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Speaker 1: The epstein Bar virus infects almost everybody on Earth. For

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Speaker 1: the most part, it's relatively minor. Occasionally it causes mono.

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Speaker 1: You get sick, you get better. But it turns out

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Speaker 1: the epstein Bar virus EBV stays in our bodies forever,

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Speaker 1: and in some people, long after their initial infection, EBV

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Speaker 1: winds up causing cancer. In other people it causes multiple sclerosis,

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Speaker 1: which is not only scary, it's weird. When I think

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Speaker 1: of viral illness, I think you get infected with the virus,

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Speaker 1: maybe you get sick, your immune system responds, and most

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Speaker 1: of the time you get better. That's it. But EBV

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Speaker 1: isn't like that. And one lesson of EBV is maybe

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Speaker 1: we need to think differently about how viruses make us sick,

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Speaker 1: because sometimes they can hide out for decades and then

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Speaker 1: through a complicated and unlucky series of events, they can

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Speaker 1: do tremendous damage. I'm Jacob Goldstein, and this is Incubation,

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Speaker 1: a show about viruses. Today on the show epstein Bar,

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Speaker 1: let me just say a quick word about pronunciation. In

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Speaker 1: the US we say epstein bar. In the UK they

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Speaker 1: say epstein bar. You will hear both pronunciations in today's show.

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Speaker 1: The show as usual is in two parts. In the

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Speaker 1: second half of the show, we'll hear about this really

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Speaker 1: major breakthrough just from the last few years linking EBV

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Speaker 1: to multiple sclerosis and other autoimmune diseases. But first we're

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Speaker 1: going to go back to the nineteen sixties. At that time,

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Speaker 1: people knew that viruses could cause cancers in animals. In fact,

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Speaker 1: we talked about that last season in our episode about HPV.

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Speaker 1: In the sixties, no one had ever identified a virus

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Speaker 1: that caused cancer in people. There were some researchers who

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Speaker 1: thought such a thing might exist. One of those researchers

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Speaker 1: was a young British pathologist named Anthony Epstein.

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Speaker 2: He was extraordinary, a one off, i would say.

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Speaker 1: Dorothy Crawford was a grad student in Epstein's lab later

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Speaker 1: in the nineteen seventies, and she went on to co

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Speaker 1: write a book about him.

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Speaker 2: He was supremely self confident. He was highly intelligent, he

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Speaker 2: was intuitive, he was persistent. He was somebody who's going

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Speaker 2: to find the bloody virus if he's.

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Speaker 1: There, Dorothy says Epstein needed more than intelligence, confidence and

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Speaker 1: persistence to discover the link between viruses and cancer. She

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Speaker 1: says he needed some lucky breaks. Epstein's first big break,

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Speaker 1: according to Dorothy, was when a doctor named Dennis Burkett

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Speaker 1: just happened to give a lecture at the hospital where

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Speaker 1: Epstein worked.

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Speaker 2: Dennis Burkett was a missionary doctor working in Uganda with children,

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Speaker 2: and he described these large tumors of the jaw that

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Speaker 2: was seemed to be very common among young children in

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Speaker 2: this particular area. He'd never seen anything like it before,

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Speaker 2: and neither had anybody else, and so he went on

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Speaker 2: a jeep ride around Africa to look at the epidemiology

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Speaker 2: of this tumor and tracking the geographical restriction of it.

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Speaker 2: The tumor only occurred where malaria was what we call

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Speaker 2: hyper endemic, so where malaria occurred all the year round

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Speaker 2: at the same level. And he thought, and many people thought,

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Speaker 2: that maybe it was caused by an infectious agent that

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Speaker 2: was transmitted by mosquitoes, because malaria is transmitted by mosquitoes.

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Speaker 1: And Burkett gives a lecture at the hospital where Epstein

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Speaker 1: works talking about his work. That's right.

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Speaker 2: It was the Middlesex hospital where Tony Epstein was working,

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Speaker 2: and Burkett came in nineteen sixty one to give a lecture,

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Speaker 2: and Tony Epstein just happened to see this notice on

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Speaker 2: a noticeboard and went along.

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Speaker 1: You read in your book that Epstein hears this lecture

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Speaker 1: and he thinks, you know, this may be it, This

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Speaker 1: may be the tumor that is caused by a virus.

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Speaker 1: So what does he do next? What does he do

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Speaker 1: after he hears this lecture?

