Pandemic as a
Natural
Evolutionary
Phenomenon

BY JOSHUA LEDERBERG

 

My main thesis is that the progress of medical science during
the last century has obscured the human species’ continued
vulnerability to large-scale infection. We fail to acknowledge
our relationship to microbes as a continued evolutionary
process. This is far from equilibrium, and we cannot take for
granted near-term outcomes that would be optimal from
either our, or our parasites’, perspective. We have a reasonable
lead on bacterial intruders; we grossly neglect the protozoan
parasites that mainly afflict the third world; we are danger-
ously ignorant about how to cope with viruses.

Pasteur and Darwin

Charles Darwin’s role in nineteenth-century thought, how
that shapes our own thinking about man’s place in Nature, is
too well known and oft discussed to bear extensive elaboration
on my part. His contemporary, Louis Pasteur, is a culture
hero, world renowned for the human benefits of his germ
theory of disease: the use of antiseptic hygiene and of vaccines
to prevent infection.

The ideological interaction of these two iconoclasts has been
given too little attention. In his correspondence, Darwin makes
enthusiastic but passing reference to Pasteur’s humanitarian

SOCIAL RESEARCH, Vol. 55, No. 3 (Autumn 1988)
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contributions.! Pasteur’s correspondence has been less exten-
sively indexed to date.? The most notable allusion to Darwin in
his published work is his address to the Sorbonne on April 7,
1864: “Great problems are in question today, which keep all
spirits in suspense: . . . the creation of man several thousand
years or several thousand centuries ago; the fixity of species, . ..
the idea of a useless God.” There is little doubt he is referring to
Charles Darwin, whose work had been translated into French in
1862 and promptly aroused a theological storm. Pasteur is de-
termined, however, to remove himself from that debate and
such mysteries. Instead, he insists on addressing only those ques-
tions accessible to experiment, namely, the contemporary claims
of spontaneous generation of microbial life. In 1864, his refuta-
tion was in comfortable support of an orthodoxy that would
invoke the Creator for the ultimate origin of life. Indirectly, it
was an argument against a Darwinian evolution of life arising in
“some warm little pond.” Pasteur did show that the plethora of
empirical claims of abiogenesis in sterilized broths exposed to air
could all be accounted for by airborne spread of existing germs.
By 1883, he had returned more optimistically to mechanistic
views of abiogenesis if only one could achieve biochemical asym-
metries, perhaps by the use of electromagnetism. Nevertheless,
there is no record that he ever achieved a sympathetic under-
standing of Darwinian evolutionary theory; and he seems always
to have been hostile to a methodology of inference, like Dar-
win’s, that deviated from the grain of laboratory experiment.*

! Darwin to Bentham, 1863; Darwin to Romanes, 1875.

? Pasteur’s correspondence is being opened to scholars at the archives of L’Institut
Pasteur, Paris.

5 Charles Darwin to J. D. Hooker (1871). “It is often said that all the conditions for
the first production of a living organism are now present, which could ever have been
present. But if (and oh! what a big if!) we could conceive in some warm little pond,
with all sorts of ammonia and phosphoric salts, light, heat, electricity, &c., present, that
a protein compound was chemically formed ready to undergo still more complex
changes, at the present day such matter would be instantly devoured or absorbed,
which would not have been the case before living creatures were formed.”

* John Farley, “The Social, Political, and Religious Background to the Work of Louis
Pasteur,” Annual Review of Microbiology 32 (1978): 133-154.
PANDEMIC 345

 

On Darwin’s side, for all his appreciation of Pasteur’s
medical contributions, he seems never to have incorporated
microbiology into his natural history. And, as we know, neither
of them had any inkling of two other contemporaries’
contribution to fundamental biological understanding. Gregor
Mendel’s foundations of genetics, articulated in 1865, were
buried until 1900. Friedrich Miescher had discovered nucleic
acids (DNA) in pus cells in 1870; we were not to begin to
understand the biological function of DNA until Avery,
MacLeod, and McCarty’s work at the Rockefeller Institute in
1944.5 The latency of DNA research may be ascribed mainly to
deficiencies in experimental technique whose repair needed
decades of drudgery and many instrumental inventions. The
barriers among Darwin, Pasteur, and Mendel were purely
cerebral and ideological.

