Survival Tricks of a Slippery Virus
Topics about interesting or local scientific developments likely to go unreported elsewhere in the newspapers have dominated this column for the 16 years it's been in existence. So this hasn't been the place to read about cold fusion or chronic fatigue syndrome, stealth bombers or AIDS.
But when the NAMES Project brought the AIDS memorial quilt to Fairbanks early in May, I was reminded that there was one item about acquired immune deficiency syndrome that I haven't seen discussed in the newspapers: the odd mutability of the AIDS virus.
The research, as reported in many magazines (such as Science, Science News, Discovery, Scientific American), suggests that AIDS is deadly partly because the causative virus has a striking weakness. Like other members of its family, the retroviruses, the AIDS virus has no mechanism to correct errors occurring as its genetic material undergoes duplication. That means whenever the virus multiplies, it's highly likely to make imperfect copies, or mutations, of itself.
An international team of researchers working in the Netherlands and England, worried about what that might mean for a human infected by the mutable virus. They theorized that a population of similar but not identical viruses would soon develop within that single person; the victim would play host to a family of subspecies. The person's immune system would recognize and fight this diverse lot of enemies, but eventually one or more variations would appear that the system detectors could not recognize. The mutants escaping detection would successfully attack key cells of the immune system itself, eventually overwhelming it.
As a crude analogy for how this works, imagine the cells of the immune system as a troop of robot dogs programmed to keep cats out of a goldfish farm. The robots' sensors recognize an array of catlike characteristics, and they chase away animals with those features. But if their program insists that cats have green or yellow eyes and long tails, then an eventual Manx-Siamese crossbred cat with a stub tail and blue eyes could enter the farm and eat goldfish without triggering a reaction from the dogs. Soon there would be few goldfish and many blue-eyed, stub-tailed cats (and if this analogy were truly accurate to AIDS, the cats would destroy all the robot dogs).
The AIDS researchers reasoned that if they had correctly understood the course of infection, then the diversity and number of viruses within a given patient would map to the progress of the disease. First, for a variable period of weeks to months, high levels of the virus would show up in the bloodstream of someone recently infected. Then the fully roused immune system would do its virus-control work, so that peak would be followed by a long period when virus numbers would be low. The immune system would be keeping up with the viruses, but they would be constantly mutating, so the number of subspecies would keep increasing. Theoretically, after the victim showed signs of full-blown AIDS, the number of subspecies should decrease. The successful mutations that had escaped recognition, the viral equivalents of the fictitious blue-eyed stub-tailed cats, would be the ones to overwhelm the immune system and multiply uncontrollably. Operating on evolutionary principles, they would be the thriving survivors---as long as their host lasted.
Preliminary results support the theory. It explains the unpredictable length of the incubation period between entrance of the virus and development of disease symptoms. Decades may pass before the virus mutates in just the right way to confuse the immune system, or the key mutations could appear within months. The theory also explains why medical scientists are having so little luck developing vaccines or cures for this modern plague. The virus is actually an enormous, ever-changing family of targets, too shifty for any medical magic bullet found so far.
