For more than 100 years, biologists who suggested that some cancers may be caused by viruses were the pariahs of genetics. However, they persevered and incrementally built their knowledge, leading to the discovery of retroviruses, the development of a test to diagnose HIV, and the creation of the HPV vaccine. Join us as we interview Gregory J. Morgan about his book Cancer Virus Hunters: A History of Tumor Virology.

Credits

Host: Alexis Pedrick
Senior Producer: Mariel Carr
Producer: Rigoberto Hernandez
Associate Producer: Sarah Kaplan
Audio Engineer: Jonathan Pfeffer
“Color Theme” composed by Jonathan Pfeffer. Additional music by Blue Dot Sessions

Resource List

Cancer Virus Hunters: A History of Tumor Virology, by Gregory J. Morgan

Transcript

Alexis Pedrick: Hey listeners, it’s me, your host, Alexis Pedrick. In this episode, our producer, Rigoberto Hernandez, sat down with Gregory Morgan to talk about his book, Cancer Virus Hunters: A History of Tumor Virology. They break down a century’s worth of research into the controversial field of cancer virology, from its humble beginnings in 1909 to its most important applications: the development of the HPV vaccine and the discovery of the HIV virus.

Rigoberto Hernandez: Your book focuses on cancer causing viruses. Today we know that the HPV virus can cause cervical cancer, and that hepatitis C can cause liver cancer. But viruses were not always seen as a culprit, right? 

Gregory J. Morgan: Well, my book covers basically a century of research from the beginnings of the 20th century to the beginnings of the 21st century.

And at the time, at the beginning of the 20th century, not a lot was known about cancer. There was various theories about what it was caused, but no one really had in mind a virus as a cause. People thought about chemicals, perhaps, thought about maybe internal dysfunction of the body itself. But not a lot was known.

It was known that chimney sweeps in England who would cover themselves in soot to clean out chimneys would get scrotal cancer. So that was known that there’s maybe something in the dust, right, in the coal dust or in the soot that you see in chimneys that was carcinogenic. And it was also known that some miners got lung cancer at higher rates than normal.

And it was also known that women that were promiscuous got higher rates of cervical cancer. So we knew a little bit, but not much at all really at the beginning of the 20th century. It was mostly a mystery. The idea that viruses were involved started in 1909 with a scientist called Peyton Rous.

Rigoberto Hernandez: So his research was with animals. Was the idea that eventually he could use that knowledge to help humans? 

Gregory J. Morgan: Yes, no, no, the idea was to eventually help humans. In fact, Rockefeller had donated the money that funded what’s now Rockefeller University and the hopes that they could make some progress on human health. But, one way of getting at human health is to study a simpler system, and sometimes animals are the way to go.

We today call these model systems, but at the time they just thought that them as an easier approach. Since the biology of animals and humans is sometimes not too different, we can make a lot of advances by understanding how it works in animals first. He was looking at chickens, and he discovered a tumor that you could transplant from one chicken to another chicken. It was closely related. And it would grow. Then he made a new experiment, which was to take the tumor, grind it up to very small pieces, then filter it, and take the filtrate, take what went through the filter, which was smaller than a cell, and inject that into a new chicken. And that would lead to a new tumor growing.

And that was, in retrospect, a revolutionary experiment. At the time, people weren’t sure what to make of it. Some people thought that maybe it was just, like, a peculiarity of chickens, and didn’t have any implications for humans. So it would take another few decades before people came around to the idea that viruses could cause cancer in humans too.

So his main accomplishment, which this is an experiment that started in 1909, was to find something in the tumor, in this chicken tumor, which could be extracted and then create new tumors. And he could do this basically indefinitely, so he could keep this tumor alive for years. What he didn’t know, which was that the substance was a virus, in 1909 there was no electron microscopes, so he couldn’t see a virus. All that was known was that it was something that could reproduce itself. And could pass through very, very fine filters. 