What lost opportunity! Darwin might have found, as
present-day investigators do, marvelous experimental material
for the study of evolution in populations of microbes—where
generation time is measured in minutes, and where natural (or
artificial) selection can be applied to tens or hundreds of
billions of unicellular organisms at small cost and less ethical
compunction. Pasteur and his successors in microbiology might
have avoided decades of muddled thinking about variation in
bacteria. The revolution in biotechnology could have had a
couple of decades’ head start. I should not complain: I had the
fun and advantage in 1946 of exploring a terra still incognita
(genetics of bacteria) that might otherwise have been blanketed
with homestead claims for four or five prior decades.®

Plagues

Darwin had placed Homo sapiens at the pinnacle of the

5O.T. Avery, C. M. MacLeod, and M. McCarty, “Studies on the Chemical Nature of
the Substance Inducing Transformation of Pneumococcal Types,” journal of
Experimental Medicine 79 (1944): 137-518.

6H. A. Zuckerman and J. Lederberg, “Forty Years of Genetic Recombination in
Bacteria: Postmature Scientific Discovery?,” Nature 327 (1986): 629-631.
346 SOCIAL RESEARCH

 

evolutionary process, but with as much emphasis on pinnacle
as on evolution. He never quite rectified the view that man has
a privileged place in nature. Man’s intelligence, his culture, his
technology has of course left all other plant and animal species
out of the competition. Darwin was oblivious about microbes as
our competitors of last resort. In experimental science, the
Darwinian and Pasteurian perspectives are at last fully
integrated. The study of mechanisms of virulence is a top
priority in research laboratories applying the most advanced
techniques of molecular genetics. Since Theobald Smith in
1934, F. M. Burnet and R. Dubos’ have offered us broad
perspectives of the natural history of infectious disease—
perspectives that leave no illusions about the feasibility of
eradicating our scourges, of the ongoing struggle. For a
period, the works of Paul de Kruif dramatized the efforts of
the “microbe-hunters.”® But one legacy of the “miracle drugs,”
the antibodies of the 1940s, has been an extraordinary
complacency on the part of the broader culture. Most people
today are grossly overoptimistic with respect to the means we
have available to forfend global epidemics comparable to the
Black Death of the fourteenth century (or, on a lesser scale, the
influenza of 1918), which took a toll of millions of lives! We
have no guarantee that the natural evolutionary competition of
viruses with the human species will always find ourselves the
winner.

I would ask the professional cultural historians for their
comment; but it appears that our half-century has turned away
from external nature and to the self-deprecation of human
nature, or of human organizations, as the central target of fear
and struggle. Not that we have to quarrel over pride of place
between virus infection and nuclear doomsday.

7 Theobald Smith, Parasitism and Disease (Princeton: Princeton University Press,
1934); F. M. Burnet and D. O. White, Natural History of Infectious Disease (Cambridge:
Cambridge University Press, 1972); Ist ed. 1940); R. Dubos, Man Adapting (New
Haven: Yale University Press, 1965). See also Hans Zinsser, Rats, Lice and History
(Boston: Little Brown, 1935).

8 Paul de Kruif, Microbe Hunters (New York: Harcourt Brace, 1926).
PANDEMIC 347

 

The countercultural protest against technology posits a
benign nature, whose balance we now disturb with diabolical
modernities. But man himself is a fairly recent emergent on
the planet; the sheer growth of our species since the paleolithic
is the major source of disturbances to that hypothetical
balance. Man as a creature of culture is a man-made species;
for better or worse, the only planet we know is a Promethean
artifact. Genesis mandates: “Be fruitful and multiply!” After
sampling the tree of knowledge, and acquiring the means, we
could return to Eden only by reducing the human population
to about | percent of its current density. We are complacent to
trust that nature is benign; we are arrogant to assert that we
have the means to except ourselves from the competition. But
our principal competitors for dominion, outside our own
species, are the microbes: the viruses, bacteria, and parasites.
They remain an interminable threat to our survival.

This harsh view may be a product of my day-to-day
laboratory experience. Most of my own scientific contributions
have entailed the relentless use of artificial selection® as a way
to detect rare differences in the genetic makeup of individuals
in large populations. These were populations of bacteria; but
they numbered in the billions in each test tube. Typically, all
but a few of these would be wiped out by the chemical or virus
intentionally added to remove that “normal background”; a
few survivors of uncharacteristic genetic composition are then
readily detected and isolated. So I have personally observed,
even contrived, the wipeout of populations on a gigascale, and
of course recognize that this is an unremitting process in
nature—for example, recovery from infection on the part of
any patient. This may come about either by the administration
of an antibiotic or the mobilization of the naturally evolved
defense mechanisms of the patient. In such confrontations,
either the human individual or billions of microbes must die.

