Q/208
10/30/02

Jan Sapp’s interview with Joshua Lederberg
“: a
July 26, 1995; [Ciba Conference on Ma, and His Future]...

L: ..that was my first venture into social commentary, at least
published social commentary. And I talked about eugenical
issues, what molecular genetics would do for us. I was in a
little bit of a debate there with H.J. Muller and with Huxley
who were the positive eugenicists, and I was saying it’s hard
to quarrel with that but why use such a clumsy method and with
such uncertain political and social overtones. If there’s a
problem, the technology fifty years downstream will be so far
Superior; but what you’re proposing that we can deal with it
more effectively and let’s use the time and the interval and
try to decide what it is we really want to do. And that’s when
I introduced the term euphenics as the counter program to
eugenics, at least for the...

S: Why? Because it’s at the phenotypic level...

L: Yeah; and a footnote yeah, that’s medicine, education.
S: Exactly. It’s all the social factors. So this is ’62.

L: Yeah.

S: What does Nigel Calder have to do with this?

L: He was the editor of The New Scientist. Yes, I actually did
publish a rather hysterical short one-page version of it in
The New Scientist - Crisis in Human Evolution, namely. The
kind of stuff Sinsheimer was touting very strongly a few years
later on. But I was saying, "Look, there’s an issue; let’s
think about it" and a lot of other people said "Oh, how awful.
Let’s shoot it down". I just wanted to look at it.

At any rate, I bumped into him a couple of times. I think this

is the COSPAR, the Committee on Space Research - the international
conglomeration of scientific activity of a lot of the non-
governmental and governmental efforts in international cooperation
in space. They had a symposium in Nice; I gave a paper about the
biologist’s interests in space exploration - worrying about
quarantine on the one hand which is another cosmic environmental
issue; and on the other the positive programs of the cosmos
determinants of biology that are around all the time.

[I coined the term exobiology around this time]. And I

think I was sitting next to him on a flight either to or from

Nice that he approached me and said, "Would you be interested in
writing a column [weekly or monthly or whatever] for The New
Scientist on social impact of science", I said, "That’s an
interesting proposition" and I mulled it over for a while. And

... this is a rule of life I’ll pass on to you: whenever you’re

faced with an opportunity, never just grab it; if you find you’re
interested in it then say, "Look, what do you really want to do
with it" rather than what’s presented to you. So I followed that
heuristic and said, "Look, if I’m going to do that sort of thing,

I want to put it some place where it’ll have a broader impact than
in The New Scientist". And I asked around some friends in the
newspaper publishing industry. I would have been very happy if
the New York Times had agreed to it, but as it turned out, the
Washington Post is the one that was receptive. I guess it was
David Hamburg who introduced me to the publisher.

S: And where were you institutionally based when you were doing that?
L: Stanford. I hadn’t been there very long, but I got there in 1959.
S: So what’s the deal with Washington Post - weekly?

L: They agreed on a weekly column. It’s dated - as you can tell by
the title - it’s called "Science and Man". Didn’t have much fuss
about that ("sexist") distinctions in those days. And so it went.
Howard Simon was my protector there. He was the science editor
for the Post, and I needed one because his publisher was
constantly badgering him - "Nobody can understand what this guy
is saying. What are we publishing it for?" - etc, etc. And he
would sometimes protect me from mutilation of my text. He was
quite keen on it. The fact is it had a pretty good play, and
my target audience were congressional staffs if I were to try
to identify what kind of person was I trying to get to.

S: Congressional staffs?
L: Yeah. These are the people who actually read the technical stuff
that might have policy implications and pass it on to their

bosses.

S: How common is it (this is what, °66?).
L: Yeah. Nobody else was doing it.

S: I was going to say... there wasn’t a science reporter or science
editorial column for ...

L: I did not know of any working scientists at that time who were
making regular contributions of this kind.

S: And later on people such as Lewis Thomas whose book I read
recently, The Youngest Science, talked about his contract
with The New England Journal of Medicine and that’s ’72.

L: Yeah. No, it’s the public press that I’m interested in.
Morowitz must have been doing it; I don’t know when Steve
Gould started. But even to this day, there is no regular
column of this kind.

S: So how long did it last?
L: About six years. It was quite a strain.

L: Well, °66 through ’71. I didn’t actually get started until ’66.
Id forgotten. It was ’64 or °65 when I talked to Nigel. And
more and more I got into environmental questions and there was
hardly any environmental reporting in those days. So issues...
hazards from lead or whatever else just thinking environment
and so on - weren’t being very much talked about.

S: But this is a demanding thing to be writing. Once a week you’re
doing this plus you’re at Stanford at...

L: Oh, yeah, running a department.
S: And were you also involved in any international affairs?

L: Not as much then as now. And in fact, this did come to some
crisis because at one point for example I was asked to serve
on the PSAC, on the President’s Senate Advisory Committee,
and I decided I couldn’t do it, that while I was writing a
column for public consumption that I really could not be the
recipient to confidential information. I would be having to
hold things back from a public that would be expecting the
contrary.

S: But was this your entry into those kinds of relationships?
L: In some measure. Not totally, but. Yeah, my connections with
government up to that time were NIH and NSF study sections which
didn’t involve broad policy considerations. I might have been
once in a blue moon asked on some other commission or whatever,
but it was not a regular commuter.

S: And can you measure how successful your series was?

L: It’s very hard to say. I keep running into people who tell me
that they used to read it and...

S: Actually, I have met lots of people.
L: But when I asked myself, I didn’t know how to measure it.
S: Isn’t that interesting?

L: But the kind of people we’re talking about told me that yeah, they
read it; they looked forward to it. I'd get a little bit of
flack in the mail and so on.

S: I was going to ask you that. So did you get governmental feedback
from these Congressmen that you were addressing?

L: From time to time. I’d get three or four letters a week of
response which sounds like it’s not very much but when I’d run
into people..well, you know: how many people bother to write?

S: Okay. Now, there was something else you mentioned on email...

L: Let me make another point about that, though. This was also
syndicated; it wasn’t just the Washington Post. It appeared
probably in a couple dozen newspapers all around the world.

In fact, you may have seen it in The Age in Melbourne. I know
it was there for a while. This is just an example.

S: And this raises another issue which is.. on the one hand we have
a scientist going into, in effect, journalism reportage but
basically bringing the public up to date with current events
within the scientific community of things of interest to
scientists.

L: And there were very few things I was a strong advocate of. It
was mostly, again, "Let’s take a look at this. There are some
issues that deserve consideration. Life is more complicated than
you think, that simple settled answers are likely to be overly
simplistic". If I had any meta message, it would be in that
dimension.

S: But what’s your other message at the level of writing? What does
it say about journalists reporting about science. I mean, did
you have a sort of chauvinist attitude of "Here’s a scientist.

I know what I’m talking about" as opposed to journalists screwing
it up?

L: Well, yes. One reason I did this was that (I can’t recall the
specific incidents, but) I was very disappointed in the way the
press ever dealt with anything I ever had to say. And I came
to the conclusion if ’'m going to be in the press, I want it to
be in my own words. I understood their constraints; I had a lot
of sympathy with what they had to do, especially when I could
sort of do it one day a week and what they do is seven days a
week. But I just felt there was a need for that alternative.

So there was some explication of current science, but it was
focused on "What does this mean for humanity"; that’s the headline

rather than a policy dimension of these kinds of discussions.

S: What about your colleagues. Did they look askance at this? Did
they say "Here’s Lederberg going..."

L: A few did, yeah. Well, yeah.