Rigoberto Hernandez: So, Rous didn’t know it was a virus, but did he suspect it was one? 

Gregory J. Morgan: Yeah, he suspected it was a virus, but he was reluctant to say so in print. It wasn’t clear exactly what a virus even was at that point in time. In fact, they were sort of thought of as, well, they’re perhaps alive, some people thought they were merely chemical, but they were known to be smaller than a cell, and perhaps responsible for a number of diseases, in plants and in animals. At the beginning of the 20th century, more and more diseases were shown to be caused by a very small organism that today we’d call a virus.

By the 1930s it became more clear that it was a virus and people became more open to calling it a virus. In the early days they called it a factor or an agent, which is sort of somewhat open ended about what that meant. 

Rigoberto Hernandez: So this eventually became known as the Rous Sarcoma virus. What happened to it in subsequent decades?

Gregory J. Morgan: So this was the first virus that was discovered right back in 1909. In the 1970s, it becomes the most important tumor virus for understanding what cancer is because we work out that what makes Rous sarcoma virus cancerous, what makes it able to create cancer in its hosts, is it’s carrying what we call today as an oncogene, and an oncogene is a, we now know, is a gene that has somehow being mutated so it doesn’t work properly.

And so it turned out that what’s probably happened was in the history of Rous sarcoma virus, it picked up a gene from a chicken, which then mutated and became sort of abnormal. And so when it got reinserted into a chicken cell, it would make that cell cancerous. This gene was called sarc. It was the first of many oncogenes discovered, and a lot of the first ones were discovered because they were in the genomes of tumor viruses and allowed these tumor viruses then to, to cause cancer in their hosts.

Oncogenes, it turns out, are not only genes that cause cancer, but they’re also genes that when they’re not malfunctioning or they’re not mutated, they play important roles in the cell itself. Normally, they play a really important role in determining how the cell cycle works, how cells know when to dive and when to stop dividing. 

Rigoberto Hernandez: And that knowledge is key to understanding cancer as a whole, right?

Gregory J. Morgan: Yes. So today, anybody that, or many people that get cancer will have their, their tumors sequenced. You’ll learn which of your oncogenes have been mutated and are important in making the tumor grow. And in theory, and in practice to a certain extent, then you can work out which cancer therapies are going to be more effective.

Rigoberto Hernandez: So after Rous, who is the next cancer virus hunter? 

Gregory J. Morgan: Yeah, he had a colleague who was working at Princeton named Richard Shope. And he was interested in a similar phenomena in rabbits and wild rabbits. Sometimes they get afflicted with these growths out of their heads, papillomas they were called. In fact, it’s probably the explanation of the mystique of the jackalope, but it’s meant to be this mythical hare or rabbit that has horns as well as ears.

But in fact, there probably was a rabbit that was infected with another virus, which we now call, um, Shope papillomavirus. Why were these rabbits growing these horn like growths? And so if you take the horn and you put it into different components, you say, what component of the horn is going to create new horns?

It turns out that it’s something that’s nothing to do with the cells that make up the rabbit. It’s something that’s smaller than the cells. And Shope basically did the same type of experiments that Rous did by showing that he could take the growths and grind them up, filter them, and then re-inject them in rabbits and cause the same growths again.

Rigoberto Hernandez: How long did it take to accept that perhaps it was a virus? Because Richard Shope also didn’t say it was a virus, right? 

Gregory J. Morgan: Yeah, he was, he was also a little reserved about how he talked about it. It really is, I think, not until the 1950s when people become more open to saying that. Right. I think it’s driven by electron microscopy.

So, we get electron microscopes that are powerful enough that actually see the viruses, and we can see these little circular objects, and that makes it easier for people to say, this is a virus, this is what it consists of, DNA or RNA in the center, covered by protein, and maybe an envelope around that, and that’s visible with an electron microscope, and we’re going to call it a virus.