9J. Lederberg, “The Ontogeny of the Clonal Selection Theory of Antibody
Formation: Reflections on Charles Darwin and Paul Ehrlich,” Transactions of the New
York Academy of Science, 1988.
348 SOCIAL RESEARCH

 

As Twort and d’Herelle first observed over seventy years
ago, such competition can be seen within the microbial world,
in nature or in the microcosms of the test tube: for bacteria
have their own viruses, often in uneasy equilibrium with their
hosts. It is not unusual to observe a thriving bacterial
population of a billion cells undergo a dramatic wipeout, a
massive lysis, a sudden clearing of the broth, in consequence of
a spontaneous mutation extending the host range of a single
virus particle. The bacteria will be succeeded by a hundred
billion viruses—whose own fate is now problematical, as they
will have exhausted their prey (within that test tube). There
may, or may not, sometimes be a few bacterial survivors,
mutant bacteria that now resist the mutant virus; if so these can
repopulate the test tube—until perhaps a second round, a
mutant-mutant virus appears.

Is there any reason to believe that such processes are unique
to the test tube, that life in the large is exempt from them? Of
course not! Only the time scale is certain to be different, by a
factor of years to minutes, of a million to one, the disparity of
generation time of human to bacteria. The fundamental
biological principles are the same. The numerical odds may be
different, by a factor hard to estimate.

As crowded as we are, humans are more dispersed over the
planetary surface than are the “bugs” in a glass tube, and we have
somewhat fewer opportunities to infect one another, jet air-
planes notwithstanding. The culture medium in the test tube
offers fewer chemical and physical barriers to virus transmission
than the space between people—but you will understand why so
many diseases are sexually transmitted. The ozone shield still lets
through enough solar ultraviolet light to make aerosol transmis-
sion less hospitable; and most viruses are fairly vulnerable to
desiccation in dry air. The unbroken skin is an excellent barrier
to infection; the mucous membranes of the respiratory tract much
less so. And we have evolved immune defenses, a wonderfully
intricate machinery for producing a panoply of antibodies, each
specifically attuned to the chemical makeup of a particular in-
PANDEMIC 349

 

vading parasite. In the normal, immune-competent individual,
each incipient infection is a mortal race: between the penetration
and proliferation of the virus within the body, and the develop-
ment of antibodies that will dampen or extinguish the infection.
If we have been vaccinated or infected before with a virus related
to the current infection, we can mobilize an early immune re-
sponse. But this in turn provides selective pressure on the virus
populations, encouraging the emergence of antigenic variants.
We see this most dramatically in the influenza pandemics; and
every few years we need to disseminate fresh vaccines to cope
with the current generation of the flu virus.!°

Many quantitative mitigations of the pandemic viral threat
are then inherent in our evolved biological capabilities of
coping with these competitors. Mitigation is also built into the
evolution of the virus: it is a pyrrhic victory for a virus to
eradicate its host! This may have happened historically, but
then both that vanquished host and the victorious parasite will
have disappeared. Even the death of the single infected
individual is relatively disadvantageous, in the long run, to the
virus—compared to a sustained infection leaving a carrier free
to spread the virus to as many contacts as possible. From the
virus’s perspective, its ideal would be a virtually symptomless
infection, in which the host is quite oblivious of providing
shelter and nourishment for the indefinite propagation of the
virus’s genes. Our own genome probably carries hundreds of
thousands of such stowaways. The boundary between them
and the “normal genome” is quite blurred; intrinsic to our own
ancestry and nature are not only Adam and Eve, but any
number of invisible germs that have crept into our chromo-
somes. Some confer incidental and mutual benefit. Others of
these symbiotic viruses (or “plasmids”!!) have reemerged as
oncogenes, with the potential of mutating to a state that we

10 £. D. Kilbourne, Influenza (New York: Plenum Medical, 1987).
"J. Lederberg, “Cell Genetics and Hereditary Symbiosis,” Physiology Review 32
(1952): 403-430.
350 SOCIAL RESEARCH

 

recognize as the dysregulated cell growth of a cancer. As much
as 95 percent of our DNA may be “selfish,” parasitic in origin.