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Speaker 2: That very day he approached Burkett and asked him if

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Speaker 2: he could send samples of the tumor to the Middlesex

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Speaker 2: Hospital for him to study. And I mean, it's all

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Speaker 2: very well to just say it like that, And they

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Speaker 2: started arriving. But you know, getting a fresh tumor biopsy

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Speaker 2: from Uganda to the Middlesex Hospital in time for it

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Speaker 2: not to have died, the cells to have died, it's

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Speaker 2: a mean feat on its own, despite everything else. In

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Speaker 2: the mid sixties, exactly in the mid sixties.

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Speaker 1: Yes, So they start arriving every week, Yes, and Tony

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Speaker 1: Epstein starts looking at them, right, he wants to find

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Speaker 1: some path that is causing this tumor. Right, So what

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Speaker 1: does he start doing.

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Speaker 2: Well, they were chunks of tumor and he straightway fixed

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Speaker 2: them for the electron microscope. So that he could look

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Speaker 2: at them under the electron microscope. And I just have

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Speaker 2: to add that, I mean, it was dead lucky that

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Speaker 2: the medal Sex had an electron microscope, but because at

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Speaker 2: that time, you know, those machines were like gold dust

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Speaker 2: and they're incredibly expensive. But pathology at the Middlesex Hospital

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Speaker 2: had one and Tony had access to it, and so

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Speaker 2: he started off preparing them and just looking at the

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Speaker 2: cells and seeing if he could see any viruses in them.

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Speaker 2: And the answer is he couldn't.

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Speaker 1: He couldn't. Why not? What was going on?

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Speaker 2: Because there weren't any no virus particles to see in

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Speaker 2: the cells. And so he also put them into tissue

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Speaker 2: culture to see if he could grow the cells, and

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Speaker 2: he couldn't.

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Speaker 1: Just to be clear, is the idea that like, maybe

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Speaker 1: there were some very small number of virus particles in

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Speaker 1: the tumor cells, and if you could you grow a

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Speaker 1: bunch more cells, you could also get more virus particles

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Speaker 1: so they'd be easier to see.

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Speaker 2: Yes, that they might increase the number of virus carrying cells,

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Speaker 2: but they didn't. He just basically spent three years getting

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Speaker 2: native results all the way through.

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Speaker 1: So three years three years is a long time it

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Speaker 1: is to look and not see. I mean, it would

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Speaker 1: be reasonable to conclude, oh, my hypothesis was incorrect, this

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Speaker 1: tumor is not caused by a virus. Like, why doesn't

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Speaker 1: he come to that conclusion?

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Speaker 2: He would never do that to Every time you asked

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Speaker 2: him why he did it, he said, because I just

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Speaker 2: knew it was right. That's what he always said. It

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Speaker 2: had to be right.

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Speaker 1: So it's during this period, right that Yvonne Barr comes

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Speaker 1: to work with Tony Epstein, and she of course becomes

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Speaker 1: the other half of Epstein Bar. So tell me about her.

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Speaker 2: Well, she joined a bit later, I mean as the

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Speaker 2: three years were coming to an end, so she was

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Speaker 2: virtually there when the breakthrough came. She was a scientist

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Speaker 2: from Ireland and her job was to set these cells

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Speaker 2: up in culture. So he looked at them under the

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Speaker 2: electron microscope and he also put them into culture, and

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Speaker 2: as I've already said, nothing grew. But that was her

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Speaker 2: job anyway.

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Speaker 1: Huh So three years in nothing, nothing, nothing? Then what happened? Then?

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Speaker 2: What happened was fog fog fog.

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Speaker 1: A common occurrence in London.

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Speaker 2: I'm told fog fog?

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Speaker 1: Yes, why is fog? Why is fog important.

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Speaker 2: Why, because it delayed the flight that the sample was

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Speaker 2: coming in on. And he throw is particularly low lying

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Speaker 2: and particularly prone to fog, and so they diverted the

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Speaker 2: plane to Manchester. Obviously, it arrived late. It was a

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Speaker 2: Friday afternoon. Everybody had gone home except on He waited

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Speaker 2: for it, and when he got it into the lab,

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Speaker 2: it came in a bottle of transport medium, as we

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Speaker 2: call it, and he held it up to the light

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Speaker 2: and it was all cloudy, and that means to everybody

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Speaker 2: that it was contaminated with bacteria. And because the temple

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Speaker 2: had been delayed, these bacteria had grown in the culture

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Speaker 2: and it would be useless.