In the very early days, virus was a little ambiguous, it maybe meant something that was sort of poisonous, it was ambiguous whether it was alive or not. It really is the new equipment that comes along, this was done in the 1930s, Shope was working in the 1930s. It takes till the 1950s before we have enough technical equipment to really push the story forward.

I think what you might call the modern conception is from the 1950s. We needed to know that DNA and RNA were genetic material. So you might know about the discovery of the structure of DNA in 1953 with Watson and Crick. So following that it became quite clear that a virus was really just like a little package of genes that could be transmitted from one animal to another or from one plant to another.

So yeah, the 1950s I would say we get the modern conception of a viral particle which is pretty similar to what we have today. 

Rigoberto Hernandez: So the next cancer virus hunter is Ludwik Gross. Can you tell us about him and kind of his personal journey? 

Gregory J. Morgan: Yeah, he was, he was also a little reserved about how he ta Yes, so Ludwik Gross was a Polish physician scientist. He was trained in medicine in Poland. He also was a popularizer of science. He wrote stories about recent medical discoveries for the newspaper. He was Jewish. He was worried about the Nazis in the 1930s and, in fact, when Germany invaded Poland, had to flee. And this story that’s sort of known in the lore of this field, he requisitioned a car from a friend of his, and he was driving as fast as he could to get to Romania and hoping he could drive faster than, uh, the German army which was coming across the border.

And at one point he ran out of gasoline. So it was sort of touch and go what was going to happen. I’m not exactly sure how he managed to get new gasoline, but eventually he got across the border and he escaped. And then he made it to Italy, and then he made it to the United States. He was what I call a true believer. He believed that cancer was caused by viruses, not just some weird rabbit cancer or chicken cancer, but actually human cancers too, and so he was determined to try and show this. So he started work in the United States eventually when he got here during World War II. He thought that viruses were going to be the key to understanding human cancer.

Rigoberto Hernandez: And how did his colleagues react? 

Gregory J. Morgan: Uh, derision mostly. The big problem was if cancer was caused by a virus, it should be contagious, you would think, like other viral agents. But cancer doesn’t seem to be contagious. Oncologists don’t catch cancer at a higher rate than normal people. Nurses don’t catch it from their patients.

So the standard view was this was sort of a slightly outlandish view. But that didn’t stop Gross. He kept on pushing his view and trying to investigate it with mice in his case. 

Rigoberto Hernandez: I read that some of his colleagues wouldn’t even shake his hand.

Gregory J. Morgan: Yeah, he gave a talk and a young pathologist wouldn’t accept it because they thought he was maybe pushing quackery or pseudoscience. They thought this was just so unlikely to be true. At that point, we did know that you could get cancer from tobacco, so there were other explanations of why people got cancer to do with chemicals and carcinogens.

Rigoberto Hernandez: Could you tell us about Ludwik Gross work. How he might not have had the most resources to do it? 

Gregory J. Morgan: Yeah, so he, when he came to the United States, he joined the U. S. Army and was serving at a veteran’s hospital in the United States, and he was trying to do research on the side at the beginning. So at one point, he had a colony of mice that he was keeping in coffee cans in the trunk of his car, because that was the only place he could do his research.

And in fact, people, when they came across this, saw him as being especially dedicated, um, that he was, couldn’t be stopped by a lack of resources. He was investigating different types of mice. Some mice, um, have a, have a more of a tendency to cancer than others. And he’s using the differences between different strains of mice, work out why some mice tend to get cancer at a higher rate than other mice.

Rigoberto Hernandez: So what did he find? 

Gregory J. Morgan: So in the early 1950s then he works out that you can transmit basically cancer from one mouse to another by injecting it with a virus. But you have to inject the mice as baby mice, like very, very young mice, before their immune systems are up and functioning. Otherwise, you can’t transmit the virus.