At evolutionary equilibrium, we would continue to share the
planet with our parasites, paying some tribute but deriving
some protection from them against more violent aggression.
Such an equilibrium is unlikely on terms we would voluntarily
welcome: at the margin, the comfort and precariousness of life
would be evenly shared. No theory lets us calculate the details;
we can hardly be sure that such an equilibrium for earth even
includes the human species. Many prophets have foreseen the
contrary, given our propensity for technological sophistication
harnessed to intraspecies competition.

In fact, innumerable perturbations remind us that we cannot
rely on “equilibrium”—each individual death of an infected
person is a counterexample. Our defense mechanisms do not
always work; viruses are not always as benign as would be
predicted to serve their long-term advantage.

The historic plagues, the Black Death of the fourteenth
century, the recurrences of cholera, the 1918 swine influenza
should be constant reminders of nature’s sword over our head.
They have been very much on my mind for the past two
decades.!2 However, when I have voiced such fears, they have
been mollified by the expectation that modern hygiene and
medicine would contain any such outbreaks. There is, of
course, much merit in those expectations: the plague ba-
cillus is susceptible to antibiotics, and we understand its
transmission by rat-borne fleas. Cholera can be treated fairly
successfully with simple regimens like oral rehydration (salted
water with a touch of sugar). Influenza in 1918 was
undoubtedly complicated by bacterial infections that could
now be treated with antibiotics; and if we can mobilize them in

12 J. Lederberg, “Biological Warfare and the Extinction of Man,” Stanford M. D. 8
(Fall 1969): 15-18; J. Lederberg, “Orthobiosis: The Perfection of Man,” in Arne
Tiselius and Sam Nilsson, eds., The Place of Value in a World of Facts: Nobel Symposium
XIV (New York: John Wiley & Sons, 1970); J. Lederberg, “The Infamous Black Death
May Return to Haunt Us,” Washington Post, Aug. 31, 1968.
PANDEMIC 351

 

time, vaccines can help prevent the global spread of a new flu.
On the other hand, the role of secondary bacterial infection in
1918 may well be overstated: it is entirely possible that the
virus itself was extraordinarily lethal. The retrospective
scoffing at the federal campaign against the swine flu of 1976
is a cheap shot on the part of critics who have no burden of
responsibility for a wrong guess. It underrates health officials’
legitimate anxiety that we might have been seeing a recurrence
of 191815—and underscores the political difficulty of undertak-
ing the measures that might be needed in the face of a truly
species-threatening pandemic. This so-called fiasco in fact
mitigated an epidemic that happily proved to be of a less lethal
virus strain. The few cases of side-effects attributed to the
(polyvalent) vaccine are undoubtedly less than would have
appeared from the flu infections avoided by the vaccination
program. However, the incentives to attach fault for damages
from a positive intervention have predictable consequences in
litigation, not to be confused with the balance of social costs
and benefits of the program as a whole.

Many outbreaks of viral or bacterial infections have
destroyed large herds of animals, of various species, usually
leaving a few immune survivors. With all the discussion of
faunal extinctions, nothing has been said about infectious
disease. It would be impossible to verify this from the fossil
record, but disease is the most plausible mechanism of episodic
shifts in populations. Incontrovertible examples of species
wipeouts are seen with fungi in the plant world: Dutch elm
disease and the American chestnut blight. Yes, it can happen.

My discussion has emphasized viruses because medical
science has still to develop effective drugs for the treatment of
virus infections—we have but a small handful, of limited use.
Keep in mind that bacteria are free-living organisms whose
metabolic peculiarities lend themselves to differential attack.
For example, the bacterial cell wall is utterly unlike any

18 Kilbourne, Influenza.
352 SOCIAL RESEARCH

 

structure found in human cells. Hence, penicillin, which
attacks the integrity of the bacterial cell wall, is all but
innocuous to human tissue, and can be given in very large
doses so as to saturate every susceptible bacterial cell. Viruses,
on the other hand, are genetic fragments which live within the
host cells and exploit their metabolism. It has so far been very
difficult to find chemicals that will inhibit a virus without
harming the host cell at the same time. Our principal strategy
for dealing with viruses is immunization, evoking antibodies
that recognize the peculiarities of the virus surface. When a
virus, like AIDS, comes along and targets the immune system
itself, we are left with dimmer hopes of being able to use that
strategy; and we have very few alternatives.

