1491_ New Revelations of the Americas Before Columbus - Charles C. Mann [60]
Genetic homogeneity can be problematic, too. In the 1960s and 1970s 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 a rhinovirus, the kind of virus that causes the common cold. (Viruses mutate quickly and are commonly present 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 the 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.