitis and also
Speaker 3: we can put the scarlet letter of hepatitis on every
Speaker 3: single person that we test.
Speaker 2: I feel like that part of hepatitis B especially is
Speaker 2: so overlooked today. Hmm, Like yeah, yeah.
Speaker 3: And yeah, a lot of these many or most of
Speaker 3: these restrictions or regulations have been overturned, but the stigma
Speaker 3: and isolation faced by many people with hepatitis B continues
Speaker 3: today and has a huge detrimental impact on their quality
Speaker 3: of life. Right after the hepatitis B virus was identified,
Speaker 3: many people began working on a hepatitis B vaccine, including
Speaker 3: Bloomberg and his colleague doctor Irving Millman, who came out
Speaker 3: with one in nineteen sixty nine, and over the next
Speaker 3: decade people would work on refining the vaccine and incorporating
Speaker 3: it into routine vaccine schedules. And I think since then
Speaker 3: it's kind of faced like continuous like tweaking, and we've
Speaker 3: gotten a pretty solid, from my understanding, hepatitis B vaccine.
Speaker 1: Yeah.
Speaker 2: Since nineteen eighty one was when the hepatitis BA vaccine
Speaker 2: was licensed like in the US widespread by the FDA,
Speaker 2: and then nineteen eighty six it was updated to not
Speaker 2: have any like human parts in it. Essentially, it's made
Speaker 2: in a yeast and it's a real combinant vaccine, and
Speaker 2: as far as I know, it's the same vaccine since
Speaker 2: nineteen eighty six.
Speaker 3: Do you know who helped work on the yeast aspect
Speaker 3: of it?
Speaker 2: Tell me who erin?
Speaker 3: Maurice Hillman are Oh, let's hear it for Maurice.
Speaker 4: He's here for Maurice.
Speaker 3: And I already mentioned one person in this story who
Speaker 3: was the recipient of a Nobel Prize for their work
Speaker 3: on hepatitis viruses, and that was in twenty twenty.
Speaker 4: But in nineteen.
Speaker 3: Seventy six, doctor Brooke Bloomberg was awarded the Nobel Prize
Speaker 3: in Physiology or Medicine for his work and identifying the
Speaker 3: hepatitis B virus.
Speaker 2: Love it.
Speaker 3: Also that same year it was co awarded to two
Speaker 3: different people, just to you know, that didn't have any
Speaker 3: work together. The other person awarded was Carlton Gadgasek. You
Speaker 3: remember him from Preon's The Bad Guy.
Speaker 2: Yes, yes, I do, uh huh.
Speaker 3: Over the decades since the discovery of the hepatitis B virus,
Speaker 3: there's been a great deal of research on understanding transmission dynamics,
Speaker 3: genotype differences, the cancer causing potential of the hepatitis B virus.
Speaker 3: New hepatitis viruses like hepatitis D, like hepatitis C, like
Speaker 3: hepatitis E, better blood tests, improved vaccines, harm reduction programs,
Speaker 3: and a growing recognition of the tremendous global burden that
Speaker 3: this virus has in a physical, economic, and emotional sense.
Speaker 3: And despite all of the advancements made in the field
Speaker 3: of hepatitis B research, the virus is still extraordinarily prevalent
Speaker 3: and transmission continues today. So, Aaron, that was kind of
Speaker 3: a quick wrap up to the future. But I want
Speaker 3: to hear where we stand with hepatitis B today. So
Speaker 3: can you fill me in?
Speaker 2: Oh, I can't wait to right after this break. Unlike
Speaker 2: our first three episodes, I have some a lot of
Speaker 2: statistics for this section, Aaron, first three episodes of this season,
Speaker 2: I mean, but they're pretty sobering. Okay. Globally, it is
Speaker 2: estimated that close to four percent of the entire world's
Speaker 2: population is living with chronic hepatitis B infection. That is
Speaker 2: close to three hundred million human beings. And believe it
Speaker 2: or not, that's an improvement because the very first paper
Speaker 2: I read was a bit older, from two thousand and four,
Speaker 2: and that started off by saying, over four hundred million people,
Speaker 2: So we're down.
Speaker 4: So those are people chronically infected.
Speaker 2: Right, living with chronic hepatitis being and how.
Speaker 3: Many people are infected newly every year?
Speaker 2: What's the The World Health Organization estimates one point five
Speaker 2: million people are newly infected every year. Wow. Yes, it's horrific.