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Speaker 1: An urmal person would throw it out and wait for

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Speaker 1: the sample next week.

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Speaker 2: Yes, but Tony didn't do that. He'd got some of

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Speaker 2: the sample out, looked at it under the microscope and

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Speaker 2: did not see any bacteria. He saw free floating tumor cells.

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Speaker 2: And so for the first time ever, he put the

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Speaker 2: free floating cells into a culture. Previously, he'd been putting

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Speaker 2: lumps of tumor into the culture, but there weren't any

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Speaker 2: lumps this time. They'd all shape, the cells had all

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Speaker 2: shaken free on the journey.

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Speaker 1: So okay, so he finally now can see the cells,

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Speaker 1: he can culture the cells, which he's been on able

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Speaker 1: to do before.

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Speaker 2: What happened, well, very soon he had enough cells to

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Speaker 2: look at them under the electron microscope, and he looked

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Speaker 2: down the microscope and in the very first grid that

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Speaker 2: he looked at, he saw viruses.

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Speaker 1: He saw a virus, this thing that he's been looking

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Speaker 1: for and not seeing for three years. Yes, there it is.

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Speaker 2: In the very first grid square he saw viruses. And

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Speaker 2: he knew immediately that they were herpes viruses by the

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Speaker 2: shape of the virus particles. And he says that he

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Speaker 2: was so excited. He was afraid, you know, he's going

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Speaker 2: to do something wrong, very unusual for Tony, I might say.

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Speaker 2: So he switched the microscope off, went for a walk

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Speaker 2: around the block in the snow, and then came back

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Speaker 2: and turned it on again and made sure that they

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Speaker 2: were still there, and they were.

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Speaker 1: Wow. You imagine like his hands are shaking or something.

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Speaker 1: He's afraid he's going to knock it down or something.

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Speaker 2: I suppose, yes, or that he's seeing things. And I

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Speaker 2: can tell you that we now know that only about

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Speaker 2: one percent at most of cells in those cell lines

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Speaker 2: contain virus particles.

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Speaker 1: You're telling me there's a one in one hundred chants

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Speaker 1: that he would see it in the first grid.

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Speaker 2: Yes, I am telling you that. Yes, I mean, you know,

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Speaker 2: it's ridiculous, but that's what happened.

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Speaker 1: So, I mean, this is this is a big moment, right,

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Speaker 1: This is him seeming to find the link between a

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Speaker 1: virus and a tumor.

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Speaker 2: Yes, but nobody believed it. I mean, I don't suppose

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Speaker 2: I would have believed it either, to be honest.

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Speaker 1: Why not? Why wouldn't you have believed it?

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Speaker 2: Because it's so ridiculous?

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Speaker 1: Tell me more what I don't why why ridiculous?

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Speaker 2: Well, because at that time, viruses were known to cause

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Speaker 2: things like flu and measles and mumps, you know, and

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Speaker 2: not tumors. I mean it just I can understand why

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Speaker 2: people just did not believe it.

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Speaker 1: It does feel that way, right, And I guess also

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Speaker 1: the fact that there can be, certainly with some viruses

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Speaker 1: and tumors, a long latency period between infection and the

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Speaker 1: development of the tumor also, I guess makes it harder

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Speaker 1: to believe, right, I mean, harder to prove causality, Like

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Speaker 1: if you know, if you got spots all over your

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Speaker 1: body and then suddenly developed a tumor and be like, oh, okay,

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Speaker 1: I get it, that's the virus. But this doesn't work

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Speaker 1: that way.

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Speaker 2: Right, Oh, no, it definitely doesn't. And I mean, okay,

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Speaker 2: in berkelnfoma, there's a long incubation period. And what that

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Speaker 2: means is that there must be other factors. The virus

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Speaker 2: is not the only thing needed to cause the tumor.

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Speaker 2: You need other things. And of course the obvious thing

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Speaker 2: in this case is malaria, which immuno suppresses the children

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Speaker 2: and causes them to be you know, more susceptible to

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Speaker 2: this virus.