But the challenge was to do this in a regular way. So you could do it once or twice. Could you do it every time? And that’s what he tried to do is to find a preparation that would lead to a cancer-causing virus that you could ship to other researchers, and they could replicate his results. Eventually, he could do this. So by the late 1950s, there were a number of people including Sarah Stewart working as a government scientist who could replicate his work and show that, yeah, there is this virus.

One virus causes leukemia. The other virus, which is actually more important historically, is called polyomavirus. Poly meaning many, because it caused many types of cancer in these mice. 

Rigoberto Hernandez: So was this when the hypothesis that a virus can cause cancer finally accepted?

Gregory J. Morgan: Yeah, the tide was definitely turning by the late 1950s. It was getting more recognition. Gross actually started winning some major scientific awards. Eventually, I think he was nominated for the Nobel Prize, but he didn’t win it. Yeah, more and more people were open to it. I think mostly because it could be replicated. We had a better understanding of what viruses were.

And you could actually see the mice getting cancer in your lab if you worked with mice. 

Rigoberto Hernandez: It seems that Ludwik Gross learned from his predecessors. There’s like a lot of baton passing. 

Gregory J. Morgan: Yeah, I think he was definitely inspired by Rous and Shope. And I think mice would probably be a better organism for biologists to work with. Like by the 1950s, a lot of people thought that, you know, mice were almost like the hydrogen atom of chemistry for biology. Uh, they were going to be a standardized animal that you could work on. It was very cheap to, to breed them. They’ve, they breed very quickly. Um, you can do many experiments with them. Um, so the choice of mice was probably better than rabbits and better than chickens. 

Rigoberto Hernandez: Why do you think people like Rous and Ludwik Gross stuck to the idea that viruses were causing cancer, even though their colleagues were ridiculing them? What is it about them that made them true believers? 

Gregory J. Morgan: Yeah, that’s a really tough question to answer with a lot of specificity, but it seems to me that they were somehow convinced that they were right and everybody else was wrong.

It maybe isn’t also a bad strategy for a career as a scientist. It’s a risky one to be a contrarian. If you can pull it off, then you become very famous clearly. But I think they all had sort of fairly noble aims and they wanted to get to the truth, no matter what the truth was. And there were real phenomenon that they were investigating, right?

So that there really were chicken tumors, and there really were rabbit tumors, and there really were mice with cancer. The big question is just how generalizable is this, right? Is this something that’s sort of a quirk of nature or, or something that’s going to tell us about the nature of cancer in general?

And that was still up in the air, I think, into the 1960s and 70s as well. I think they saw themselves as looking for the truth and not being too concerned that a lot of their contemporaries thought that they were misguided. 

Rigoberto Hernandez: So the next cancer virus hunter to receive the baton was Howard Temin. What kind of person was he, and how was he perceived by his peers?

Gregory J. Morgan: So Temin, I think, is a new generation of biologists that is emerging in the 60s and 70s that is more steeped in molecular biology. He was a very smart young child, a valedictorian, obsessed with biology. He went to a liberal arts school, Swarthmore, and then he was upset they didn’t have enough molecular biology in the biology curriculum at the time he was doing it.

So he had to sort of rectify that with graduate school and postdoctoral work and he ended up at one of the more important places for molecular biology at the time, which was Caltech. He was ambitious, and people looked up to him as sort of a guru. He was obsessed with the idea of cancer. He was upset that people still smoked cigarettes. And we knew that was one effective way to reduce risk of cancer.

Um, and he got his lab, he, after he got his PhD and worked in virology at Caltech, he got a lab at University of Wisconsin. He’s very young. In fact, he nearly didn’t get one of his first grants because the granting agency thought he was perhaps too young to even get the money. But Temin was convinced that one type of tumor virus, called an RNA tumor virus, actually integrated into the genome of its cellular host.

And he also was derided for this idea, because at the time people didn’t think you could get DNA made from RNA. That seemed to go against what was known as the central dogma of molecular biology. 

Rigoberto Hernandez: Can you explain to us, for those who missed biology class, what is the central dogma of biology? 