S: Was it seen as political activity?

L: Yes. It was mixed. And even some of the same people said, "Gee,
I’m really glad you’re doing this for us” and at the same time
said, "Gee, that’s not really science, is it?" But I wasn’t
playing headlines the way that Carl Sagan does. I was not
personalizing it in that sense.

S: It wasn’t a huge money maker.

L: Oh God, no. No, it was nothing.

S: And so from the point of view of scientists, for you doing this...
L: I had mostly positive reinforcement: "I’m glad somebody’s doing
it, but it does mean dropping your science, doesn’t it?” I said,

"Well, I try to walk with two feet".

S: What does it do for breadth? Does it give you more breadth?

L: Let me explain why I stopped. I would read my columns and I
would get even more interested in the subjects that I raised, and
Pve got a foot of files for every topic that I brought up which
might have taken ten columns over a period of a year or two to
talk all around a given set of issues. But I would continue my
self education and self criticism far beyond the time the thing
as published. Well, that’s not a journalist’s approach; that’s

a scholar’s approach. And I decided in the end that I was a
scholar and not a journalist and I just couldn’t keep doing

that, that I really should go into more depth on the topics

that I did want to study and be able to do a better job.

So there was just the mental indigestion that was involved. It
was close to six years’ worth.

S: That’s a long time.
L: There were about two hundred fifty columns.
S: Is that right?

L: Yeah.
S: And where are they now? Have you even pulled these out?

L: I’ve checked my own copies of them. I’ve had them all transcribed
so they’re ready for publication.

S: You’ve got them on CD ROM or something?

L: Not yet; they will be. I’ve just got them in computer files at
this stage.

S: How did you get them into computer files?

L: [had my staff here transcribe them. If I had been more patient,

I might have waited to get them scanned and done in that way.
But don’t kid yourself: by the time you’ve edited a text like
that, you’re not very far from the amount of effort required to
just type it in in the first place. I think it was not an
inappropriate choice. The columns could be scanned by a

human interpreter about as efficiently that way as the formal
scanning. When you get scientific material, there’s an advantage
to scanning it in, having the page images on tables and things

of that sort.

S: Okay. So this takes you far off the bench, but from the point
of view of a bacterial geneticist.
L: Very few of the...well, one in ten might literally have to do
with genetics or microbiology. I didn’t avoid that topic, but
it was much broader. So nuclear policy, arms control. got
kind of excited about Vietnam and wanted to be some voice of
temper and campus revolt and that sort of thing. So some of
that crept in. But I’d get a little admonition now and then
from Howard who said, "Look, we've got a lot of other people
who think they know as much about that as you do",

S: Who’s Howard?

L: Howard Simon, my editor. It was not a heavy hand, but a little
reminder now and then. So he gave me some latitude. But I
couldn’t go week after week on things that didn’t have an obvious
centre of scientific and technical expertise. It was my
credential for being the one to do it.

S: I know when you sent me the article on the Sea Level Canal, it
was quite interesting what you said from the point of view of a
geneticist interested in evolution. I’d be interested in first
of all the taxonomy of the organisms in the Caribbean before the
Pacific Ocean rushes in.

L: Well, there’s an analogue to that with planetary quarantine.

S: I was about to say the exact same thing. It reminds me of your
story about the moon, when you were worried about the moon being
contaminated.

L: Mars is what I was worried about.

S: Excuse me; Mars, that’s right.

L: Pd given up on the moon. If we’re going to send astronauts
to the moon, the moon’s going to be contaminated.

S: Well, is the moon contaminated?

L: Undoubtedly stuff has been left there. I’m not sure how
consequential it is; there’s no atmosphere and it’s probably
heavily bombarded with radiation from space, so it’s self
Sterilizing in very large measure. But if we were to find a
spore on the moon, we’d have to seriously worry that it was
not the result of terrestrial traffic.

S: Do you remember when Carson’s book came out?
L: Rachel Carson? That was in the late 50s, so it was a little bit
before I was responding to...

S: It came out in 62.
S: Did it have a big influence on you when it came out? It didn’t
go smack right between the eyes with respect to environmentalism?

L: Not to me, but I could see what was happening to the public more
generally. It was certainly a major point of arousal. I thought
it was greatly hyperbolic, and I thought the toxicity of DDT was
greatly exaggerated and so on. The one thing that’s come up that
we didn’t know then is what it does to egg shells and birds. I
think that part is indisputable. But I think that’s the only
part of its ecological impact that’s really reliably founded.
So I tended to take a quietistic attitude about some of that
stuff, but I felt against the vacuum that we’d had before, it
was a matter of if the pendulum’s gonna swing violently from

one side to the other, let’s find what some central point might
be.

S: Okay. Can we jump now to emergent viruses for a minute?
L: Yeah.

S: I have two questions. I need to understand what happens in 88,
what you people are doing in Washington, what the alarm is. And
then I have another question which I’d like you to think about
and undoubtedly you already have which is "Is there a new paradigm
for understanding virus outbreaks that has emerged in the last
ten years or less" which seems to be indicated in Morse’s book,
"Emerging Virus” and things of that nature. I keep seeing
pictures of this stuff. There is an ecology of viruses as
opposed to killing them.

L: Well, I can mostly give this in a personal perspective which is
what you want. I had been exercised ever since I can remember
about the hazards in biological weaponry and the subversion of
microbiology as military agencies. I was quite well acquainted
with the programs that had emerged since World War II. A lot
of folks who had been at Fort Detrick during the war were at
Wisconsin afterwards; there was no secret about any of that.

I felt we had to defend ourselves, but I was appalled at the idea
that these things would ever be used. At the time, I didn’t

think much about terrorists in the lower level activity but

more as it’s being incorporated into the arms race in the U.S.

and the Soviet Union. That’s sort of background Item 1. I didn’t
do much about it during the 50s up to the middle of the ’60s.
And 2), I was very much impressed by the outbreaks of Marburg
and Lassa fever in the middle ’60s, and I wrote a couple of
columns about it. I also remarked that this is nature’s war

and I also connected them with how much more terrible it would be
if these kinds of agents were to be adopted as well as BW agents..
So I had a dual program - one at the political level, the arms
control aspects of it - and the other is to worry about these
emerging viruses. I didn’t use that expression at that tirne.

I think the paradigms are mostly rhetorical ones; I think the

basic ideas go back a very long time.

In ’67 and/or °69 (I forget which one of those it was) I brought
this issue up again at a Nobel Foundation conference and didn’t
get very far with it.

S: What issue?

L: The hazards of emerging viruses. I talked in particular about
influenza through recombination. We’d had two major antigenic
shifts of flu, one in °57 because I remember that happened when
I was in Melbourne -- the Asian flu -- and there was another one
in the ’60s. And I read up on it, had long known about the
influenza epidemic in 1918 and what a devastating impact that
had.

Oh, there were seminal books on this. I did medical school, had
microbiology and so on, but Hans Zinsser wrote Rats, Lice and
History and that’s probably the guiding text on this issue.
O’Neil wrote essentially the same book a little later on plagues
in history -- not much that’s different in there. The Zinsser

book is really the paradigmatic

S: So as far as the influenza epidemic of 1918, 1919 -- is that what
you mean?