Speaker 2: If we look at the entire spectrum or the whole
Speaker 2: alphabet of hepatida or viral hepatitis is viral hepatitis caused
Speaker 2: an estimated one point three four million deaths in twenty
Speaker 2: fifteen alone, which is more than HIV. It is substantially
Speaker 2: more than malaria, and it's nearly as much as tuberculosis.
Speaker 4: So why does it feel like it's not talked about?
Speaker 1: Why?
Speaker 2: Erin, I don't know, Okay, And that's all of the
Speaker 2: viral hepatitis hepatidi Okay. Of all of those deaths, ninety
Speaker 2: six percent are estimated to be from chronic hepatitis. And
Speaker 2: of that ninety six percent, sixty six percent of those
Speaker 2: are from hepatitis B. So if we do some erin math,
Speaker 2: just kidding, just kidding, the World Health Organization did this
Speaker 2: that that is eight hundred and twenty thousand humans that
Speaker 2: are dying from chronic hepatitis B infection every single year. Ah.
Speaker 2: Now you asked why we're not talking about it. Yeah,
Speaker 2: here's probably a large part of it. That burden is
Speaker 2: not born equally across the globe, of course not. The
Speaker 2: World Health Organization, you know, divides the globe into different regions.
Speaker 2: The Western Pacific region by far has the highest incidents
Speaker 2: and prevalence of hepatitis BE, followed by the World Health
Speaker 2: Organization African region. And in these areas the prevalence can
Speaker 2: be as high as six percent or greater in some cases, wow,
Speaker 2: oh my gosh, whereas in some parts of the world,
Speaker 2: like in Europe or in North America, the prevalence may
Speaker 2: be less than one percent. And so I think that
Speaker 2: huge global discrepancy can lead for some countries to not
Speaker 2: think a lot or talk a lot about hepatitis B.
Speaker 4: Yeah, it's oh, well, it's not a problem here, so.
Speaker 2: Exactly, Aaron, I think I wrote those exact words later on. Yeah,
Speaker 2: And it gets more sobering because it's also estimated that
Speaker 2: only ten percent ten and a half percent of people
Speaker 2: that are living with hepatitis B know their status. And
Speaker 2: it's also estimated that only twenty two percent of those
Speaker 2: that are diagnosed that know their status are on treatment
Speaker 2: for chronic hepatitis. Be that statistic I want you to
Speaker 2: take with a grain of salt, because not everyone who
Speaker 2: is diagnosed with chronic hepatitis B necessarily needs treatment, at
Speaker 2: least not right away, So that statistic at least might
Speaker 2: not be quite as bad as it sounds. But ten
Speaker 2: percent of people knowing their status is pretty bad.
Speaker 4: Yeah, that's I mean, that's yeah.
Speaker 2: Yeah, it's also I have more numbers as a number
Speaker 2: heavy one and these numbers are from a modeling study
Speaker 2: from twenty sixteen data. But of this almost four percent
Speaker 2: of the global population that is infected with chronic hepatitis B,
Speaker 2: between one point six to two point two million are
Speaker 2: children under the age of five, and the World Health
Speaker 2: Organization most recent data does suggest that it's now finally
Speaker 2: just under one percent of all children worldwide under age
Speaker 2: five that are chronically infected. That's down from around five
Speaker 2: percent of all children in the pre vaccine era. Oh
Speaker 2: my gosh, I know, and still like just under one percent,
Speaker 2: essentially one percent of all kids under age five globally
Speaker 2: living with this chronic infection that I can't emphasize enough
Speaker 2: is entirely preventable At this point. We have had a
Speaker 2: vaccine for hepatitis B that is ninety eight to one
Speaker 2: hundred percent effective for seventeen to thirty years, like not
Speaker 2: a lot of waning immunity, incredibly effective vaccine for forty years.
Speaker 4: So I have a question about that.
Speaker 3: So is it part of every single routine vaccine schedule.