Gregory J. Morgan: So Francis Crick, who discovered the structure of DNA with Jim Watson and using data from Rosalind Franklin, he proposed that there was this sort of one way flow of information in the cell, and the information flowed from DNA to RNA to protein, and the flow couldn’t go backwards.

That’s a really simple way of putting it, but, so, genetic information was in the gene, the DNA, it got made into RNA, and then that RNA got directed to the building of proteins, which we need to make it have our cells work. And what Temin was saying was actually it was possible for there to be RNA that could then direct the generation of DNA.

And that seemed to run counter to the standard view of what was going on at the time. If Temin was right, would inject the RNA into the cell and then somehow generate a DNA copy of their genome and integrate that into the genome of the host cell. 

Rigoberto Hernandez: That almost sounds like science fiction. 

Gregory J. Morgan: Yeah, it’s scary in the sense that it would, might mean that viruses, once you get infected with them, you’re kind of stuck with them because they have their genomes built into your own cells.

And if the cell reproduces, they reproduce along with it in the genome of the cell. These viruses are called RNA tumor viruses in the beginning. They actually get renamed in the 1970s as retroviruses. And a lot of the worst human pathogens are retroviruses. HIV is a retrovirus. For example, there’s another virus which is related to herpes called Epstein-Barr virus, which practically all of us have been affected with Epstein-Barr virus. It causes cancer of the jaw in Sub-Saharan Africa, but also causes mononucleosis, um, and maybe is related to other diseases as well.

I think one of the things that we’re discovering is a lot of these viruses that are integrated into our genomes can have an effect later on in their life when various things happen. 

Rigoberto Hernandez: So are you saying that when we get a virus, it can stay in our bodies and then something activates it? 

Gregory J. Morgan: Yeah, it can, it can lie dormant for years and years and then if some, some sort of event can, can make it basically jump out and start replicating again.

And the early cases, it was actually UV radiation and bacteria. This happened. When you irradiated cells with a, what was called a provirus, integrated into the genome. It can be reactivated by UV. And presumably, in the human case, other things can cause the virus to sort of jump out and become active once again.

Rigoberto Hernandez: So this reminds me of a commercial I keep seeing about the HPV vaccine. 

HPV Commercial: Numbers move you, but some can stop you in your tracks. Like the tens of thousands of people who were diagnosed with certain HPV related cancers. For most people, HPV clears on its own. But for those who don’t clear the virus, it can cause certain cancers.

Rigoberto Hernandez: The commercial says that most people would just pass it, but others can develop more serious complications like cancer, right? 

Gregory J. Morgan: Yeah. So HPV and the HPV vaccine is sort of one of the success stories of the history of tumor virology because HPV is actually a papilloma virus, just like the Shope Papilloma virus, which infected rabbits.

It’s one that infects humans. And, uh, zur Hausen, who was a German biologist, was able to show that there are a couple of different strains, I think, uh, 6 and 18 cause cervical cancer, also throat cancer and other types of cancers as well. And it’s, it’s a success story because we worked out how to make a vaccine.

We actually use the protein of the virus, not the genetic material of the virus. 

Rigoberto Hernandez: So what you’re saying is that it was thanks to the a hundred years of perseverance by these cancer virus hunters that we got something like the HPV vaccine. 

Gregory J. Morgan: Yeah. I think one of the lessons of this whole history is that these big discoveries take a long time.

This has taken really a century of research to go from. From Rous in1909 to the FDA approving the HPV vaccine in 2006. And yeah, these scientists who were dedicated, some of them for decades, working on the same issues, same problems, just making very small incremental progress, a number of different lines of research sort of coalescing into, into our current understanding.

Rigoberto Hernandez: So we can trace the discovery of the HPV vaccine back to ideas proposed by Howard Temin. But when he proposed them, was it a revolutionary idea at the time?  