L: Well, about the role of plague as a historical phenomenon, that
it had as much to do with shaping human destiny as wars had. Then
as far as the ecology of microbes are concerned, the books by
Dubos especially, Theobald Smith and Mac Burnet -- Mac wrote one
on the natural history of Viral Disease I think it’s called; it
goes back quite a way. It’s provided the main intellectual
substance of thinking about it and the paradoxes of co-evolutionary
adaptation of micropredators and their hosts. The short run is
towards higher virulencies through transmissibility - those are
pyrrhic victories; and the long run is co-adaptation closer to
symbiosis.
10

Now, I am reminded also of the general background of my interest
in symbiosis that you know all about, the 1952 paper and so forth.
So that’s even part of the background -- the ecological

relationship -- which comes under the general heading of symbiosis
study.

: Agreed. But when I look at -- and you mentioned a moment ago --

that perhaps there is no new paradigm but there’s a sketch for
rhetorical purposes or polemical purposes - but what is that
polemic? Is it a polemic that, "Oh, we’ve killed these damned
things"? And our aim is to kill them. And, by the way, if we
get reinfected or if there’s an outbreak, this is because they’re
new viruses. And the new paradigm would Say your object is not
just to kill them, it’s to learn how to live with them and the
reason for that is that -- guess what -- they may not be new
viruses at al] and that this is not simply a matter of mutation
but a matter of transmissibility; and maybe what we’re doing is
speeding up the rates of cycles of infestations or cycles of
epidemics. Is that an accurate depiction of -- that’s what I...

L: Td have to put at somewhat greater length and more subtly than

S.

L:

that. If we could only do it, our aim is to kill them; but

they’re hard to kill, and that’s a huge biosphere out there. I’d
calculate there are about a mole of potential pathogens! And
those are very big numbers. So you better take that into account
if you’re going to talk about eradication as a paradigm. I’ve been
skeptical about eradication, maybe overly so. It took me a long
time to when I was....

: Maybe overly so, did you say?

: Yeah. In some particular context, I was something of a hold-out

on Advisory Committee on Medical Research at WHO on declaration
that smallpox had been eradicated. And it was okay to wait

another year or two before claiming victory on that. It probably
didn’t do any harm, but turned out...

: When was that?

: 781

And what did it turn out? Was there eradication?

Yeah. It’s never shown up again. Now, it still lives in the
freezers in the laboratories, and there’s a debate going on
about destroying them. It may still live in the frozen Arctic
11

in the old cemeteries, and Sandakcheev is digging them up to
see. And I think it’s very important to find out whether that
potentially exists. I’d rather have them dug up in very
carefully-controlled conditions than have it happen inadvertently
with unvaccinated personnel and so forth.

S: So eradication to you as a paradigm -- you’re skeptical about it
because of the impossibility of success and because of the large
numbers of variations of these organisms. Is that...

L: I think there are so many ways in which there might still be
lurking remnants and quite apart from the issue about reformation,
de novo from its evolutionary progenitors that... There’s a
tacit assumption of special creation that public health people
have about infectious agents. They really have not understood
their continued evolutionary process. The ease with which they
talk about the Great Plague of the 14th century being
Yersinia. Okay, maybe it was. I wouldn’t guarantee it. But
they don’t have another category to think of it. And if it is
pestis, what’s the identity, the strains and so on and so forth?
But I’ve been working on microbial evolution all my life, so the
idea of plasticity is one that I’m much more deeply imbued with.

S: And is it the plasticity of the viruses, for example, that makes
them so difficult to eradicate.

L: Yeah. Well, the whole set of issues. We don’t have good
chemotherapy for them. They’re easy to eradicate if they have
unique hosts, and that’s what makes smallpox almost a unique
paradigm; there’s no other known host for it nor another reservoir
for it. Maybe the same will be true for polio. So far, that’s
worked in the western hemisphere. What we will do if we’re smart
is to replace virulent polio with Sabin polio and have that still
circulate as an essentially innocuous attenuated virus that will
get around a little bit so it isn’t only the inoculated individual
who gets the benefit of it.

S: Does it make sense to talk about -- as in other kinds of
invasions, not the kind of invasions that Elton talked about in
terms of the transmission of plants and animals by humans like
the zebra mussel kind of stories but -- other kinds of, let's
call it, naturally occurring outbreaks? Does it make sense
to talk in terms of virus outbreaks in the sense of cycles,
thousand-year periods of cycles; where are we in this wave?

I mean, there’s a way in which one speaks about...

L: I don’t know why there would be a thousand year cycle. I could
12

imagine there being a fifty year cycle having to do with immunity
and that certainly has happened with flu. So an outbreak leaves
survivors with a very high degree of immunity. Until those have
died out, you’re not gonna have a fresh wave. But that’s about
the only basis for any cyclical behavior that I could visualize

and that implies that there’s some continued reservoir, either

in an animal host per se or recreation through regeneration.

S: But if you talk about an ecology of viruses, how can you talk
about for example -- and again, comparing it to other kinds of
invasions where we may argue, "Well, we may not be causing these
outbreaks but we may be increasing the frequency of recurrence of
these outbreaks"...

L: Oh, human behavior has a lot to do with opportunities of viral
spread. A lot of people want to pin down all the awful
consequences of capitalism and so on. I say, "Yes, and there’s
One outstanding one and that is people travel a lot and to an
unprecedented degree". And the statistics I throw out is that
a million people a day fly across an international boundary.

A million people a week travel between developing and advanced
countries. That’s a new fact in human existence. I don’t think
we need to go into climate change or... I think the other matters
are all trivial by comparison.

S: So does that have any evolutionary.....

L: ... their rather poorly-regulated mechanisms for adaptation and
above all the immense population numbers, even with very low
mutation rates. When you’ve got a mole’s worth of bugs, that’s
a lot of opportunity for variants. So the issue is, then, do they
find their host and once having found them, will they have a good
opportunity to spread.

S: Yeah, exactly.

L: The human population, first the total numbers of the population
and then the hosts that are available and the way they stratify.
And these convocations of very large numbers of people live in
very crowded conditions, very poor hygiene; you couldn’t design
a better setup for new outbreaks to expose. I think, I’m certain
that will happen.

S: Pm asking for a little biology lesson here which is about the
notion of virulence. As I understand it, in the 1918-19 pandemic,
one of the reasons at least that people are giving in the 1990s
in reconstructuring those events for the increased virulence was
13

the frequency by which this virus could be transmitted because
of the trench warfare, because of people going back to their
towns and villages, that this is going to have an evolutionary
impact on the organism itself, using a sort of game theory

to account for...

L: When there are fresh hosts readily available, there’s likely to
be selection for enhanced virulence as it goes along. Just as in
standard Darwinian theory... as long as the hosts are there
and as long as the first host doesn’t die too quickly but there’s
a nice balance on that score, you can expect selection for more
rapid replication. The virulence is sort of a side effect.
For a viral pathogen it’s sort of indifferent whether the host lives
or dies. In fact, it’s to its disadvantage if the host dies as
opposed to a bacterium, by the way. Bacteria can multiply in
putrefying flesh; viruses cannot. That’s a severe limitation.

S: What does virulence mean?

L: Virulence is an operational term; it’s a black box. Virus in,
disease/death out. And just think of all the considerations
involved.

S: I see. Okay, so does it mean...

L: It’s everything involved. Ease of transmission, rapidity of
replication, side effects of formation of toxins, disabling
of the host’s defenses -- you have to include drug resistance
plus the de facto situation of that black box is that drugs
are going to be thrown at it. So you think what are all the
defense mechanisms and what are all the things that keep the
organism capable of coping with the virus. So you really have
to think of it in those operational terms.

S: Okay.

L: It’s generally correlated with rapid multiplication. A virus
that multiplies slowly is not likely to be virulent just because
there would be less of it around.