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Speaker 1: Aha. So that explains that original link between the tumor

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Speaker 1: and the geographic areas where malaria is especially prevalent. Yes,

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Speaker 1: So tell me about the rest of Tony Epstein's he

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Speaker 1: makes this big discovery, people don't believe him. Eventually they

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Speaker 1: do believe him. How does his career play out?

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Speaker 2: Well, he was nothing if not single minded.

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Speaker 1: You know, he was.

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Speaker 2: Persistent in what he did. He never gave up. He

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Speaker 2: was highly self confident, and he was also an obsessional worker.

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Speaker 2: And so you know, as soon as he in his

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Speaker 2: own mind believed that this was a tumor virus. He

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Speaker 2: knew that what he had to do was make a

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Speaker 2: vaccine to stop the tumor.

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Speaker 1: Right, it follows, right, Oh my god, we can prevent

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Speaker 1: cancer with the vaccine, yep.

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Speaker 2: So it's a totally direct way of thinking, and he

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Speaker 2: just went for it. So you know, we're still on

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Speaker 2: a learning curve, frankly, and Tony was part of the

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Speaker 2: learning curve and had a huge, huge impact.

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Speaker 1: I really appreciate your time of truly fascinating conversation. Thank

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Speaker 1: you so much, No problem. Dorothy Crawford is a retired

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Speaker 1: professor of medical microbiology and co author of the book

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Speaker 1: Cancer Virus, The Story of Epstein Barr Virus. Today, there

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Speaker 1: is still no vaccine for EBV, but people are working

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Speaker 1: on it. Since Epstein's original discovery, EBV has also been

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Speaker 1: linked to other forms of cancer, including Hodgkin's disease and

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Speaker 1: cancers of the nose, throat, and stomach. Epstein died earlier

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Speaker 1: this year at the age of one hundred and two.

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Speaker 1: As for Yvon Barr, she moved to Australia in nineteen

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Speaker 1: sixty six and became a high school math and science teacher.

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Speaker 1: She died in twenty sixteen, at age eighty three. We'll

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Speaker 1: be back in a minute to discuss new research linking

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Speaker 1: EBV to multiple sclerosis. It's been clear for decades now

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Speaker 1: that EBV causes certain cancers, and there's been speculation that

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Speaker 1: the virus may also be linked to multiple sclerosis and

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Speaker 1: other autoimmune diseases, but until recently, that's all it was speculation.

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Speaker 1: Bill Robinson is a professor of medicine and chief of

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Speaker 1: the Division of Immunology and Rheumatology at Stanford. He specializes

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Speaker 1: in autoimmune diseases, and he says for a long time

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Speaker 1: he and his colleagues didn't really buy the idea that

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Speaker 1: EBV causes MS.

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Speaker 3: We had dismissed it as epiphenomena, meaning ninety four percent

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Speaker 3: of all humans are infected with EBV, and how could

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Speaker 3: it actually be the cause of MASS given only about

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Speaker 3: one in nine hundred people developed mass.

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Speaker 1: Was that your own view?

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Speaker 3: That was definitely my view.

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Speaker 1: Basically, almost everybody has EBV, almost nobody has MS. There's

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Speaker 1: no way there can be a cause of link. The

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Speaker 1: numbers just don't make sense exactly. So this idea is

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Speaker 1: out there for decades really, and only just in the

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Speaker 1: last couple of years, right in twenty twenty two, there

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Speaker 1: were two studies that really seemed compellingly to demonstrate a

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Speaker 1: link between epstein barvirus and multiple sclerosis. And I want

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Speaker 1: to talk about both studies. Of course, I want to

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Speaker 1: talk about the study you did, but before we get

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Speaker 1: to that, let's talk about the other study. Let's talk

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Speaker 1: about the epidemiological study. Tell me about that work.

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Speaker 3: Yes, so, in the military, people are getting tested every

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Speaker 3: several years for HIV disease and other things, and the

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Speaker 3: military has banked samples from those collections. And Alberto Asherio

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Speaker 3: at Harvard School of Public Health, who's been a leader

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Speaker 3: in the field on the association of epstein bar virus

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Speaker 3: with multiple scrosis, completed a lot of paperwork and went

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Speaker 3: through a lot of regulatory requirements and with that received

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Speaker 3: blood samples that were did from individuals who developed multiple scrosis,

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Speaker 3: either in the military or following service, and basically use

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Speaker 3: these to show that essentially everybody who developed MS was

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Speaker 3: infected with EBV prior to developing MS. Huh More, specifically,

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Speaker 3: they had eight hundred one patients total, and eight hundred

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Speaker 3: out of the eight hundred and one, so ninety nine

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Speaker 3: point nine percent were infected with EBV before they developed

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Speaker 3: clinical multiple scrosis.