Speaker 2: Over one hundred and eighty countries have hepatitis B as
Speaker 2: part of their universal vaccine program, and it's estimated that
Speaker 2: eighty seven percent of infants worldwide received the three dose
Speaker 2: B vaccine series in their first year of life, which
Speaker 2: is great, but only forty six percent likely had a
Speaker 2: timely birth vaccination that critical twelve to twenty four hour window,
Speaker 2: and even less, this study estimated about thirteen percent got
Speaker 2: both the hepatitis B vaccine and if needed, that IVIG
Speaker 2: to actually treat and provide more passive immunity. But with
Speaker 2: IVIG and the vaccine within twelve to twenty four hours
Speaker 2: of birth, it's still about ninety one percent effective to
Speaker 2: prevent B infection in those babies. But it's even more
Speaker 2: effective if you can treat the pregnant person to lower
Speaker 2: their viral load. Okay, And it's estimated that only about
Speaker 2: one percent of pregnant people are actually getting that testing
Speaker 2: and then treatment one percent. Yeah, one percent or less,
Speaker 2: And so that contributes a lot to the overall burden
Speaker 2: and why we still have such high infection rates.
Speaker 4: We have the tools, just not the delivery.
Speaker 2: Yeah, so we have a lot of improvements to still
Speaker 2: be made.
Speaker 4: Yeah.
Speaker 2: Overall, this is a massive, massive disease. I honestly didn't
Speaker 2: even realize how massive it was before researching for this episode.
Speaker 2: And because it's such an enormous global problem, I'm glad
Speaker 2: that we were able to highlight so many different parts
Speaker 2: of this really important disease. But there are still several
Speaker 2: aspects that we didn't fully cover in this episode, especially
Speaker 2: the substantial stigma and discrimination faced by so many people
Speaker 2: living with hepatitis BE around the world.
Speaker 3: Right, And because this is such an important part of
Speaker 3: the hepatitis B story, I am so excited to be
Speaker 3: able to take a deeper dive into it in a
Speaker 3: bonus episode coming out next week.
Speaker 2: Woo oooh, you heard that right, bonus episode.
Speaker 3: So I enlisted the help of the amazing doctor Sherry Cohen,
Speaker 3: who is senior vice president of the Hepatitis B Foundation,
Speaker 3: to discuss some of the drivers of stigma and discrimination
Speaker 3: in hepatitis B and what's being done about it. I
Speaker 3: also got to pick doctor Cohen's brain about what it's
Speaker 3: like to work in the public health nonprofit world, what
Speaker 3: the differences between a doctor of public health and a
Speaker 3: PhD is, and some fantastic advice for people who might
Speaker 3: be interested in pursuing a career in public health.
Speaker 2: And we know there's a lot of you out there.
Speaker 4: There's a lot of you out there.
Speaker 3: Yes, it was so much fun chatting with doctor Cohen,
Speaker 3: and you should definitely mark your calendars so you don't
Speaker 3: miss the app. It comes out next Tuesday, February first. Okay,
Speaker 3: but should we maybe wrap up this episode for now?
Speaker 2: I think we should time for sources. It is a right.
Speaker 3: So I have a lot of papers for this, and
Speaker 3: I'll post them all on our website, But I do
Speaker 3: want to shout that one book in particular, and that is,
Speaker 3: of course, Hepatitis B The Hunt for a Killer Virus
Speaker 3: by doctor Bruke Blumberg.
Speaker 2: I have a few papers, not as many for this
Speaker 2: as some episodes, but a few really nice review papers.
Speaker 2: Most of them are from the Lancet and they've just
Speaker 2: been like updates on each other. So the most recent
Speaker 2: one that I read was published in twenty eighteen and
Speaker 2: called Chronic Hepatitis B Virus Infection has a lot more
Speaker 2: detail about the different phases of chronic infection. And we'll
Speaker 2: post the sources for this episode and every one of
Speaker 2: our episodes on our website. This podcast will kill you
Speaker 2: dot com. We sure will.
Speaker 3: A big thank you again to doctor Wong for taking
Speaker 3: the time to chat with us and being willing to
Speaker 3: share your experiences with hepatitis B. And also thanks for
Speaker 3: all the awesome work you do.
Speaker 2: Yeah, thank you so much. Thank you also to Bloodmobile
Speaker 2: for providing the music for this episode and all of
Speaker 2: our episodes.
Speaker 3: And thank you too, exactly right of whom we are
Speaker 3: a very proud member.
Speaker 2: And thank you of course to you listeners. We love
Speaker 2: making this podcast and we couldn't do it if you
Speaker 2: didn't listen to it.
Speaker 4: That's very true.
Speaker 3: And also an extra big thank you as.
Speaker 4: Always to our wonderful patrons. We love you. You're amazing,
Speaker 4: We love it.
Speaker 3: Okay, Well, until next time, wash your hands
Speaker 2: You filthy animals.