S: Right. So can I assume, then, logically that with the speeding
up of the transmission of viruses that you were speaking about
a moment ago with a million people crossing borders per day that
we would then be enhancing a virulence of viruses?

L: Its a second order effect, but it provides the setting in which
that evolution is more likely to occur. Where you will start
14

limiting those selective forces is if you run out of hosts. Then
there’s no new place for a virus to go, there can be no selected
drive for it to enhance its virulence. Then those viruses which
last longer than the host of origin are the ones that are going

to survive, and that’s less virulence. The ones that don’t kill
their hosts -- and this is what we see with AIDS -- the virus

is going to be there ten years later. The ones that kill their
host promptly -- the host is dead, the virus is dead. So that’s
why there’s a paradox in the evolutionary trends. The short run
will tend to favor rapid multiplication and what goes along with
it; the long run would tend to favor a more symbiotic/
mutualistic relationship.

~”

: A classic dilemma.

: Let’s go to 1988, then. In ’88 you’re talking about what, the
AIDS pandemic; there is new cholera; there’s lots of emerging
new viruses. What do you people do? Is that what you...

nm

L: Okay. Again, you’re asking that at a sort of personal level. I
didn’t publish it. I was one of the very first people... when
the initial report about HIV and I had this conversation with
Igor Tamm in biology. He said "It’s gotta be a virus". There
was a lot of skepticism about it at that time; we even thought
[amyl] nitrite would help it and so on. I remember talking about
this with a number of people and saying, “What would happen in
its further evolution” and so forth. But I don’t recall my
having gone public with it right then.

S: Public with what?

L: My concerns about the further evolution of AIDS. Then I was
invited to appear at a symposium that was organized by the
New School for Social Research on plagues. And I think I sent

you a copy of this. If not, do you have "Pandemic as a Natural
Evolutionary Phenomenon"?

S: No.

L: Pll get that for you right now.

S: What year are we talking about?

L: Let me look at it. How I came to be invited.
S: What was January ’88?

L: That was the conference at the New School on plagues. And I
i)

talked just to that title; I gave that ecological genetic
evolutionary picture.

But AIDS was the central aspect of it. I don’t recall if I had
written anything ... this issue of Social Research has several
other very interesting papers in it.

S: May I have a copy of this?

L: Yeah. Oh, but there’s a place which could confuse you if I don’t
correct your copy. There’s a typo with "antibodies" instead of
“antibiotics. I refer here to some of the columns that I’d
written on the same things, but I'd been fairly quiet about it
for about twenty years on this particular topic. And it was
AIDS that sort of brought it back to me. It was sort of "Okay,
it’s happened". I hadn’t guessed that it would be as insidious,
the high latency kind of aspects in this multi transmission.

But new bug had come out of Africa and it was devastating".

But I sort of left it at that. But then Elie Wiesel organized
a conference of Nobel laureates; I think that was also in 1988
in December.

S: What is this person’s name?

L: Elie Wiesel, the poet of the Holocaust. That’s when I got to
know him and I’ve gotten to know him very well since then. And
he had the illusions that the Nobel laureates, of which he is one,
were all such wise and human people. And he wanted to collect
them to make some statements about how the world might be better
through good thinking at the time that some of them might have
to offer. I cautioned him that it wasn’t going to work out quite
that way.

S: About what?

L: No, about Nobel laureates. But he was committed to it. There was
certainly a lot of hoopla. Francois Mitterand who was co-sponsor
with the Majesty of the French state was -- part of it was held
at the Elysee. I sort of wondered, "Well, what could my
contribution to that be?” I said, "Okay, I'll pick up this
and I'l] talk about it". And I wrote a somewhat more passionate
version of this paper which in the end was published in JAMA.

A medico, a close friend of mine who is a physician, made that
suggestion -- an inspired one. And it was more of a column.

I read it and I said, "You know, Josh, it’s time to make an issue
of this again. This is serious business. Nobody was paying much
16

attention to you twenty years earlier, but they will now”. And
that’s sort of the genesis of my own current involvement.

I ran into Steve Morse at one of the cocktail parties at the
President’s House, found out he was interested in similar
matters and told him I would back him up very strongly if he
wanted to organize a conference on it. So he talked to some

of the folks at NIH and did organize that first conference

in Washington on this. We got some virologists in the country
and a few biologists from elsewhere.

S: What is the theme?

L: Is there a problem with emerging infections. I think that’s
where he started.

S: And what to do?
L: Not quite.

S: So is there a problem? What does that mean? Are we speeding
up the process of infections, or are there going to be more
of them?

L: Well, just what’s there. A threat analysis. Some discussion
about the ecological historical background of it, but I needed
to get some credibility that AIDS was not just suigeneris,
that there were people in a wide range of other areas of virus
research who felt equally troubled. And I found plenty of them.
The only rhetorical exception was Howard Temin. (I'll explain
that in a minute); they all spoke up very strongly and the gist
of it was, "Yeah, the bugs I’ve worked on really trouble me
a great deal. I’m really interested and impressed that all of
you other specialists and all of your other favorite bugs
have exactly the same feeling. The aggregate is something we
really ought to be concerned about". I’ve never gotten that
kind of scientific consensus because the mood until then was
roughly, "Yeah, we take the terrible vaccines, antibiotics and
so forth” and there are many quotes from the 1960s that infectious
disease had been conquered. So this was the counter manifesto --
"No, we have lots of problems". But there had never been an
aggregation of those kinds of scientific interests.

S: So what are they? There’s not just the viral outbreaks; there’s
also bacterial plasticity, which antibiotics aren’t working.

L: Yeah. The major element of virulence in bacteria to be concerned
17

about is antibiotic resistance. The selective pressures there

are enormous, and I think we see that happening but not nearly
as obviously and overtly. We only see these new cholera strains
coming along, in the Shigella toxin showing up in E. coli, strains
like the so-called E. coli 0157; we have other instances

of it. But antibiotic resistance is just happening all over

the place.

S: So °88’s just taking inventory. So now there’s something
called "germs are back again” in the sense that it’s a
term, and the question is taking inventory of how many of
these kinds of problems do we have.

L: The first conference in Washington was "Is there a scientific
base of concern” and the answer was a resounding "Yes" with a
lot of detail about individual areas. Howard Temin was the
only one who spoke up and said (well you interpret his terms)
"Well, maybe there’s a problem but we oughtn’t to put it this
way. We’re gonna get very inhumane treatment of people who
are carrying HIV if they are pictured as being threats to the
rest of the community, so let’s play that down entirely.

S: Play what down -- play AIDS down?

L: The possibility of further evolution of HIV. I was just raising
an issue for analytic inquiry -- what could happen in its mode
of transmission, could it become more rampant and contagious
pariah. They’re close enough to being that already.

And I said, "Look, I know the empirical evidence as well as
anybody. I feel greatly relieved about it, but I think there
ought to be more research on what are the barriers to person-
to-person transmission by aresol", and that’s never been
satisfactorily answered. There is still, I would say, a flimsy
empirical basis of confidence it’s not spread that way.

S: What about ebola? When was ebola outbreak in Zaire,
the first one?

L: In ’67. I don’t know if I brought up ebola in my columns. I
did Lassa and Marburg which were the analogues.

S: Why I mentioned ebola in that note is that with ebola, you
have quarantine; in AIDS there’s never a quarantine. And if
you use AIDS as your benchmark of what’s politically correct
but sensitive and so on, it could be very dangerous to.......