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Speaker 1: So that study shows very elegantly and very compellingly that

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Speaker 1: EBV is basically necessary but not sufficient to get MS.

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Speaker 1: It doesn't tell us anything about why, about the mechanism,

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Speaker 1: about what's going on, and that's what your work tells us,

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Speaker 1: and I want to get to that, but before we do,

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Speaker 1: let's just talk briefly about multiple sclerosis as a disease,

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Speaker 1: both what happens to patients and also so well what

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Speaker 1: happens to patients sort of clinically and then what happens

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Speaker 1: at the cellular level tell me about multiple sclerosis.

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Speaker 3: Yeah, so, in MS, the immune system attacks the milin sheath,

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Speaker 3: which is the insulating coating on neurons, and it's essential

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Speaker 3: for effective nerve conduction and thus sensation and you know,

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Speaker 3: muscle movement. I think of the milin sheath as you know,

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Speaker 3: the equivalent of the insulation around a wire. If you

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Speaker 3: cut the insulation on a wire, it's short circuits and

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Speaker 3: doesn't conduct. And likewise, if the immune system attacks and

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Speaker 3: damages the milin sheath on individual nerves, those nerves also

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Speaker 3: won't conduct. In us won't receive sensory signals or be

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Speaker 3: able to transmit signals to activate muscles in thus move.

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Speaker 1: So okay, so this is what goes wrong in patients

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Speaker 1: who have multiple sclerosis. Their own immune system attacks the

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Speaker 1: milin sheath that's for their nerves. When you set out

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Speaker 1: to study the role of EBV and MS, what are

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Speaker 1: you what's your hypothesis?

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Speaker 3: We were very focused on taking the B cells from

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Speaker 3: human multiple scrosis patients and then isolating the specific individual

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Speaker 3: antibodies produced by each B cell.

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Speaker 1: A B cell is a cell that's part of the

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Speaker 1: immune system, right, So you're looking at the antibodies produced

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Speaker 1: by the B cells in a multiple sclerosis patient.

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Speaker 3: Yes, And to our great surprise, many of the antibodies

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Speaker 3: were antibodies against viruses, of which EBV was a prominent virus.

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Speaker 1: Huh. So, in a sense, these are immune cells doing

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Speaker 1: what immune cells are supposed to do. They're creating antibodies

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Speaker 1: to attack pathogens.

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Speaker 3: And protect that individual against you know, viral pathogens such

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Speaker 3: as E as well as other herpes viruses.

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Speaker 1: When you put it that way, seems good, right, Oh great,

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Speaker 1: there's a virus has infected my body. My immune cells

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Speaker 1: are creating antibodies to attack that virus. That's what's supposed

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Speaker 1: to happen. Where does it go wrong?

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Speaker 3: So we discovered that some B cells made antibodies that

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Speaker 3: not only bound to EBV, but they cross bound to

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Speaker 3: human milin, meaning that.

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Speaker 1: The same antibody could essentially attack both the epstein bar

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Speaker 1: virus and the patient's own the person's own milin.

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Speaker 3: That's correct.

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Speaker 1: So was there like a specific moment when you realize

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Speaker 1: that MS patients have these antibodies that attack both EBV

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Speaker 1: and their own milin.

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Speaker 3: The lead author, Toby Lance on our Nature paper emailed

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Speaker 3: and called when he first found that these antibodies that

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Speaker 3: we had isolated from human MS patients spinal fluid B

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Speaker 3: cells when he found that they bound EBV. The email

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Speaker 3: may call me and they're like, Bill, they're reactive with EBV,

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Speaker 3: and I think we were both shocked.

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Speaker 1: Yeah, what'd you say? What'd you think when you got

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Speaker 1: that call?

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Speaker 3: I was floored. I couldn't believe it, and I was like, wow,

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Speaker 3: this is real. Because it's one thing to be statistically

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Speaker 3: or epidemiologically associated, and a second component is to have

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Speaker 3: a mechanistic basis, And our work provided the mechanistic basis

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Speaker 3: by which EBV was causing a subset of MS and

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Speaker 3: thus enables people to further believe the statistical finding that

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Speaker 3: it's strongly associated.

