The second type of vulnerability [The first he describes being the kind where you have yet to acquire immunity via trained antibodies -- MF] stems from a quirk of history. Archeologists dispute the timing and manner of Indians' arrival in the Americas, but almost all researchers believe that the initial number of newcomers must have been small. Their gene pool was correspondingly restricted, which meant that Indian biochemistry was and is unusually homogeneous. More than nine out of ten Native Americans -- and almost all South American Indians -- have type O blood, for example, whereas Europeans are more evenly split between types O and A.
Evolutionarily speaking, genetic homogeneity by itself is neither good nor bad. It can be beneficial if it means that a population lacks deleterious genes. In 1491, the Americas were apparently free or almost free of cystic fibrosis, Huntington's chorea, newborn anemia, schizophrenia, asthma, and (possibly) juvenile diabetes, all of which have some genetic component. Here a limited gene pool may have spared Indians great suffering.
Genetic homogeneity can be problematic, too. In the 1960's and 1970's Francis L. Black, a virologist at Yale, conducted safety and efficacy tests among South American Indians of a new, improved measles vaccine. During the tests he drew blood samples from the people he vaccinated, which he later examined in the laboratory. When I telephoned Black, he told me that the results were "thought-provoking." Every individual person's immune system responded robustly to the vaccine. But the native population as a whole had a "very limited spectrum of responses." And that, he said, "could be a real problem in the right circumstances". For Indians, those circumstances arrived with Columbus.
Black was speaking of human leukocyte antigens (HLAs), molecules inside most human cells that are key to one of the body's two main means of defense. Cells of all sorts are commonly likened to biochemical factories, busy ferments in which dozens of mechanisms are working away in complex sequences that are half Rube Goldberg, half ballet. Like well-run factories, cells are thrifty; part of the cellular machinery chops up and reuses anything that is floating around inside, including bits of the cell and foreign invaders such as viruses. Not all of the cut-up pieces are recycled. Some are passed on to HLAs, special molecules that transport the snippets to the surface of the cell.
Outside, prowling, are white blood cells -- leukocytes, to researchers. Like minute scouts inspecting potential battle zones, leukocytes constantly scan cell walls for the little bits of stuff that HLAs have carried there, trying to spot anything that doesn't belong. When a leukocyte spots an anomaly -- a bit of virus, say -- it destroys the infected or contaminated cell immediately. Which means that unless an HLA lugs an invading virus to where the leukocyte can notice it, that part of the immune system cannot know it exists, let alone attack it.
HLAs carry their burdens to the surface by fitting them into a kind of slot. If the snippet doesn't fit into the slot, the HLA can't transport it, and the rest of the immune system won't be able to "see" it. All people have multiple types of HLA, which means that they can bring almost every potential problem to the attention of their leukocytes. Not every problem, though. No matter what his or her genetic endowment, no one person's immune system has enough different HLAs to identify every strain of every virus. Some things will always escape notice. Imagine someone sneezing in a crowded elevator, releasing into the air ten variants of the rhinovirus, the kind of virus that causes the common cold. (Viruses mutate quickly and are commonly resent in the body in multiple forms, each slightly different from the others.) For simplicity's sake, suppose that the other elevator passengers inhale all ten versions of the virus. One man is lucky: he happens to have HLAs that can lock onto and carry pieces of all ten variants to the cell surface. Because his white blood cells can identify and destroy the infected cells, this man doesn't get sick. Not so lucky is the woman next to him: she has a different set of HLAs, which are able to pick up and transport only eight of the ten varieties. The other two varieties escape the notice of her leukocytes and go on to give her a howling cold (eventually other immune mechanisms kick in and she recovers). These disparate outcomes illustrate the importance to a population of having multiple HLA profiles; one person's HLAs may miss a particular bug, but another person may be equipped to combat it, and the population as a whole survives.
Most human groups are a scattershot mix of HLA profiles, which means that almost always some people in a group will not get sick when exposed to a particular pathogen. Indeed, if laboratory mice have too much HLA diversity, Black told me, researchers can't use them to observe the progress of an infectious disease. "You get messy results -- they don't all get sick." the opposite is true as well, he said. Peole with similar HLA profiles fall victim to the same diseases in the same way.
In the 1990's Black reviewed thirty-six studies of South American Indians. Not to his surprise, he discovered that overall Indians have fewer HLA types than populations from Europe, Asia, and Africa. European populations have at least thirty-five main HLA classes, whereas Indian groups have no more than seventeen. In addition, Native American HLA profiles are dominated by an unusually small number of types. ABout one third of South American Indians, Black discovered, have identical or near-identical HLA profiles; for Africans the figure is one in two hundred. In South America, he estimated, the minimum probability that a pathogen in one host will next encounter a host with a similar immune spectrum is about 28 percent; in Europe, the chance is less than 2 percent. As a result, Black argued, "people of the New World are unusually susceptible to diseases of the Old."
[He goes on to detail the experience of Siberian native populations with European borne diseases, reasoning on the basis of the close ancestry American and Siberian natives share. Not entirely relevant to the explanation here, however, as he includes it mostly to bolster his case about 70-90% death rates over the centuries - MF]
After learning about this sad history [The Siberian experiences - MF] I again telephoned Francis Black. Being genetically determined, Indian HLA homogeneity cannot be hanged (except by intermarriage with non-Indians). Did that mean that the epidemics were unavailable? I asked. Suppose that the peoples of the Americas had, in some parallel world, understood the concept of contagion and been prepared to act on it. Could the mass-death have been averted?
"There have been lots of cases where individual towns kept out epidemics," Black Said. During plague episodes, "medieval cities would barricade themselves behind their walls and kill people who tried to come in. But whole countries -- that's much harder. England has kept out rabies. That's the biggest success story that comes to mind, offhand. But rabies is primarily an animal disease which helps, because you only have to watch the ports -- you don't have many undocumented aliens sneaking in with sick dogs. And rabies is not highly contagious, so even if it slips through it is unlikely to spread."
He stopped speaking for long enough that I asked him if he was still on the line.
"I'm trying to imagine how you would do it," he said. "If Indians in Florida let in sick people, the effects could reach all the way up to here in Connecticut. So all these different groups would have had to coordinate the blockade together. And they'd have to do it for centuries -- four hundred years -- until the invention of vaccines. Naturally they'd want to trade, furs for knives, that kind of thing. But the trade would have to be conducted in antiseptic conditions."
The Abenaki sent goods to Verrazzano on a rope strung from ship to shore, I said.
"You'd have to have the entire hemisphere doing that. And the Europeans would presumably have to cooperate, or most of them, anyway. I can't imagine that happening, actually. Any of it."
Did that mean the epidemics were inevitable and there was nothing to be done?
The authorities, he replied, could "try to maintain isolation, as I was saying. But that ends up being paternalistic and ineffective. Or they can endorse marriage and procreation with outsiders, which risks destroying the society they supposedly are trying to preserve. I'm not sure what I'd recommend. Except getting these communities some decent health care, which they almost never have."
Except for death, he went on, nothing in medicine is inevitable, "But I don't see how it [waves of epidemics from European diseases] could have been prevented for very long. That's the terrible thought. But I've been working with highly contagious diseases for forty years, and I can tell you that in the long run it is almost impossible to keep them out.