L: Well, we knew about person-to-person transmission with ebola
18

although with the most recent outbreak you wonder how much of
that was contaminated needles that would have been the same
with HIV. But the overall epidemiology of ebola does suggest
that isolation precautions will make a big difference in
transmission whereas with AIDS, we talk ourselves into the
view that if you avoid needles and if you avoid unsafe sex

that you’re perfectly safe. And to a reasonable approximation
that’s turned out to be correct. But there is more that we

don’t know than we do about ebola, we don’t really understand
how readily it is transmitted but it does look as if infection
control procedures have worked so quarantine has been
justified. So it’s an isolated outbreak. If we knew that

there were twenty people suffering from AIDS and that was all
there were, I'd have no hesitation about quarantining them.

I'd say, if that’s the way to contain them, even if it’s only

a question of sexual behavior that is involved. Of course,
when you have tens of thousands/hundreds of thousands....

S: And worse still, isn’t there the period of incubation when a
virus is latent.

L: Yeah.

S: whereas you’re not going to tell whether or not they’re
infected until after...

L: and conversely, it has to go on forever, so saying "We’re
going to isolate people for three weeks and if they’re still
healthy and well, we are going to let them go at that time.

S: No, but wouldn’t it effect the virulence of the AIDS virus

through quarantine? Isn’t the virus gonna mutate and say
"Okay, this is a bad strategy to kill these organisms"?

L: If I deprive it of new hosts, it can’t get very far.
S: Right. But will it change substantially the structure of the
DNA in the virus by doing that eventually in any ecological

time?

L: The structure of the DNA will change to the extent that it’s
able to proliferate.

S: But what time frame do you think of when you think of that?

L: We must be talking about something other....
19

S: No, no. When you talk about the mutation rate or the increase
of virus through quarantine or through lack of quarantine, what
kind of time frame does one think about when you think about
the plasticity of viruses?

L: The purpose of quarantine is not to first order, to modify the
evolution of virulence; it’s to keep it from getting out from
those people who have been infected and spreading into the wider
herd.

S: Correct.

L: If you had substantial spreading into the wider herd, that by
itself is likely to provide selective factories that will enhance
virulence, so it has to do with how many passages are there. So
at the end of ten or twenty passages of one individual to another
to another to another, I would expect there would have been
enough selective pressure...

S: That’s what I’m asking.
L: ...to be surprised that there is no enhancement of virulence.

S: That’s what I’m asking. So ten. I didn’t realize that; that’s
fast, isn’t it?

L: Well, it’s only ten passages, but think how many generations
there are within a given host. Twenty generations in that
host...thirty.

S: Now, in ’88 you mentioned the sensitivity of the AIDS issue.
What about Cassandra? Was there talk about "What do we do,
how do we behave once we determine that maybe, okay, there is
a problem. How do we speak to the public about this, how do

we speak to agencies and..."?

L: Well, I was loath to talk to the public about theories of AIDS
changing its mode of transmission. My message was to the research
community, saying, "it’s important to rely on shallow empiricism
as the basis of our conclusions". I didn’t want to entangle
public reaction. I’m still a little more cautious about that,
but on a very narrow balance if you want to get some sort of
action you have to talk to the public. But I sympathize with a
lot of what Howard had to say. I wanted any action to be
effective action and not hysterical.

S: But did you have effective action?
20

L: It’s only just beginning, but I’ll give you the latest on that.
Here, you can take that. It was just issued yesterday.

So anyway, after that first Washington conference, I then
thought, "Okay, that was much more successful than I anticipated
it was going to be. We’ve now gotta move towards what are we
going to do about it". I wanted to see this done in stages;

I wanted to have absolute certainty about the credibility of the
threat before going any further. And even with Howard’s caveats
that it didn’t apply to other viruses and so on, I was very
gratified. And had a lot of bolstering from my colleagues there
and so on, so I didn’t feel...

S: How many people there?

L: About fifty.

S: And did you pay your own way to go there? Or any agent sponsoring
the committee?

L: I think the NIAID took on the expenses of it and so on. Now if
there’s a political agenda, this has to do with the justification
for that particular agency. People like Tony Fauci worry that
nobody cares about infectious disease any more; we’d have all
the microbiologists in the world worrying about the rice bowls,
so I can’t deny those kinds of factions.

S: Sure. Everybody’s got to win here in order for it to work.

L: But I don’t think it contaminated their scientific judgment on
this point because say, you know, ten years earlier they weren’t
thinking that way.

S: But it would certainly give them some motivation to attend and to

L: Right. So the next step then was to try the Health Sciences
Policy Committee of IOM and I brought up a whole policy
orientation.

S: What’s IOM?

L: The Institute of Medicine. That’s the principle organ for health
policy pronouncements of the National Academy of Sciences. I’m
one of the founding members of that. In fact, a little story
on that. I have to dig up my files (I can’t find them), but I
think I invented it and I did so when I was on President Kennedy’s
21

health transition team when he was first appointed. At that time,
The AMA was the only organized vehicle for professional expression
on health policy matters, and it was totally dominated by
practitioners; and academic physicians sometimes had very

different views; before Medicare and things of that sort had

come into place, really had no place to go, and I said "Let’s

have a national academy of medicine as part of the NAS complex",
so that we'd have an authoritative group that could talk about

health science policy and so on.

I don’t know if there’s a direct continuity. That was in the

report we gave to Kennedy. Wilbur was to be Secretary of Health;
he was the chairman of this task force, and there were a lot of
conversations. And a few years later the Institute of

Medicine was born at the Academy to do exactly what I was
proposing and has been fairly effective in that role. The

AMA’s come a long way since it’s inception. It had monopolized
the lobby on health issues and they had done a lot to hold things
back,

S: So this another politic. That’s right: whose jurisdiction is
this?

L: Correct. That was as political as I ever got when I worked with
Kennedy during that month or two, on the transition team. So I
am reminded I wasn’t totally insulated in those things.

S: Is infectious diseases normally the domain of the AMA or NIH?

L: Well, NIH is the research aspect of it. This wasn’t an issue
for the AMA at that time. At that time health policy had to do
with government role in insurance, Medicare in particular and
things of that sort.

So back again here, so to explain the IOM -- the IOM was the
constituted body. I knew I could get authenticity through that.
I was named chairman of the Task Force, but I insisted on
having a co-chair, someone who already had an established
reputation as a virologist which I’m not. And that was Bob
Shope; that was a splendid choice. So he and I co-chaired

it. He was head of the Virology Unit at Yale at that time

and knew more about all the viruses than the rest of the world
put together and that actually.

S: What’s his name again?

L: Bob Shope who had an impeccable scientific reputation. So we
22

labored for a couple/few years and came out with this little
turquoise book on emerging infections report. Have you got
one? I hope your library has it. It’s deemed to be a scarce
collector’s item at this point, but Pll show you what it

looks like. Information on specific organisms and how to find
out more about them and so on. That’s become...

S: The way you describe this, Josh, it’s very, very rudimentary.
All you can say is what you do so far -- correct me if I’m
wrong -- in the late ’80s and ’90s is taking inventory of what
we've got out there.

L: This is a set of policy recommendations, step by step, and I
still held back the way I guided the committee and said "Let’s
be very careful about assigning tasks to specific government
agencies. Let’s drive this to what are the things that need
to be done but don’t tell people in government how to go about
it because then you get into all their turf fights". I wanted
to have an absolutely solid ground, that there’s something we’ve
got to pull together and agree on that there’s a threat or a
few measures to be taken and "then we’|I work on the organization
of it". And I think that was sound advice, as a matter of fact.
This nailed it down for sure, and this has been cited over and
over and over again. You’ll find it repeatedly cited in this
document, for example.