Gregory J. Morgan: Yeah, he had some experimental data to try and show that this was happening. But almost nobody was convinced by his data in the early 60s, but he stuck with his hypothesis, and then he did some work which was Nobel Prize winning work. He was able to show that the virus actually had an enzyme inside the virus that it brought along with it that could turn the RNA into DNA, that is what it needed for its life cycle And that enzyme is called reverse transcriptase.

And it is not found in normal human cells. It’s only found in, in these viruses. Two different labs basically came on this, discovered reverse transcriptase at the same time. Temin’s lab, um, in Wisconsin, and David Baltimore also found the same enzyme inside a virus. And they actually had a funny little conversation where they talked to one another to tell each other their results and didn’t realize that each other had actually found the same thing.

So they were obviously very happy. Temin had been hoping to find something like this for years and years. Baltimore had managed to do it much quicker. He had more training in biochemistry. And that’s what you needed to show that this enzyme existed. It also gives you then a way for looking for retroviruses because if only retroviruses have reverse transcriptase, if you can somehow test for reverse transcriptase, you can now have a way of searching for viruses. The natural thought was, okay, we’ve been talking about chickens and mice. What about in humans? Are there retroviruses in humans that cause cancer? And now we had, in the 1970s, with reverse transcriptase, we had a way of trying to test for them. And so, uh, Robert Gallo, which some people may have heard of with, with the HIV pandemic and he, who worked on HIV, he was one of the first people to search very hard for a retrovirus that caused cancer in humans.

Rigoberto Hernandez: Well, that was the logic all along, right? That’s why they were studying animals because, if tumors happen in animals, chances are that they’re also happening in humans, right? 

Gregory J. Morgan: Right. That was what motivated a lot of these scientists, yeah. Some people, I think, thought that animals and humans are somewhat different, and that we shouldn’t expect one, something to happen in mice to happen in humans, but I think more and more, as more and more time goes by, it becomes more clear that the biochemistry of mice and the biochemistry of humans are pretty similar.

And actually, by the 1970s, we don’t even need mice anymore, really, because we can just grow cells and just do all the research. Or most of the research using cells, cell culture, so cells that have been shown to grow indefinitely. 

Rigoberto Hernandez: So let’s go back to Gallo and HIV. So in the 1980s, HIV is affecting predominantly gay men in cities like San Francisco and New York. And so this is what’s going on in the news. What did people like Gallo and those who were studying retroviruses think? 

Gregory J. Morgan: Right. So Gallo, he had already discovered a human virus called HTLV which he thought that HIV was another example of a human retrovirus that, in this case, infected white blood cells, right? That was what made it quite difficult to focus on. So, one of the first things which allowed us to fight back was to work out a test for if someone was infected. And luckily, because we’d been working on retroviruses for like the preceding decade, we had this basic understanding of how they work, how they reproduce themselves, which led us to first, a test for HIV infected people, and second, some drugs that would actually fight back.

I think the first being AZT, which attacked the reverse transcriptase of HIV. 

Rigoberto Hernandez: So we’re used to thinking that science works really slow, but in this case, some things actually happen relatively quickly, right? 

Gregory J. Morgan: Some things happen fast, some things happen slow, right? So, the test for HIV came very quickly because of the basic biology, and some of the drugs came relatively quickly. What came very slowly was a vaccine. In fact, we don’t have a vaccine for HIV even today. And in some cases, it’s sort of luck. Some viruses, it seems like, were more easily amenable to the vaccines against them, and others are not. 

Rigoberto Hernandez: However, with HIV, it seems like we have actually made a lot of progress. 

Gregory J. Morgan: Yeah, I think so. I think we understand the genome of HIV, what all the genes do in the genome. What are potential targets for drugs and now of course there are cocktails of drugs, which if you’re HIV positive, you can take which will basically bring your viral load to zero and you’re no longer infectious. So that’s yeah, one of the great success stories of retro virology. 

