AlaskaDenise
In Memoriam
http://bodyandhealth.canada.com/channel_health_news_details.asp?news_id=10991&news_channel_id=1020&channel_id=1020&rot=11
Provided by: Canadian Press
Written by: HELEN BRANSWELL
Oct. 29, 2006
TORONTO (CP) - The accepted notion that influenza viruses are constantly changing in a bid to outsmart the human immune system may not be entirely accurate, a new study says.
The work, by U.S. scientists, suggests flu viruses evolve in a pattern of fits and starts, perhaps spurred by a competition between the two circulating types of influenza A that infect people, H3N2 and H1N1.
The finding, if confirmed by other researchers, could offer clues on how best to select the influenza strains that go into the annual flu shot, in particular in the years when H3N2 is undergoing the major changes that precede a bad flu season.
"Our hope is one, we could do a better job of being ready for those big changes, which is important because a lot of people get sick those years," said David Lipman, senior author of the paper, which was published in the online journal Biology Direct.
It might also help scientists predict if the avian influenza strain H5N1 is evolving in a way that should set off alarm bells, said Lipman, director of the U.S. National Center for Biotechnology Information, one of the National Institutes of Health.
The authors suggest the dominant human subtype, H3N2, occasionally goes into brief periods of evolutionary suspension or stasis, lasting months and even a year or so. Spotting an opening, H1N1 surges forward to become the main circulating subtype for a flu season, an occurrence that snaps H3N2 viruses back into action, they say.
"When H1N1 wins, that's basically a sign that H3N2 is in a stasis period," said Lipman, who wrote the paper with colleagues from the National Institutes of Health and the Pennsylvania State University.
Their work, which may raise eyebrows among flu scientists, is one of the first to draw on the Influenza Genome Sequencing Project - an ambitious U.S. program aimed at cataloguing the genetic blueprints of as many garden-variety flu viruses as possible from different parts of the world.
The project is a bit like a genetic census of influenza. The growing database gives scientists the chance to study the genetic codes of a large number of flu viruses and look for patterns that may provide insights into everything from how flu evolves to how best to design new flu drugs and vaccines.
Joshua Plotkin, a researcher who specializes in molecular evolution at Harvard, called the work "an awesome use of these data."
Plotkin is also looking for ways to predict the evolution of influenza viruses. While he didn't challenge the findings, he suggested this paper doesn't turn flu dogma on its ear, but rather fine-tunes it.
"It's been known for a long time that . . . it sometimes takes two or in rare circumstances even three years" for a sufficiently new strain of H3N2 to emerge and cause a serious epidemic, he said, adding the study conclusions "really fill in the detail of that story."
But one of the reviewers of the paper remained skeptical Lipman and his co-authors had captured a real pattern, suggesting the collection of 1,000 or so viruses they studied might not have been representative of what was going on around the world. The viruses studied for this paper were from New York state and New Zealand.
"I am not convinced that the view of long periods of stasis . . . described here is not primarily due to the use of a biased (incomplete) dataset," Ron Fouchier, a virologist from Erasmus University in Rotterdam, wrote in his assessment of the study. (Biology Direct posts the comments of its academic reviewers along with the articles.)
In the paper, Lipman and his colleagues charted the evolution of H3N2 and H1N1 viruses between 1995 and 2005.
They saw a pattern in which H3N2 viruses would evolve to the point where they were sufficiently different that they could cause a serious annual epidemic. That's because the changes made the viruses unrecognizable to the immune systems of many people worldwide.
Those big influenza years occurred in 1997, with a flu strain named A/Sydney and in 2003 with a strain named A/Fujian.
But because those strains made so many people sick, the H3N2 viruses would have had to acquire significant new changes in successive flu seasons to again infect lots of people. They did not and in the year or two after, the flu seasons were milder.
Eventually, the evolutionary progress of those strains of H3N2 appeared to stall, allowing H1N1 to come to the fore. Being overtaken by the rival strain seemed to push H3N2 back into action.
Lipman said a mild H3N2 season followed by an H1N1 season - H1N1 typically causes even milder disease than H3N2 - could be a signal a bad flu season is on the way.
"We don't know if it's going to take off next season. Or the season after. What this . . . tells us though, is that we need to come up with a better way to analyze the sequence data, to do the (strain) surveillance, to see when it's going to explode on us," Lipman said.