S: Okay.
L: So the next stage (Let me get one more document).

S: Emerging Infections Book: Microbial Threats to Health in the
U.S. Institute of Medicine published by the National Academy
press in 1992 and Lederberg and Shope are the editors.

L: Ultimately it starts getting out of my own hands as it had to
do, and this is the first government agency to respond. And
this picks up immediately on the IOM report. It’s an outline
of what are they going to do about it. Now, that’s only a
piece of the problem. This has to do with public health
measures, surveillance, diagnosis, monitoring; it doesn’t
cover the vaccines, doesn’t cover the health care aspects
of it. It’s very limited in the international side of it.

But the background of that is the astonishing degree to which
that kind of public health activity has deteriorated over the
last twenty or thirty years.

Basically what’s happened is the budgets are flat, states are
23

poorer and so those are going down. And then the special
problems of AIDS and TB have gobbled up what’s there, so about
60% of their budgets are devoted for monitoring and surveillance
are devoted to those two diseases. There’s nothing left over

for a systematic inquiry of things like "flesh eating

streptococci" and so forth. Basically no good statistics

on things like that. We don’t know if that’s an emerging

disease or not.

S: Fascinating. So how do you do benchmarks" Is there long-term
monitoring for other kinds of....

L: Well, they’re trying to set up systems to do that, and it takes
a little money; not a lot, but CDC may have gotten --I’m never
clear how much is gonna be taken back overnight -- another $6
million to set up more comprehensive monitoring for a wider
range of infectious disease conditions.

S: Worldwide monitoring?

L: No. Mostly U.S. We actually heard yesterday. Here’s an extra
copy of that; that shows you the current status of these
activities. That’s in the U.S. alone. So the next stage is
the report I just gave you - that’s as I said - this is now
elevated to a broader federal inter-agency activity, and I’ve
played some role in knocking on doors and trying to provoke
some further action and interest. And that report has just
come out. And now the agencies have gotten together and they
decided on a division of labor and what things they would like
to do, so I didn’t have to get into the turf fights. They
argue it out by themselves.

S: Okay. In terms of base lines and monitoring, in your first
meeting in ’88 -- as you described it to me at least -- the
quick and dirty was that it was very easy to do in effect
of this polemic with people in the ’70s who said, "Look,
we’ve eradicated all these diseases". And so if your base
line is zero in that sense of ... then you can talk about,
"Well, look. We now have a serious problem". Is that right?

L: No, I don’t understand what you’re saying.

S: Well, how do you know if you have emerging viruses? How do
you know if there’s increase in epidemics?

L: Well, some things are so spectacular you can’t avoid it; some
things you discover by happenstance, like what happened with
24

hanta virus in the southwest. It’s been going around for

a long time and you didn’t know that this was emerging as a
distinctive entity, but a very shrewd internist remembered that
there had been another case just like it and guess what? It

was the fiance of the person he was treating right now and he
said "Oh, we’ve got something alarming on our hands. A very
sudden progression of disease in young people. They come into
the hospital, acute respiratory distress and twenty-four hours
later they’re dead." So then you get into all the machinery:
okay, what’s the agent; you pull in the PCR stuff and you
identify the virus. It’s called Hantavirus but there’s a new
syndrome connected with it. So now suddenly we have a new
emerging entity, but that’s by recognition of something that
had been going on for some time before.

S: I see.

L: But it’s by happenstance. And so you say, "How many of these
things are going on? We don’t filter the amount of the noise.
And we need to do that if we’re going to advise people. Now
the CDC issues an advisory to people living in suburbia, because
we now realize this virus is in total of the United States.

You be very careful how you handle rodent droppings. They
might well be contagious and there have been at least a couple
of cases that have been clearly identified - one here in New
York -- from that kind of a source. So where is Hanta going

to go, I haven’t got the foggiest idea. It’s all over the

mice, all over the continent. You ought to be thinking about
that in Canada too, by the way; no respect of that boundary.

So far nothing observed in the natural history of the mice

that they get any disease from it. And quite sporadically it’s
showing up in people who have been in contact with them. It’s
obviously readily transmissible from mouse droppings to people.
What about human droppings to people and other effluvia things?
We don’t know anything about that. There’s no known example
of secondary transmission person to person, but we don’t know
why not.

It has the favorable aspect that it’s a rapidly-fulminating
disease so these people don’t stay menaces very long. There’s
a very short interval of potential of transmission.

S: So what does monitoring mean in this context? Does monitoring
mean once you’ve set up long-term monitoring, does it mean

measuring increased numbers of different kinds of outbreaks?

L: Basically that’s correct. And then if you don’t really know
25

for sure what’s causing them is to do the not so logical work
so you can figure that out, so you can provide a proper
taxonomy. That’s not just to make tidy pigeonholes. I suppose
different disease entities.

We could institute quarantine; a legal base does exist.

Peggy Hamburg has invoked it. She’s the Commissioner of Health
Care. By the way, that’s David Hamburg’s daughter and that’s
David Hamburg over there.

S: She’s invoked quarantine?

L: For people suffering from TB who are not compliant with
medication and who therefore remain infectious. She’s locked
up a dozen of those folks and keeps them in an isolation ward
and pumps medication down their throat until they are no longer
infectious and then lets them go out and they’re essentially
on parole at that stage. For TB, the legal authority for that
has existed, and she could call an emergency for any other
disease that would warrant it. And could actually get by even
the civil rights advocates and so on. I mean, they do recognize
a threat to the community. The difference with AIDS was that
with AIDS, you couldn’t do anything to help them and it was
very ambiguous whether quarantine would make any difference.
I mean, as long as sexual transmission was the only issue and
we don’t at this stage use quarantine to control sexual
behavior.

S: Right. Now, you’ve never - especially in terms of your advocacy
in political roles -- been someone to shy away from public
controversy and political action. In most outbreak stories
what I’ve been noticing is a trend, especially as I interview
scientists who, (in fact I can document this) have been very
reluctant to get involved in doing outbreak research because
of it’s political nature. That is to say, especially when
governments get involved, is it a natural occurence? Is it
anthropogenic? Or, as I could imagine in the case of AIDS,

18 if...

L: That’s not my experience. I know any number of people who would
be more than happy to do the research. Getting funding for it has
been more the issue, getting support for it to happen. And there
are other political obstacles, getting across those boundaries.

S: I’m thinking of Cassandra. I’m thinking of what happens to you.

L: I think we’ve passed that at this stage. I think that’s one of
26

the advantages. I mean, you can’t talk Cassandra when you’ ve
had this group coming out with that conclusion. That was the
whole purpose of doing that.

S: You did mention to me on email once that you indeed experienced
Cassandra.

L: Yeah, that was in the ’60s.
S: Oh, it was in the ’60s. So in the 80s there was no..

L: In the ’80s when I brought up the possibility of airborne
transmission, I had a few folks decrying it saying, "Why do
you want to invoke public hysteria and so on", I reminded them
I wasn’t talking to the public. It did spill over. I couldn’t
totally exclude reporters picking that up. Whenever I had the
opportunity I would say, "Look, that’s a research agenda. There’s
no evidence for airborne transmission. It’s a hypothetical
thing to worry about in the future" and I did try to lower the
profile on that. It’s a tightrope -- trying to say anything
about it addressing one community without fuelling the kinds
of things that Howard Temin was worried about. He was willing
to go much further, and I think suppose what I think he
actually believed of because of what he thought were social
distortions that would come from scientifically-accurate
statements.