Our main concern about bacterial plagues is for the
emergence of antibiotic-resistant strains of familiar threats—for
example, chloramphenicol-resistant typhoid. Plasmids are
known to travel among bacterial strains and confer antibiotic
resistance. Hence selective pressures favoring antibiotic-
resistant mutations in the bacteria in cattle’s intestines (by our
routinely feeding them antibiotics) have ended up making it
more difficult to treat human disease with the same drugs.
Probably even more important, and more difficult to control,
is the inappropriate use of antibiotics for trivial human disease,
or often for viral infections which antibiotics cannot control
anyhow, with the same result. In effect, any antibiotic will have
a limited lifetime of practical use; but we have devised no way
of rationing that to be sure it saves the most lives. (On the
other hand, it has been surmised that the indiscriminate use of
penicillin, by purely incidental effect, is the main cause for the
drastic mitigation of syphilis in the United States, most cases
having been treated unintentionally. Here we have been
unaccountably lucky that penicillin-resistant syphilis just hasn’t
emerged. We don’t know why.) We have been in a
well-chronicled race: human wit in the development of new
antibiotics versus the evolutionary drive for the emergence of
resistant mutants. We gained an enormous lead during the
PANDEMIC 353

 

1940s’ discoveries of these magic bullets; on the whole we
probably have the appropriate incentives and _ scientific
understanding to retain that lead, at least in the developed
countries. As must be reiterated, our neglect of infectious
disease in the poor majority of the world is not just a
humanitarian disgrace; it leaves unchecked the seeds of our
parochial infection.

Besides drug-resistance, bacteria do have some surprises for
us: in recent history, the spreading tick-borne epidemic of Lyme
arthritis and the storied Legionella show what can emerge over-
night; and how perplexing that can be until the parasite is
isolated and identified. Other mysterious variations in lethality
of bacterial infections come to notice from time to time. Besides
the fluctuations of environment that are usually invoked, closer
attention should be given to the likelihood that the bacteria
themselves may undergo genetic evolution. This may be alarm-
ing, insofar as we cannot be sure that the plague bacilli we see
today, and believe we can control, are just the same as those
responsible for the fourteenth-century pandemic.

Technology’s impact is not all on the human side of the
struggle. Monoculture of plants and animals has, of course,
made them more exposed to devastation. In like fashion, the
increasing density of human habitations, inventions like the
subway and the jet airplane, all add to the risks of spread of
infection. Paradoxically, improvements in sanitation and
vaccination leave the larger human herd more innocent of
microbial experience, and may in the long run make us the
more vulnerable. On the other hand, the loosening of ethnic
barriers has made the human population a mite more variable,
and in principle better equipped to deal with biological
challenges. Evolutionary modes of adaptation, we must never
forget, carry a terrible cost in the lives of extant individuals.
The best-known example in the human is the sickle cell trait,
evolved in Africa as an adaptation to malarial infection. The
ancestral benefit to the heterozygotes is exacting a cost today in
sickle cell disease among the homozygotes, about two births
354 SOCIAL RESEARCH

 

per thousand among American blacks. The evolutionary
calculus tells us this will come to equilibrium only when as
many homozygotes have died (or will not be born) as ancestral
heterozygotes had been saved from malaria. Infectious disease
has undoubtedly loomed large among the selective factors
shaping the human genome, and eventually will help explain
the polymorphisms in blood groups and in histocompatibility
(tissue-graft) antigens. We have had plausible speculations that
genetic diseases like the Tay-Sachs syndrome may have
conferred some protection against tuberculosis.

Technology, manifest in the opening of wild lands to human
occupation, has also exposed people to unaccustomed animal
viruses, to zoonoses. Yellow fever has sustained reservoirs in
jungle primates, and the same source is the probable origin of
the HIV virus in Africa. It is mystifying that yellow fever has
not become endemic in India, where competent mosquitoes
and susceptible people abound. We will almost certainly be hav-
ing like experiences from the “opening” of the Amazon basin.

More remote, perhaps more farfetched, is the interplanetary
transfer of infection. My own concerns, since Sputnik,!+ have
addressed the need to quarantine the planets, more to protect
them from contamination from a germ-laden earth than vice
versa. The main values at stake are in scientific understanding,
which will certainly be confused should we find bacterial spores
on Mars and have not undertaken hygienic precautions before-
hand. So long as we do not rush people to Mars (which bears
the concomitant imperative of returning them to earth), we can
do all the necessary preliminary science with clean, unmanned
missions, as has been internationally agreed policy to date.

