Published by Communications and Public Affairs (519) 824-4120, Ext. 56982 or 53338
May 31, 2001
Gene 'fingerprint' offers clue to foot-and-mouth virus
A University of Guelph researcher studying foot-and-mouth disease has found a “fingerprint” that indicates the virus may share certain adaptive characteristics of longer-lasting viral infections such as HIV.
The research by Daniel Haydon, a post-doctoral fellow in the Department of Zoology, focused on six different types of foot-and-mouth virus (FMDV) and was published by the science journal Genetics. He also collaborated on a paper published in the May issue of Nature magazine that documented how foot-and-mouth disease in the United Kingdom was brought under control.
In the Genetics study, Haydon reported that he had discovered a “fingerprint” in the genes of FMDV that reveals the virus uses its extremely high mutation rate to selective advantage. Although FMDV poses no risk to humans, this variation has also been found in human viruses such as HIV that must change quickly and often enough to outsmart an immune system for lengthy periods. Until recently, it was unknown whether shorter-lasting viral infections such as FMDV, which usually clear up in two to three weeks, could benefit from rapid mutation rates in the same way.
“Rapid mutation rates allow viruses to dodge around natural immune responses and vaccines and avoid being eliminated,” Haydon said. “This is why longer-lasting viruses such as HIV must be treated by a cocktail of drugs. The viruses mutate so fast that they could become immune to one drug very quickly. But when you throw three drugs at them at once, it’s less likely they can mutate fast enough to dodge them all simultaneously.”
The fact that FMDV changes so rapidly means an initial infection could be prolonged or intensified, increasing the potential for transmission, Haydon said. A virus that mutates quickly “tricks” its host’s immune system. “Halfway through an infection, it looks like a different virus, and the body doesn’t recognize it as something it has already mounted an immune response to. From the virus’s standpoint, this is a good idea as it stands to benefit from confounding the immune system either of its immediate host or other hosts that the virus's offspring may adopt.”
Discovering that a virus is mutating and changing is one thing, said Haydon, but figuring out whether change is actually advantageous to the virus is something else altogether. It is much harder to document. “Is the high mutation rate of FMDV actually intrinsic to its ability to persist, or is the fact that it’s mutating and surviving just an accidental coincidence?” The researchers concluded that although the high mutation rate in FMDV is well documented, it appears that the new mutant virus actually does better and is more likely to persist through time than a virus that stays the same.
Haydon conducted the study while at the Centre for Tropical Veterinary Medicine in Edinburgh, Scotland and collaborated with researchers from animal health institutes in England and South Africa. In the Nature article, Haydon and researchers from the United Kingdom concluded that the foot-and-mouth disease outbreak was brought under control a month after the disease was first noticed. There have been nearly 1,600 foot-and-mouth cases since the outbreak was first confirmed in Britain in February. At the epidemic’s height, as many as 40 new cases were being confirmed daily.
Although the researchers say the initial outbreak is on the way out, they caution that new epidemics in previously unaffected areas would have to be immediately contained.
“If there was an outbreak in a new part of the country, the whole story could change quite dramatically,” Haydon said. “Chances are the disease would have been in that new area for some time without anyone knowing about it, and the process could start all over again. A new outbreak would be the tip of the iceberg, a whole new cancer, so to speak.”
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