Plagues and Peoples (2 page)

For a long time, I felt that the remarks on
this page
about how the age-old balance between host and parasite remained a permanent feature of human (and of all multi-celled forms of) life were sufficient to explain the appearance of AIDS and the emergence of resistant strains of older infections. In fact, I still do, and so have not altered anything in these pages. A second reason for saying nothing explicitly about AIDS was that accurate information about its origins and spread was impossible to find. This is still the case, but alternate theories have emerged with the passage of time, and
some statistics about the scale of the epidemic worldwide and within the United States are now available. Let me therefore offer a few brief observations on the AIDS epidemic and how it appears to conform to familiar ecological and sociological patterns.

First, origins. When AIDS was newly discovered in the 1980s and doctors were still expecting to come up with a quick and easy cure for the HIV-1 infection, a related virus was discovered to exist among a species of African monkeys. This suggested that the human form of the infection might have arisen recently, when the virus shifted its parasitism from monkeys to humans. Routes of transmission, from Africa to Haiti and so to the United States, were swiftly inferred, offering a plausible account of how AIDS had arisen and spread.

But there were difficulties with this theory. The virus that existed among monkeys in Africa had a relatively mild human equivalent in the form of HIV-2; but the lethal HIV-1 virus that causes AIDS was so different in details of its structure that recent derivation from the form of infection existing among a few African monkeys and humans seemed implausible. This led a distinguished medical historian, Mirko Grmek,
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to propose in 1989 that AIDS was in fact a longstanding human infection, widely dispersed around the earth, but hidden from medical attention both by the diversity of symptoms sufferers developed and by the infrequency with which it occurred. According to Grmek, changes in medical science on the one hand and changes in human behavior on the other were what provoked the AIDS epidemic.

Assuredly, without techniques of molecular biology introduced within the past fifty years or less, the HIV-1 virus could not have been identified. Moreover, symptoms later associated with AIDS were observed as early as 1868, when the so
called Kaposi’s skin cancer was diagnosed and named in Vienna. And beginning in the 1930s, doctors encountering strange infections sometimes stored tissue samples in hope that later advances in science might solve their puzzlement. In a few cases, analysis of such tissues has turned up evidence of HIV infection decades before AIDS was first recognized.

But the most persuasive evidence that HIV-1 is a longstanding human infection rests on the fact that slightly divergent strains of the virus exist among human populations in different parts of the earth, and now appear to be evolving toward a recombinant, global form as local strains intermingle and the most vigorous, viable viruses multiply themselves at the expense of less successful variants. It is even possible that the AIDS epidemic, as recognized in the 1980s, was itself provoked by recombination of older viral strains, producing what is now called HIV-1 from different ancestral forms of the virus. No one is sure; but a recent transfer from some African reservoir of HIV infection no longer seems necessary or even probable.

Whatever pathways HIV viruses may have followed in the deeper past, it seems certain that the sudden outburst of AIDS in the 1970s depended on changes in human behavior that favored transmission of the viruses from host to host. One such change was an increase in sexual promiscuity among homosexual men in the United States and elsewhere, partly as a result of gay liberation. A second factor was an increase in the intravenous injection of heroin and other mood-altering drugs beginning in the 1970s, when cheap plastic syringes first became available. As these practices became more common, it became far easier than before for HIV viruses to spread from host to host. The infection had previously remained rare because opportunities for direct entry into the bloodstream of a new host, which the virus required, were narrowly restricted. Presumably, only the fact that hosts lived a long time before lethal adventitious infections killed them had allowed the chain of HIV infection to continue, sporadically and precariously. But shared needles and sexual promiscuity
among infected individuals abruptly widened chances for the virus to transfer from an infected individual to a new host; and it appears that the result was indeed spectacular.

For example, retrospective analysis of blood samples collected from gay men in San Francisco showed that in 1978 (before AIDS had been diagnosed) 4.8% of them were HIVpositive. A mere six years later, the figure was 73.1%.
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By then, knowledge of how the infection is transmitted had hit home. Sexual practices in the homosexual community of San Francisco changed abruptly and infection rates among gay men ceased to grow, but only after blood samples showed that the majority of gay men in the city had become bearers of the disease. I have not seen comparable figures for intravenous drug takers, and they may persist in reckless behavior. After all, fear of dying of AIDS far in the future is unlikely to deter someone whose craving for a quick “fix” eclipses any and every long-range consideration.

But in American society at large, it seems clear that awareness of how AIDS is transmitted put a chill on sexual promiscuity and made intravenous drug-taking a lot less attractive than before. It therefore seems almost certain that the future incidence of the disease will reflect resulting behavioral changes. Only a few reckless individuals are likely to remain high risks, concentrating very likely at the social extremes—on the one hand, gilded youth who suppose themselves immune from sexual or any other sort of mischance; and on the one hand, poor, down-and-out drifters who do not know or care enough about themselves or others to take precautions against HIV infection. This was what happened to syphilis, and is probably also happening to AIDS in the United States and other similar societies today. If so, the epidemic will be contained and never have any very noticeable demographic effect on society at large, just as was true of syphilis.