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Speaker 1: So I know that your study applies to something like

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Speaker 1: a quarter of MS patients. And then, as I understand it,

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Speaker 1: there's other researchers that shows similar things, quite similar things

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Speaker 1: going on in other patients, essentially antibodies that bind you know,

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Speaker 1: both the EBV and tamiolin. Is that right?

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Speaker 3: Yes, there's several groups studying other antigens that are mimicked

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Speaker 3: by EBV, including our own. And it turns out that

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Speaker 3: EBV infections also associated with other diseases such as systemic

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Speaker 3: loopus or SL and it's also associated with rheumatoid arthritis.

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Speaker 1: So these are all autoimmune disease, these diseases where the

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Speaker 1: body's immune system is attacking itself. Basically, yes, I mean

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Speaker 1: is this like, are we right now? Are you right

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Speaker 1: now finding the answer to this question that people have

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Speaker 1: been asking for whatever fifty years, eighty years, like, are

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Speaker 1: you finding the virus that is causing autoimmune diseases?

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Speaker 3: We believe we are, and we are performing experiments to

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Speaker 3: further bear out the mechanisms that would encompass one hundred

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Speaker 3: percent of MS and as well as of lupus and

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Speaker 3: other autoimmune diseases that are EBV associated.

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Speaker 1: And just to be clear, in these other autoimmune diseases,

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Speaker 1: what are the immune cells? What are the antibodies attacking?

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Speaker 3: In the other autoimmune diseases, They're not attacking myelin' They're

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Speaker 3: attacking their corresponding tissue anogens. So in loopus, the immune

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Speaker 3: system attacks the nucleus of cells and also the kidney.

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Speaker 3: In rheumatoid arthritis it attacks the joints.

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Speaker 1: So I mean, why does this one virus, EBV, Why

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Speaker 1: does this one virus cause us to make antibodies that

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Speaker 1: attack so many different parts of the body, Like, what's

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Speaker 1: going on?

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Speaker 3: You know? I think we don't know. We only you know,

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Speaker 3: hypothesize and speculate. My sense is that given EBV as

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Speaker 3: a herpes virus that's present in a person's B cells

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Speaker 3: as well as epithelial cells for life, and that it's

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Speaker 3: transiently reactivating on a periodic basis, that those properties make

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Speaker 3: it reimmunize the individual multiple times repeatedly over the courses

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Speaker 3: of their life.

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Speaker 1: So basically, most people get this virus when they're a kid. Right,

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Speaker 1: So you have this virus not just in your body

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Speaker 1: for your whole life, but in your B cells, in

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Speaker 1: your immune cells, and it periodically sort of turns back

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Speaker 1: on basically and causes an immune response. And it's the

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Speaker 1: idea that it's happening again and again and again. That's

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Speaker 1: fundamentally the problem.

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Speaker 3: I think that that's contributing to the problem.

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Speaker 1: Almost everybody gets EBV, has EBV. Very few people get

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Speaker 1: autoimmune diseases, certainly relative to the share of people who

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Speaker 1: get EBV. What's going on there? Like, why do only

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Speaker 1: some people get autoimmune diseases if we all have EBV.

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Speaker 3: Yeah, that's the big question, and that's why more than

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Speaker 3: five years ago we were skeptics that there was any

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Speaker 3: relationship between EBV and MS or these other autoimmune diseases

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Speaker 3: like lupus.

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Speaker 1: Well, so presumably it's sort of necessary but not sufficient, right,

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Speaker 1: Like you need to have EBV and something else or

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Speaker 1: in some other set of phenomenon, characteristics, risk factors, whatever

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Speaker 1: to develop autoimmune disorders? Do you have a sense of

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Speaker 1: what the other things are.

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Speaker 3: Recently, investigators in Germany Christian Muntz is showing that some

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Speaker 3: of these classic multiple sclerosis. Genetic risk factors are actually

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Speaker 3: risk factors for inability to mount a robust T cell

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Speaker 3: response to EBV. So they're basically preventing you from having

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Speaker 3: a T cell response that controls the EBV and that's

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Speaker 3: known to be associated with more rounds of reactivation.

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Speaker 1: Huh. So, just to be clear, T cells are are

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Speaker 1: an immune cell. And so basically this finding is if

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Speaker 1: your body is bad at controlling EBV, if you're genetically

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Speaker 1: bad at controlling EBV, you are more likely to get MS.