Rigoberto Hernandez: So, in the 20th century, there were several labs that were working in cancer viruses, like Cold Spring Harbor, the National Institutes of Health, MIT, Caltech. How did these teams of scientists interact with each other? Was there cross pollination? Were they amicable? 

Gregory J. Morgan: Yeah, I mean, I think there was a mixture of competition and cooperation. The key institution, I think, is Cold Spring Harbor Laboratory, which is in Cold Spring Harbor, New York, um, in Long Island.

They had a very productive tumor virology lab there that was assembled by Jim Watson, the co-discoverer of DNA with Francis Crick. And he thought that tumor virology was the key to understanding cancer. And he organized these big international meetings in the summers. So a lot of the scientists from various labs would assemble in Cold Spring Harbor and present their results to one another.

And then also discuss things afterwards at the bar on campus. And, uh, it was sort of almost like summer camp for, for scientists. I called it Mecca for tumor virology because there was sort of this annual pilgrimage to Cold Spring Harbor for various meetings that they held there. It’s, it’s a wonderful place.

It’s almost unique, I think, in terms of a center for molecular biology where Cold Spring Harbor is not a traditional university, it doesn’t have undergraduates. It’s sort of singly devoted to research, and it has these many large meetings there, including some in the history of biology, where you can see why scientists would want to go there and meet up. In addition to the scientific data to share, you can actually sort of have almost a vacation. 

Rigoberto Hernandez: You know, some of the people that we talked about earlier, like Ludwik Gross and Rous they had these kind of lone wolf personality, and they seemed to do everything by themselves. But that is not the case anymore, right?

Gregory J. Morgan: No, I think it illustrates a general theme in biology, which was At the beginning of the 20th century, it was easier for an individual person to make a huge breakthrough and to discover something really significant. But today, biology is a lot more complex, and it’s done by teams of people in large labs or collaborations between different laboratories.

So a lot of discoveries involve a lot more people. Actually, this makes it quite contentious when Nobel Prizes are given out, because the Nobel Prize can only be given to three people. But in a lot of discoveries, a lot more than three people are relevant. 

Rigoberto Hernandez: And not only is it different labs in the U. S., but also internationally, right?

Gregory J. Morgan: Yeah, no, I think biology is quite international. There’s a lot of work done in Europe. We haven’t mentioned some of the other people in my book, but there’s Australians and Germans and Chinese scientists who all sort of contributed to the overall development of the field. And now, of course, with journal publication being electronic, like results can be seen by anyone in the world straight away. In some ways, the annual conferences aren’t quite as important as they used to be. The results can be shared more easily. 

Rigoberto Hernandez: I want to touch on the conflict that arose in the discovery of the HIV virus and the HIV diagnostic tests. There was some work that was done by the Pasteur Institute in France, and some of the work that was actually done by Gallo here in the United States, but they didn’t always get along, right?

Gregory J. Morgan: It was the Pasteur Institute, Institute Pasteur, by a scientist called Montagnier. And he was working on HIV at the same time as, as Gallo was, in fact, in some sense they were competing about who was going to discover what caused AIDS first. At one time collaborators and at one time competitors. And it involved quite a bit of acrimony at one point in time because it turned out that it wasn’t clear if the virus that Gallo was working on was one that he discovered in America or he had somehow had been transferred somehow to his lab from France.

And since there was also a lot of money and patents at stake with the HIV test, it became almost an international dispute between France and the United States. 

Rigoberto Hernandez: Yeah, and earlier we were talking about who gets credit or how people are credited. In this case, who got the credit? 

Gregory J. Morgan: Part of the issue was that the terminology for HIV hadn’t been crystallized yet, so Gallo was actually calling it HTLV-III, and the French were calling it LAV, so that the patent office, I don’t think, realized that they were giving tests for the same thing, and the French applied for their patent first, but the Americans got theirs awarded first, and then there was lawsuits following that about who should get credit, and eventually the lawsuits were settled, and they kind of shared credit.