This may not be the case in some parts of sub-Saharan Africa where AIDS appears to be widespread among the general
population. But reliable statistics do not exist; and blood samples collected from urban areas may exaggerate the prevalence of the infection. As elsewhere in the world, the disease appears to be new in Africa, and changes in sexual behavior associated with massive migration from the countryside into urban shantytowns presumably lie behind its propagation. These changes affect both men and women and are not associated with homosexuality. That makes the impact of AIDS different in Africa from what it has been in the United States. But it is too soon to be sure that the disease will not be contained by changes in human behavior on the one hand and by the global process of HIV-1 evolution on the other. So far at least, official population statistics from African countries do not show any demographic effect that is clearly attributable to AIDS. Population growth rates are diminishing, but remain higher than anywhere else in the world. Nothing remotely like the disease disasters of the deeper past has yet become evident, but the long gap between initial HIV-1 infection and death from AIDS means that no one can yet be sure how statistically important the AIDS epidemic in Africa will prove to be.

Similar uncertainty prevails in countries like Thailand, where HIV-1 infections are believed to be widespread. Worldwide, uncertainty is even greater, but so far at least, AIDS simply does not compare with the ravages of the Black Death or with the disease destruction of Amerindian and other isolated peoples in the more recent past.

A really efficacious medical remedy for AIDS would alter the situation, of course; but so far chemical treatments only prolong sufferers’ lives without definitively curing the infection. Meanwhile, only partially understood changes in the HIV-1 virus itself are presumably taking place—partly in response to chemical attacks and partly in response to encounters among diverse strains coming from different parts of the world.

Modern air travel assures continuation of this accelerated
process of disease homogenization, not merely for HIV-1 but for all other human, animal, and plant infections as well. It means that whenever a new, especially successful form of an infection emerges, it will spread rapidly around the globe. The pattern of the flu virus, evolving a new variant almost every year, is archetypical. Other, usually unidentified viruses afflict us constantly as well. It is obvious that human (and nonhuman) diseases are evolving with unusual rapidity simply because changes in our behavior facilitate cross-fertilization of different strains of germs as never before, while an unending flow of new medicines (and pesticides) also present infectious organisms with rigorous, changing challenges to their survival.

AIDS therefore is not the only infection to threaten human lives; but overall and in the long run, the familiar ecological pattern of mutual accommodation between host and parasite is almost sure to prevail. That means endemic will tend to replace epidemic infections while less lethal strains and chronic infections gain in importance against more virulent germs.

Plants and animals share with us in the process of disease homogenization. Probably, local wild-animal populations are most at risk simply because they have not previously encountered some of the infections that speedy, intensified global transportation exposes them to. Other changes in habitat, due largely or entirely to human activity, also affect wild plant and animal populations. Overall, the result is massive extinctions of isolated species, with long-range consequences we cannot anticipate.

In short, organic evolution is operating in high gear nowadays, largely because of human intervention in natural ecosystems. Our exposure to infectious disease is altering very quickly, but this is only part of a wider adjustment and readjustment of ecological relations whose future trajectory remains as mysterious as ever. Perhaps one can say that biological evolution has, in effect, been overtaken and accelerated
beyond all precedent by human intervention in natural processes, guided and directed by modern science on the one hand, and driven by multiplying human numbers on the other.

In a sense, this is as old as humanity itself, for even our remotest predecessors also altered their environments by deliberate, concerted action, directed by conscious intentions and defined by shared meanings that were expressed mainly through words. But modern science and technology, by tapping inorganic sources of energy, enormously enlarged human capabilities for changing natural balances among competing life forms. The apparent conquest of infectious diseases between 1884, when Robert Koch first identified the cholera bacillus, and 1976, when WHO succeeded in eliminating smallpox, was assuredly one of the most drastic disturbances of older ecological balances ever achieved by human beings. Nonetheless, the way infectious diseases have begun to come back shows that we remain caught in the web of life—permanently and irretrievably—no matter how clever we are at altering what we do not like, or how successful we become at displacing other species.

This book explores one important aspect of our extraordinary capability for altering natural balances, and the limitations of those capabilities. Nothing that has happened since it was written contradicts its general thrust. We remain part of the earth’s ecosystem, and participate in the food chain whereby we kill and eat various plants and animals, while our bodies provide a fair field full of food for a great variety of parasites. No conceivable change in the earth’s ecosystem will alter that fundamental condition of human life, even though changes in our knowledge and behavior can and will continue to alter the incidence of disease and the array of what we eat.

This book explores the notable landmarks of the shifting balance between human hosts and infectious organisms. It is a dramatic story whose importance for political and cultural history is only beginning to be widely understood. I therefore
invite you to read what I wrote more than twenty years ago and see for yourselves how infectious disease affected our predecessors’ lives.

W. H. McN.
15 March 1997

Introduction

H
OW
T
HIS
B
OOK
H
APPENED

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early twenty years ago, as part of my self-education for writing
The Rise of the West: A History of the Human Community
, I was reading about the Spanish conquest of Mexico. As everyone knows, Hernando Cortez, starting off with fewer than six hundred men, conquered the Aztec empire, whose subjects numbered millions. How could such a tiny handful prevail? How indeed? All the familiar explanations seemed inadequate. If Montezuma and his friends first thought the Spaniards were gods, experience soon showed otherwise. If horses and gunpowder were amazing and terrible on first encounter, armed clashes soon revealed the limitations of horseflesh and of the very primitive guns the Spaniards had at their disposal. Cortez’s skill in finding allies among the Indian peoples of Mexico and rallying them against the Aztecs was certainly important, but most of his Indian allies committed themselves to the Spanish side only when they had reason to think Cortez would win.