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Speaker 1: And that makes sense because if you're bad at controlling EBV,

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Speaker 1: it's gonna you can have more sort of outbreaks within

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Speaker 1: your body of EBV and you're gonna have more rounds

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Speaker 1: of this kind of mutation of antibodies.

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Speaker 3: Yes, let me give you another recent developments that's profound.

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Speaker 1: Okay.

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Speaker 3: A investigator in Germany, professor yorg Chet, gave human lupus

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Speaker 3: patients that had refractory disease that was refractory to all therapies.

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Speaker 1: Refractory meaning treatment doesn't work.

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Speaker 3: Treatment doesn't work. Yeah, he gave them a cancer drug

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Speaker 3: that completely depletes their B cells in a profound deep depletion.

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Speaker 3: So to get this drug, you have to be admitted

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Speaker 3: to the hospital for two weeks and receive chemotherapy for

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Speaker 3: a Boemero transplant, and then you receive this drug that

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Speaker 3: attacks all the B cells and removes them all from

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Speaker 3: the body.

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Speaker 1: So this is like a hardcore, nasty cancer drug.

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Speaker 3: Yes, okay, but he effectively cured these lupus patients.

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Speaker 1: Huh.

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Speaker 3: They're now three years out off all therapies, completely healthy.

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Speaker 1: So is the basic idea that if you destroy all

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Speaker 1: of the B cells, these B cells that have evolved

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Speaker 1: essentially in a way that is causing them to attack

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Speaker 1: the body, get well, they're extinct. You basically make them

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Speaker 1: go extinct and you get to start again. Is that the.

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Speaker 3: Idea there, exactly? And they term it an immune reset,

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Speaker 3: which I believe it is because after this Boemere transplant

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Speaker 3: type of B cell depletion merges our naive B cells

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Speaker 3: and then those repopulate the whole repertoire.

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Speaker 1: Yeah, you're starting from scratch, you get to start over, Yes,

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Speaker 1: and the finding suggest that when you start from scratch,

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Speaker 1: you get better. Your new B cells are not creating

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Speaker 1: antibodies that attack your own body, if I understand.

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Speaker 3: Correctly, that's correct. But you also have to rego through

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Speaker 3: all of your childhood infections and vaccines.

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Speaker 1: Oh right, so it's just carpet bomb. You're just carpet

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Speaker 1: bombing the B cells. You're not immune to anything anymore.

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Speaker 3: That's correct. You're starting from scratch, But compared to having

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Speaker 3: bad lupus or bad autoimmune disease, it's a huge win

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Speaker 3: for the individual patient.

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Speaker 1: So what you want, presumably in the same way, we

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Speaker 1: have developed targeted cancer therapy, so you don't have to

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Speaker 1: carpet bomb whatever rapidly dividing cells. It seems like if

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Speaker 1: you could just target the B cells you don't like

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Speaker 1: and let all the other B cells be, that.

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Speaker 3: Would be great, absolutely, and we're working hard to develop

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Speaker 3: therapeutic approaches that would do exactly that.

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Speaker 1: Thank you so much for your time. I really appreciate

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Speaker 1: it great.

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Speaker 3: Thanks for featuring EBV in our work.

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Speaker 1: Bill Robinson is a professor of medicine and chief of

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Speaker 1: the Division of Immunology and Rheumatology at Stanford. Thanks to

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Speaker 1: my guest today, Dorothy Crawford and Bill Robinson next week

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Speaker 1: on incubation. Why did he jump on the boat or

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Speaker 1: train or boat and train or whatever and go to

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Speaker 1: this remote island in the North Sea.

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Speaker 2: Why did he do that?

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Speaker 1: A family doctor goes to great lengths to figure out

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Speaker 1: the relationship between chicken pox and shingles. Incubation is a

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Speaker 1: co production of Pushkin Industries and Ruby Studio at iHeartMedia.

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Speaker 1: It's produced by Kate Ferby and Brittany Cronin. The show

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Speaker 1: is edited by Lacy Roberts. It's mastered by Sarah Bruguier,

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Speaker 1: fact checking by Joseph Friedman. Our executive producers are Lacy

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Speaker 1: Roberts and Matt Roman. I'm Jacob Goldstein. Thanks for listening.