Medical researchers trying to combat SARS are learning lessons from a more familiar but equally shifty viral disease: influenza. Every year, new flu strains emerge resistant to existing vaccines. And every year, epidemiologists worry that the next flu epidemic could turn as disastrous as the 1918 Spanish flu pandemic that killed at least 20 million people around the world. So Neil Ferguson, a biological modeler at Imperial College London, has been trying to develop a mathematical simulation that explains how new strains appear. That, he says, could point to ways to boost our immune system.The influenza virus puzzles researchers because it mutates rapidly, yet few variants are found in the wild at any given time. “Most of the new strains quickly go extinct,” says Ferguson’s collaborator, molecular evolutionist Robin Bush of the University of California at Irvine. So how does the virus bounce back to infect again and again? Bush and Ferguson searched for an answer by modeling the interaction between the virus’s mutations and the human immune response. The model reveals that a little-understood temporary immune response largely controls flu virus evolution. “It seems to provide general immunity against all types of influenza for a couple of weeks after infection. You can’t get the flu, no matter what kind it is,” Bush says. Most of the mutant strains that emerge during that initial period die out. But the rare variants that survive can reinfect the host when the transient response shuts down, and then spread and replace the older influenza strains. If researchers can deduce how temporary resistance works, they might be able to exploit it to design vaccines that provide long-lasting immunity.Excerpted from an article in ‘Discover’, July 2003In seeking to understand the remarkably deadly 1918 flu pandemic scientists have focused on the influenza virus, combing its genes for clues to its malevolence. But demographer Andrew Noymer of the University of California at Berkeley thinks people are overlooking a second culprit: Mycobacterium tuberculosis, the tuberculosis bacterium.Noymer reached his iconoclastic conclusion after poring over acres of data on 20th-century death rates in the United States. One statistic stood out. The rate of deaths from TB plunged from 157 per 100,000 in 1918 to 103 per 100,000 in 1921, right after the flu pandemic. He found no similar decrease in mortality from other chronic ailments such as cancer. That pattern implies that many of those who died from the flu were already infected by TB. And he notes that M. tuberculosis carves out cavities in the lung. Those cavities would have been perfect breeding grounds for pneumonia, which finished off most flu victims in 1918.Excerpted from an article in ‘Discover’, March 2001
