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