Virology: Early Infection, Late Disease

Each year since the 1930s, an estimated 35,000 Americans have fallen victim to Parkinson’s disease, or “shaking palsy.” Each year, scores of the Chamorros of Guam develop some of the symptoms of Parkinson’s, along with a form of muscle degeneration best known in the U.S. as “Lou Gehrig’s disease.” Just as regularly, hundreds of sheep in a score of different countries begin rubbing their backs against barbed wire, ruining their wool and revealing themselves as victims of scrapie. On North American fur farms, mink of many colors get sick with a sort of softening of the brain, while smoke-hued, so-called Aleutian mink get liver and kidney disease, with added symptoms suggestive of human arthritis. Each year, in the highlands of New Guinea, a hundred or more members of the Stone Age Fore tribe die of kuru, an incurable degeneration of the brain.

What do these diseases of man and beast have in common? Probably, says Dr. D. Carleton Gajdusek, a top researcher at the National Institute of Neurological Diseases and Blindness, they are all caused by extraordinarily slow-acting viruses—none of which has yet been definitely seen, even with the electron microscope.

Short Tests. To formulate such a theory, admits Gajdusek, is to call into question much of the traditional thinking of virologists. Generations of researchers have been accustomed to thinking of viruses as microbes that behave somewhat predictably. Typically, as in the case of measles, German measles, chicken pox, the common cold and influenza—of the Hong Kong variety, or whatever—they seem to appear from nowhere, spend a few days, or at most two or three weeks, incubating in the victim’s body, then cause a brief, feverish illness.

A few, like the measles and polio viruses, may cause permanent damage. Others, like those of hepatitis and rabies, may spend months in incubation before they cause apparent illness. But these, it had been thought, were the exceptions. A researcher trying to indict a virus as the cause of a still unexplained disease has ordinarily injected his test materials into small lab animals and waited a few months. If none of the animals got the disease in that time, he killed them and wrote off the experiment as a failure.

That, Gajdusek says, may have been a mistake. Some of these delayed-fuse viruses may take years to exert their malign effects in small animals, and decades in long-lived Homo sapiens. Virologist Gajdusek, a human whirlwind who goes around the world half a dozen times a year, decided to become a model of patience. At the institute, he set up a long-range study program with a variety of animals, ranging from tree shrews to sheep and goats, a dozen species of monkeys, and a number of forbiddingly expensive chimpanzees.

Age and Parkinsonism. His patience paid off. From New Guinea, Gajdusek brought back parts of kuru victims’ brains. He injected some of the material into chimpanzees, and waited—for two years. Then the chimps began to show the wobbly gait, slavering and eye-crossing that mark the human disease. When they died, their brains showed essentially the same type of damage as those of human kuru victims.

It now seems certain that kuru was the result of a slow-acting virus, transmitted from one Fore to another by cannibalism. Women and children who ate the brains of tribesmen who died of kuru far outnumber men as kuru victims. Cannibalism was stamped out—or so the Australian government thinks —about twelve years ago. Gajdusek reports hopefully that there has not been a single case of kuru among children born in the past twelve years.

The opposite kind of age phenomenon occurs in Parkinson’s disease, or Parkinsonism. At Massachusetts General Hospital, Neurologists David C. Poskanzer and Robert Schwab found records of only 22 cases in 42 years before 1917; since then, there have been more than 1,800 cases. Virtually all recent victims were born within ten years of 1897, and their age at the time their disease developed has been going up steadily—from an average of 34 in 1920 to at least 61 now. The Poskanzer-Schwab explanation: most recent Parkinsonism victims were infected during a 1915-26 epidemic of encephalitis lethargica, the virus of which disappeared in 1931. The virus may have damaged or lain dormant in the part of the brain that controls the movements affected by Parkinsonism. A telling point in favor of their hypothesis: Poskanzer and Schwab can trace only one Parkinsonism victim born since 1931.

Minlc and Man. To researchers, there are many suggestive similarities between scrapie in sheep and multiple sclerosis in man. Poskanzer has suggested that MS may be a late manifestation of a childhood infection similar to that of non-paralytic polio. Gajdusek sees a striking resemblance between Aleutian mink disease and a lethal congenital detect in partially albino children.

Gajdusek believes that slow-acting viruses may be to blame for no fewer than 30 human diseases of the nervous and muscular systems, some rare, some common. In the hope of explaining them —and thus, eventually, of curing or preventing them—he is weaving together all the seemingly disparate threads of disease in mink, sheep and men, and painstakingly amassing information for which earlier virologists would not wait.