S: Can I raise one other conceptual issue? I know you’ve got other
things to do, but this is something I see pervasive in the
outbreak stories I’ve looked at that which is this anthropogenic
versus natural argument. And that, it seems to me, seems to exist
against a backdrop of something called The Balance of Nature.
That is, if there is...

L: Yeah.

S: So does that play out, does that have any meaning with respect
to viral outbreaks, is balance of nature -- checks and balances --
and somehow if there’s an outbreak we’ ve caused it; therefore
(that’s what anthropogenic means)..... does that paradigm work?

L: Well, I think different communities take a different view of the
matter. I have a lot of environmentalists begging me to come
along with them and say, "Well, one of the hazards of climate
change is going to be viral outbreaks".

S: Yes, yes.
27

L: and I can’t go along with that.

S: Are you serious? When did they come up to you and say this
to you?

L: There are a couple of conferences being organized on it, there

have been in the past. I was down at the Smithsonian a few
weeks ago.

S: This is fascinating.

L: So everybody in the climate change area is eager to recruit
this, and there is going to be health impacts with another
change coming up in a couple of months. It also came up --
T was on a climate change review group when climate change
is the center of activity. I wrote a section about
infectious disease impact. I said it’s unpredictable.

I said there’l] be changes in precipitation, there’ Il

be changes in vector distribution. Some places may

dry up and have fewer; other places may get wetter and

will have more. But that all of these effects in my view
were quite small relative to the dominant ecological change
which is happening over that time scale, and that’s the human
population.

S: I see. And transportation.

L: And I continue to hold that view. I can’t deny there’ll be some
effect there, but it will be really second order. And over the
time scale we’re talking about, we should have the technology
of vector control. So it’s not high on my list of either the

source of worries for infection or why we worry about climate
control.

S: It seems to me that it’s a more generic argument.

L: Yeah.

S: Against why be so concerned about global warming. There are
more immediate things that are going to get us before that
which is over population.

L: Now, there are anthropogenic diseases well known. I guess the
snails in the Aswan Dam (and Schistosomiasis) is the
outstanding example, so we know those kinds of things can
happen. I’m probably more conservative on this than most of
28

the people who have working on this issue with me, but you'll see
Argentina arena-virus when you have agriculture moving into
forested areas, those sort of zones. Jungle yellow fever

is an outstanding example of that. So those things happen.

But I don’t think they begin to compare with the sheer issues

of travel and density, even there.

S: Okay. You took my question in a different direction than I
wanted to go, but I’m glad you went that way. What I was
thinking was that if you talk about something anthropogenic
in terms of outbreaks, you’ve got to have a baseline. Is
the baseline no epidemics? Is the baseline the world is now
balanced and that somehow when humans knowingly screw up that
balance? Does that model work for viruses?

L: Well, I don’t believe it for a minute. I don’t think nature is
benign. In that regard I think nature has a lot of warring
constituencies. Balance may be the ultimate outcome, but
balance may be the disappearance of some species as a part
of that outcome, and I can’t guarantee that won’t include us.
T used exactly that expression. So I think that’s totally
unpredictable.

S: When you say that, is that a polemic?
L: Yeah.

S. Why? I know coral reefs are a beautiful place to look for this
because in coral reefs you think of them as checks and balances
that have evolved over ions; therefore when you see an outbreak
you say "Oh, anthropogenic”.

L: Okay, I'll epitomize it. I think I may have asked you already.
I’ve been very struck with the phrase that man is a man-made
species, and I think that probably captures most of the rest
of it. Of course we’re out of balance; we’re intrinsically out
of balance. Population more than 5 Million Homo sapiens on
this planet generates an enormous imbalance, and we’ll never
recapture it.

S: Okay, I understand that. And that’s in a different sense of what
we're talking about, though. In respect to coral reefs in the
’70s, people wake up and they dragged Darwin’s book out and said
“Guess what? Coral reefs have never had a complete "balance of
nature". And the whole polemic against something being
natural, something that’s anthropogenic is "First let’s get rid
of the paradigm - a balance of nature -- because that’s garbage.
29

There never was this balance of nature". This is the myth upon
which you...

L: I wouldn’t go so far, but I don’t want to mix a balance of nature
with a preferred status of Homo sapiens. A balance of nature
might exclude Homo sapiens.

S: And the balance of nature may be over a period of time, that is
geologic.

L: That’s back to the man-made species again.

S: What do you mean by that? It resonates in my mind in a different
way. What do you mean when you keep saying that"Man is a man-made
species"?

L: The current status of the human condition is much less a
consequence of natural evolution than it is a cultural change.

S: In that sense, we’re controlling our own evolution to an extent.

L: Well, control may be too strong a term. We’re unwitting pawns
of social and cultural evolutionary processes as much as an
actual but biological evolution plays a relatively small role
at this stage. And there’s as much difference between homo
sapiens of 20,000 years ago and homo sapiens today as there is
between other homo species.

S: When studying outbreaks, I understand when debates are what
is anthropogenic and what’s natural, people usually try to find a
pristine system in which humans haven’t intervened and say,
"Okay, that’s the baseline upon which we can monitor?”

L: I don’t believe for a minute those pristine circumstances rendered
those people immune from pandemic crises.

S: That’s my question.

L: Of course not.

S: Okay. So there’s no, I mean, these viral outbreaks, in your
mind, are working consistently in evolution. And what are we

doing - enhancing the frequency of outbreaks?

L: The density of the human population more than any other factor
is doing that.
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S: Okay. You mentioned to me one time about four years ago.

L: We do other things as well. We invade the forests, we expose
ourselves to the Zoonoses and the vector borne diseases and
from those sources as well. There are people who point to
antibiotic resistance and say, "Well, we shouldn’t use
antibiotics”. Of course, that’s crazy. You’re going to
deny yourself the advantage of it? It won’t make any
difference whether they’re resistant or not, under those
circumstances let’s try and find a balance - the most
effective compromises that you can make to optimize
whatever measures we can take that will protect our
health.

S: And that’s good for the individual, maybe bad for the species
and vice versa.

L: That’s right. There’s the commons problem very seriously.
S: What do you call it?
L: The problem in the commons.

S: Exactly. Tragedy of the Commons. You mentioned to me and this
is something that preyed on my mind since I last saw you --
which was when you were talking about viruses as modes of
evolutionary change and you said to me that you thought the
chances of a virus doing something that may be adaptable to
the organism would be equivalent to throwing a dart into a
computer.

L: Yeah. I would have said that about mutation. It’s the same
paradigm. I guess that’s right. I think I have to temper
that a little bit; Pve learned a few things since then.
Above all, I’ve taken Kimura very seriously about drift in
evolution. Most darts that we throw into our computers
don’t do anything -- change nucleotides with no consequence
whatever. The other as a lot of evolutionary change involves
systems a little bit more highly integrated than just random
short circuits, that we have modules. The individual exons
to be even more precise about it -- being tried out in various
experimental configurations. So a lot of genetic experiments
are a little bit more structured than that, I think.

S: Okay. When you talk about the ecology of viruses -- this is
again, give me a quick biology lesson here -- what is the
predator of a virus? Can you talk about predator relationships
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in terms of viruses?

L: Nobody keeps viruses to their advantage. They don’t have that
much flesh on them. So to that extent, it’s more a question
of defending yourself against them rather than getting any
positive advantage from them. So there really is no predator.

S: Does that make them unique among....
L: Pretty much.

S: It takes them into...