I definitely think that it often involves very ambitious, smart people who would like to get credit and they get credit by in science for doing things first. So one of the worst things that can happen to you in some sense is to be scooped by someone else where you’re working on something, and someone else does it first. So I think there is a lot of competition.

As I said, it’s, it’s combined though with cooperation, the idea that you can’t do a lot of this by yourself, you need a team of people. And even the French and the Americans actually worked together to publish in the same journal at the same time, uh, it was in the journal Science, that HIV was the cause of AIDS, which was a very significant discovery.

So I think it’s a mixture of the two. That’s it’s not just competitive, competition all the time, and it’s not just cooperation all the time either. I know that’s a somewhat unsatisfying answer, but, uh, and the competition, of course, can be among different things, even within people within a lab about who’s getting credit for what happens.

Jim Watson intentionally set up his lab so that people can, there’s a lot more competition than usual. He thought that drove the research forward faster. Other people disagree with that and think, well, no, you need to have more collaboration, and it’s not good to have many people working on exactly the same problem.

Rigoberto Hernandez: What can future scientists learn from these cancer virus hunters of the past? 

Gregory J. Morgan: Well, there’s a number of things to learn, I think. One is that you need to a lot of basic research to be done in order to get applied results. And just trying to go for applications straight away. Maybe it’s not the most efficient thing I mean. This is a refrain that a lot of historians of science would say that, you know, a lot of basic research is needed before you do the applied research. And in this case it was research on rabbits, right, and on mice and on chickens, which don’t seem that relevant to humans. But, in fact, this was an efficient way of getting to understanding more about human cancer.

I think the idea that you need to coordinate things like Cold Spring Harbor. It was a really important place for the development of biology that got scientists from all around the world together. So everybody can sort of be aware of what is known. And I think that the versatility of viruses is another thing that we can learn there are now people trying to re-engineer viruses to attack cancers rather than cause them, and I’m hoping that this is going to be a productive area of 21st century biology Where virotherapy, as sometimes it’s called, could be another tool for oncologists to treat people with cancer.

Rigoberto Hernandez: Why is it important to know who these cancer virus hunters were? Why should we learn about them? 

Gregory J. Morgan: Well, I think it’s important to see that science is done by people. The average person, unfortunately, doesn’t know any scientists, personally. So, I worry that in our current climate, there’s a lot of distrust of science, and it’s sort of a growing distrust.

And part of it is driven, I think, because science seems so abstract. And may be driven by large pharmaceutical companies that people distrust, but the basic research at least is often done by individual scientists who really just care about getting the truth and trying to help people and eradicate disease.

Rigoberto Hernandez: What impacts did virology have in biology as a whole? 

Gregory J. Morgan: It had a huge impact. I, I believe viruses were the most important experimental organism of the 20th century for biology. So without viruses, we would have none- we’d be nowhere near the understanding we currently do of how normal cells work of a number of different important proteins and cells and treatments for cancer even, right?

So our contemporary understanding of cancer is really driven by this idea of oncogenes .And then it’s oncogenes, so mutated genes which are causing your cancer, and the mutations you can inherit from your parents in some cases and other cases it can be mutations that accumulate during your life because of UV radiation or tobacco use or other, um, chemical carcinogens that way of thinking about cancer comes directly out of the history of tumor virology.

Alexis Pedrick: Distillations is produced by the Science History Institute. Our executive producer is Mariel Carr. Our producer is Rigoberto Hernandez and our associate producer is Sarah Kaplan. This episode was reported by Rigoberto Hernandez and mixed by Jonathan Pfeffer, who also composed the theme music. You can find all our podcasts as well as videos and articles at sciencehistory.org/stories. And you can follow the Science History Institute on Facebook, Twitter, and Instagram for news about our podcast and everything else going on in our free museum and library. 

For Distillations, I’m Alexis Pedrick. Thanks for listening. 

---