.
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Provided by: Canadian Press
Written by: HELEN BRANSWELL
Oct. 29, 2006
TORONTO (CP) - The accepted notion that influenza viruses are constantly changing in a bid to outsmart the human immune system may not be entirely accurate, a new study says.
The work, by U.S. scientists, suggests flu viruses evolve in a pattern of fits and starts, perhaps spurred by a competition between the two circulating types of influenza A that infect people, H3N2 and H1N1.
The finding, if confirmed by other researchers, could offer clues on how best to select the influenza strains that go into the annual flu shot, in particular in the years when H3N2 is undergoing the major changes that precede a bad flu season.
"Our hope is one, we could do a better job of being ready for those big changes, which is important because a lot of people get sick those years," said David Lipman, senior author of the paper, which was published in the online journal Biology Direct.
It might also help scientists predict if the avian influenza strain H5N1 is evolving in a way that should set off alarm bells, said Lipman, director of the U.S. National Center for Biotechnology Information, one of the National Institutes of Health.
The authors suggest the dominant human subtype, H3N2, occasionally goes into brief periods of evolutionary suspension or stasis, lasting months and even a year or so. Spotting an opening, H1N1 surges forward to become the main circulating subtype for a flu season, an occurrence that snaps H3N2 viruses back into action, they say.
"When H1N1 wins, that's basically a sign that H3N2 is in a stasis period," said Lipman, who wrote the paper with colleagues from the National Institutes of Health and the Pennsylvania State University.
Their work, which may raise eyebrows among flu scientists, is one of the first to draw on the Influenza Genome Sequencing Project - an ambitious U.S. program aimed at cataloguing the genetic blueprints of as many garden-variety flu viruses as possible from different parts of the world.
The project is a bit like a genetic census of influenza. The growing database gives scientists the chance to study the genetic codes of a large number of flu viruses and look for patterns that may provide insights into everything from how flu evolves to how best to design new flu drugs and vaccines.
Joshua Plotkin, a researcher who specializes in molecular evolution at Harvard, called the work "an awesome use of these data."
Plotkin is also looking for ways to predict the evolution of influenza viruses. While he didn't challenge the findings, he suggested this paper doesn't turn flu dogma on its ear, but rather fine-tunes it.
"It's been known for a long time that . . . it sometimes takes two or in rare circumstances even three years" for a sufficiently new strain of H3N2 to emerge and cause a serious epidemic, he said, adding the study conclusions "really fill in the detail of that story."
But one of the reviewers of the paper remained skeptical Lipman and his co-authors had captured a real pattern, suggesting the collection of 1,000 or so viruses they studied might not have been representative of what was going on around the world. The viruses studied for this paper were from New York state and New Zealand.
"I am not convinced that the view of long periods of stasis . . . described here is not primarily due to the use of a biased (incomplete) dataset," Ron Fouchier, a virologist from Erasmus University in Rotterdam, wrote in his assessment of the study. (Biology Direct posts the comments of its academic reviewers along with the articles.)
In the paper, Lipman and his colleagues charted the evolution of H3N2 and H1N1 viruses between 1995 and 2005.
They saw a pattern in which H3N2 viruses would evolve to the point where they were sufficiently different that they could cause a serious annual epidemic. That's because the changes made the viruses unrecognizable to the immune systems of many people worldwide.
Those big influenza years occurred in 1997, with a flu strain named A/Sydney and in 2003 with a strain named A/Fujian.
But because those strains made so many people sick, the H3N2 viruses would have had to acquire significant new changes in successive flu seasons to again infect lots of people. They did not and in the year or two after, the flu seasons were milder.
Eventually, the evolutionary progress of those strains of H3N2 appeared to stall, allowing H1N1 to come to the fore. Being overtaken by the rival strain seemed to push H3N2 back into action.
Lipman said a mild H3N2 season followed by an H1N1 season - H1N1 typically causes even milder disease than H3N2 - could be a signal a bad flu season is on the way.
"We don't know if it's going to take off next season. Or the season after. What this . . . tells us though, is that we need to come up with a better way to analyze the sequence data, to do the (strain) surveillance, to see when it's going to explode on us," Lipman said.
.
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