L: There’s an iota. There’s a little bit of DNA in a cell that

manages somehow to defeat that viral DNA maybe incorporated
a few nucleotides, but it’s just so trivial. The

selective factors involved in relationships with viruses

really have to do with defense. That’s why there is...

selfish DNA show that’s the case. If that DNA can get past

the point where it’s either a threat to the host ... a lot

of the DNA that we have in our genome is living there

essentially as innocuous passengers. It isn’t costing very
much.

S: But where does it put them in ecology? At the top of the food
chain?

L: That’s a good question, yeah. The answer is yes. In fact, I
wrote a little piece called "Crowded at the Summit".

S: Are you serious?

L: Yeah. Vl get that out for you.

S: Please.

L: And it is the food chain. They’re not anybody’s food in any
significant fashion and the....

S: So it’s hard to play. I’m thinking of an insight that has
been used now to understand outbreaks, mathematical models
for catastrophre theory that are based on predator relation-
ships. These kinds of modelling then, well, when I think of
outbreaks from a metascientific point of view, I’m looking
at the structure of the controversy, the problems that
scientists have in conceptualizing what counts as evidence--
is this just new techniques for measuring for something or
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is there really a new phenomenon here -- all those kinds of
of methodological and meta problems. So I can see them as
being very similar. But if I look at the modelling aspect

of viruses, I’m wondering why (in the same problem with
symbionts) and if viruses have to be considered

differently than, say, understanding zebra mussels in the
Great Lakes, understanding the invasion of plants and
animals that Elton was talking in his ’°57 book which was a
brilliant book on how each species....

L: Well, they are different in detail, and I think you and I
are very familiar with those differences onethey’re
not food, and two they can enter into intense symbiotic
relationships. And I startle people by telling the story
of the mitochondria, the parasitic bacteria that ended up
in us. It goes back to another paradigm. I said it comes
from Van Neil, but I can’t verify that. People who hate
microbes will learn about them than people who respect
them and may even love them.

S: Sure.
L: And that again is learning to live with them, I guess.

S: But -- and this goes back to the paradigm business -- and I'll
keep looking at it -- it’s something that you see is much more
continuous with understanding viral evolution, viral ecology.

L: Well, maybe I remember texts that other people have forgotten.
Theobald Smith had pretty much said it all, and then Dubos followed
it up.

S: But this is all autobiographical; this is your continuity.
L: Yeah.

S: There may not be a continuity in a population sense of the
visibility of the problem, the way in which one thinks about
the problem.

L: Oh, I think that’s absolutely right. But I think the public
perceptions were that we had taken care of infectious disease
and there was a twenty-year gap and now suddenly they’re back
again. How come? Some mistrust of science, and we must have
messed it up with the anthropogenic ideas and so forth.

S: Well, I was looking through and twenty years ago an expression
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like "viral ecology" was an oxymoron. I mean, it seemed like
virus,

L: I can’t buy that.
S: No? Okay.

L: On a technical level, I think Burnet had come in very readily -
the Natural History of Infectious Disease.

S: Well, there you go.

L: There wasn’t enough of that. A lot of gut feelings were not
being well informed by those kinds of discussions, but there was
certainly a level of discourse that tended to operate there.

But Pll go back to another point that almost contradicts it.
In the public health community, bugs were products of special
creation.

S: Exactly, exactly.
L: They were not thinking about evolution.

5: So what’s new here? What’s new here may be the actors who are
in the front line making policy such as yourself as opposed to
this.

L: Reviving an evolutionary perspective.

S: Correct. And maybe putting this evolutionary/ecological
perspective in the face of medicine and saying "Now deal
with it”.

L: That’s correct. The people who study infectious disease in
departments of medicine have very little by way of evolutionary
background. In their thinking they’ve learned a little bit about
it. They had to with drug resistance and plasmids and so on,
but yeah, I gave a talk on the future of infectious disease,
and I have given out what I would regard as the most simplistic
discussion of these evolutionary considerations. I did this for
the Infectious Disease Society of America. It got raves --
“Innovation, illumination, insight". I was giving what I
regarded as baby talk. It’s what they needed.

5: Who are these people -- the infectious disease people?
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L: The people who manage infectious disease at the hospital you
go to.

S: Right. And when you talk about them thinking in terms of
special creation, you’re talking about that every virus is
a new virus.

L: Mm huh.
S: They don’t think of continuity.
L: No.

S: And they don’t think of all those things that we were talking
about.

L: That’s right.

S: So this is what I’m saying -- so that when you come into this
domain with these new books of emerging infectious and emerging
viruses, it’s new for me and I remember when I picked up Morse’s
book and a whole series came out on the evolution of viruses --
not the Coming Plague. I think that is more just a....

L: That’s journalistic.

S: Yeah, exactly. But the others say "No, there’s something new
here and it’s literature". There’s something new in terms of
maybe what I’m detecting is who’s speaking. And also this
sounds like evolutionary biology now, it reads like biology, finally
this is what Dubos had argued long ago in the ’60s with the
virology people, “your poor cousins in the mansion of pathology."
Why don’t we get some biology of these things and study the
natural history of these things.

And this is something that needs to be studied, then, is how
people that do get the power to come in and not end up ina
turf battle with these people in hospitals and saying

Do have the legitimacy to speak about this and why this wins
in the *80s and perhaps didn’t win in the 60s"?

L: Look, let’s go back to the ’40s; the idea of a bacterial
genetics was a nullity and especially in the medical community.
Medical bacteriology had evolved without the benefit of any
evolutionary thinking whatsoever with the notable exception of
Theobald Smith. His book on parasitism is really a very special
35

perspective through there, but it did not get into medical
teaching. If you go through textbooks of medical bacteriology,
I mean, that’s the place to find these kinds of transitions.

A few of them give some lip service, you know, new findings in
genetics and so on. But there’s a twenty or thirty year lag in
that kind of teaching.

: Yeah. And something else by way of conclusion. It seems to be that
I think needs to be explored from a historical point of view

is your medical training. And this seems to me to be something
that I think needs to be explored more for many people in the
twentieth century across disciplines and then study their
paradigms. I can understand your 1952 paradigm a lot better
once I know the medical training. And I realize that both

now. And I noticed in my interview with Jean Brachet and then
some other things that Brachet mentioned afterwards that he was
trained in medicine, had a certain approach to doing biology.
And it seemed that those people like yourselves who come in -
and you were obviously a lot younger but you’d been doing the
work in the same period - that there seems to be something that
needs to be explored there, that you’re crossing over and you
essentially as an individual, constantly crossing over in the

turf of policy, of medicine, of hospital practice, AI in

Australia and so on with, what was it, associated with diagnostic
treatments and things of that nature? Weren’t you involved with
McFarlan Burnet? Okay. That’s another talk, another
interview.

L: Well, I was in some ways predisposed, but I was also in the

right place? Here I was an undergraduate in a department that
Dobzhansky headed and then going on to medical school and
getting the basic medical sciences part of it which is
cross-disciplinarian in the other ways and a great educational
advantage over the graduate student who focuses on microbiology

or biochemistry or whatever. So it just all fell in on it.

: And also taking microbes and treating them as a biological
entity and I think this may be...

L: If there’s any figure that I could compare myself with it’s

Rene Dubos who I guess is not medically trained, as a
matter of fact.

S: And is a microbiologist. Did you know him?

L: Yeah. The answer is yes. His books influenced me much more

than the personality. Well, this is helpful to me, Jan, if you
want to continue this some time.

S: I would indeed. Thank you.

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