AIDS and Other Plagues

The sudden and tragic spread of AIDS has brought us back

14]. Lederberg, “Sputnik 1957-1987,” Scientist, Oct. 5, 1987.
PANDEMIC 355

 

to earth in our speculation on plagues: who among us has not
been personally touched already! A host of social and ethical
issues come right to home, and will be the main focus of this
conference. As always, the third world is paying the heaviest
price, in the dying of whole villages and in the stigma of the
biological origins of the virus. We are all in fear of what will
come next. Will the virus spread still further? What are the
prospects of a vaccine? Of a cure?

You will have professional epidemiologists speak to the
current statistics. There is nothing hopeful about them. But
you should not think that AIDS is our only plague. In the third
world, tuberculosis and malaria are until now just as
devastating in their public-health impact, and are likely to
remain deathly competitors to AIDS in toll on human life.
Unlike AIDS, most of the third world endemics are most
painful as chronic diseases, which kill millions to be sure but
leave many more in debilitation and suffering, still-hungry
mouths to be fed. On top of those, over 3 million children a
year die of diarrheal disease, a like number from infections for
which effective vaccines exist but have not been available
where needed. This enormous mortality is entirely prevent-
able. The neglect of it is related to the history of a new disease
that must have been spreading unremarked in Africa for ten
or fifteen years before it emerged in the Western Hemisphere.
Nor will AIDS be the last example of its kind.

We are all too familiar with the factors that have made AIDS
an especially ugly challenge. Unlike other virus infections,
which leave some survivors immune to further attack, there is
nothing in the natural history of AIDS to point either to a cure
or to a vaccine. Victims develop antibodies, then go on
notwithstanding to develop more aggravated disease, with the
eventual collapse of the immune system. The fact that this is
still mysterious makes it the most promising avenue for new
discovery and possible intervention. Most of the factual
knowledge we have is unremittingly discouraging.

The long latent period multiplies the opportunity for
356 SOCIAL RESEARCH

 

spread; the victim may be unaware of carrying the virus, even
less his contacts. Nothing could provoke more anxiety than this
protracted uncertainty. The targeting of the immune system
also encourages the seeding of other infections—we are
already starting to see a recrudescence of tuberculosis in the
United States and aggravations of syphilis and a host of
opportunistic organisms rarely seen before. It would be far
worse were HIV still more readily spread, but its substantial
confinement to special high-risk groups worsens the social
tensions around efforts at control. The long latent period
guarantees a large number of momentarily healthy carriers
whose civil rights—for example, to continued schooling and
employment—are in instant conflict with a quarantine mental-
ity for public-health control. I was labeled an alarmist twenty
years ago for raising a “specter” of pandemic. My most
pessimistic imagination did not fetch the constellation of
attributes that we observe with AIDS. AIDS is already so
prevalent in the United States today that none of the
approaches of public-health control of other acute infections
are pertinent. There is little merit in targeting a handful of
individuals, generally the most compliant, when there are a
score as many freely walking the streets.

So much is unknown about AIDS that a large amount of
testing is essential just to understand the scope and localization
of the problem. We may soon find that many hospital and
medical procedures aggravate AIDS infection: that will
obligate broader testing of AIDS among hospital admissions,
simply for the patients’ benefit. And they will sue for not
having been routinely tested. Health-care personnel have an
ethical obligation to care for all the sick; but this is
complemented by a right to know what they need to protect
their own health. We will not work out the most viable balance
between individual rights and the community’s needs without a
great deal more compassionate thought and inevitable political
stress. Both need to be informed by more reliable knowledge.

Will AIDS get even worse? It may already be worse than we
PANDEMIC 357

 

believe—there is a fair possibility that some potential carriers
are still uncounted, that they will have a long latent period
after primary infection, before the virus reemerges and before
antibodies begin to appear. Such a stage at least is not fraught
with transmitting the disease to others. We have yet to learn
more precisely how readily it can be transmitted by heterosex-
ual contact; there is not much point trying to predict the future
course of AIDS prevalence by simple arithmetic extrapolation,
when utterly different communities and vehicles are involved.
We have Africa as a dismal historic example of progressively
broad spread; and I am not much impressed by arguments
that speak to cultural idiosyncrasies (as opposed to mere time)
as the difference between their experience and ours. Regard-
less, with what we know we have on our hands, we have a
rough road ahead.

As with some health-care workers, we are likely to
experience a few cases of AIDS transmitted outside the
“high-risk behaviors.” As such, these will have a_ political
impact far beyond their public-health importance, in contrast
to the recognized, dominant modes of transmission. We have
to be careful not to be stampeded by a few tragic accidents
statistically equivalent to lightning bolts. Rarely in human
history has so much rested on the clarity of social decision-
making, subject to extraordinary constraints of group interest,
prejudice, and ignorance.

Will AIDS mutate further? Already known, a vexing feature
of AIDS is its antigenic variability, further complicating the
task of developing a vaccine. So we know that HIV is still
evolving. Its global spread has meant there is far more HIV on
earth today than ever before in history. What are the odds of
its learning the tricks of airborne transmission? The short
answer is, “No one can be sure.” But we could make the same
attribution about any virus; alternatively the next influenza or
chicken pox may mutate to an unprecedented lethality. As
time passes, and HIV seems settled in a certain groove, that is
momentary reassurance in itself. However, given its other ugly
358 SOCIAL RESEARCH

 

attributes, it is hard to imagine a worse threat to humanity than
an airborne variant of AIDS. No rule of nature contradicts
such a possibility; the proliferation of AIDS cases with
secondary pneumonia multiplies the odds of such a mutant, as
an analogue to the emergence of pneumonic plague. Such
cases warrant and receive close-isolation precautions; but who
will ensure that in Africa? We must particularly look more
deeply into the biological mechanisms that govern how AIDS
can or cannot be transmitted; our current assessments are
crude empiricisms. And with so much at stake we must
multiply our vigilance for evidence of extraordinary channels
of spread.

Our preoccupation with AIDS should not obscure the
multiplicity of infectious diseases that threaten our future. It is
none too soon to start a systematic watch for other new viruses
before they become so irrevocably lodged. The fundamental
bases of virus research can hardly be given too much
encouragement—and they have made extraordinary leaps,
particularly with the help of recombinant DNA technology.!5
Such research should be done on a broad international scale,
both to share the progress made in advanced countries and to
amplify the opportunities for fieldwork in the most afflicted
ones.

We also have some political lessons learned. Hard-won
human rights, the autonomy of individuals, will be in conflict
with the quietude of the community. At severe cost, if at all,
will it be possible to impose traditional disease-control methods
like isolation and quarantine on new viruses. Compulsory

‘° The sensational publicity given ca. 1975 to the hypothetical hazards of
recombinant DNA research ignited public fears and regulatory reactions that boded ill
for the opportunity to continue research on methodology of the most crucial
importance for the understanding of virus infection. Some participants at the
much-heralded Asilomar Conference treated such research as if it were an idle
diversion for the amusement of scientists; therefore what harm in an indefinite
moratorium? See J. Lederberg, “DNA Research: Uncertain Peril and Certain
Promise,” in J.D. Watson and J. Tooze, The DNA Story: A Documentary History of Gene
Cloning (San Francisco: Freeman, 1981).
PANDEMIC 359

 

vaccination has all but passed the pale. Claims for redress for
individual harm from medical accidents from vaccines necessi-
tate that we find new social-insurance approaches to indemni-
fication. Failing that, we have already seen a collapse of the
pharmaceutical industry’s incentive and capability for pursu-
ing new vaccine developments. The most stunning victories
will be quiet ones, against viruses we have learned enough
about beforehand to keep them from planting a foothold.

The stresses on democratic civility posed by AIDS have no
precedent in U.S. history. They are compounded by our
scientific uncertainties as to where this epidemic is heading.
The best available advice is incorporated in the program
advocated by the leadership of the federal health agencies and
the expertise of groups like the National Academy of
Sciences.!6 That advice can be no more authentic than the
empirical findings to date. It is of the greatest urgency that
these be bolstered by a more robust appreciation of virus
biology and of the human immune mechanism. At present,
nothing we know gives us assurance of finding satisfactory
cures or vaccines for AIDS infection. We can take small
comfort that much more remains to be explored—but only if
we mount that exploration with the most urgent priority.

16 Institute of Medicine, National Academy of Sciences, Confronting AIDS: Directions
for Public Health, Health Care, and Research (Washington, 1986).