TORONTO - Unproven assumptions about the course of the 1918 Spanish flu pandemic may be leading to misperceptions of what the swine flu virus has in store for the world, the scientist who decoded the genetic blueprint of the 1918 virus suggests in a newly published commentary.
Virologist Dr. Jeffery Taubenberger, along with co-author and medical historian Dr. David Morens, argues there is no firm evidence that the 1918 virus ratchetted up in virulence in a fall wave - because there is no solid proof outbreaks of illness in the U.S. in the spring of 1918 were caused by the same virus.
Their commentary, published in this week's issue of the Journal of the American Medical Association, suggested changes in virulence or transmissibility of the current pandemic virus are not inevitable. In fact, they wrote, there are reasons to hope for "a more indolent pandemic course and fewer deaths" than seen in many previous pandemics.
"I think every pandemic is completely different," Taubenberger said in an interview from Bethesda, Md., where he and Morens work at the U.S. National Institute of Allergy and Infectious Diseases.
"It emerges in a different way. Its genetics are going to be different. The population immunity by age is going to be different depending on what it is. So I think it's very difficult and perhaps a disservice to assume that a new pandemic is going to behave in a way like 1918."
The scientific community is split about what happened in the opening days of the notorious Spanish flu pandemic, which is believed to have killed upwards of 50 million people in 1918-1919.
The prevailing view is that spring outbreaks of largely mild disease in the United States and then in Northern Europe was actually the opening round - the so-called herald wave - of the pandemic. The received wisdom is that over the summer the virus mutated, making the disease it caused more severe.
The concept that an initially mild pandemic virus could change into something nastier has featured prominently in the logic of public health officials as they have explained why the world needs to respond aggressively to the new H1N1 virus.
But Taubenberger and some others have repeatedly noted that there are no virus samples from the spring wave, so there is no way to confirm that outbreaks were caused by the same virus or that the virus changed to become more virulent.
"So that is an hypothesis. But it is one of several. And we don't know that that's really true," he said.
Taubenberger and a team of collaborators excavated enough particles of the 1918 virus that its genetic code could be sequenced. The virus was then reconstituted at the U.S. Centers for Disease Control and remains the subject of ongoing research in select high-security laboratories.
But the fragments of viral RNA used in the painstaking task were taken from tissues of people who died in the fall of 1918. To date no one has found samples of the virus or viruses responsible for illness in the spring of 1918.
There is some high-profile support for the argument Taubenberger and Morens make.
Dr. Walter Dowdle, a retired former head of the influenza program at the U.S. Centers for Disease Control, suggested so much has changed in the world since previous pandemics - the last was in 1968 - and so much is unknown about why flu behaves the way it does that it is impossible to predict the course of this pandemic based on previous ones.
"I think what this article recognizes is that this is very, very complex," Dowdle said from Atlanta. "And in fact our understanding of the factors is so incomplete and so insufficient that I think we have to be very careful about coming up with any simple theories to explain any flu behaviour."
One of Dowdle's former CDC colleagues, Dr. D.A. Henderson, thinks there is a model for the current pandemic, but it's not 1918.
Henderson, an infectious diseases expert at the Center for Biosecurity at the University of Pittsburgh Medical Center, recently published a review article suggesting if authorities are trying to figure out how to gauge public health responses to the swine flu pandemic they should look to the lessons of the 1957 Asian flu.
"I think that what we've seen in '57 and what we see now are very similar," he said in an interview.
"And I think they (Taubenberger and Morens) feel the same way I do that we have really no evidence that this (virus) is likely to become more virulent ... or more infectious."
But another researcher who has spent a lot of time mining records from 1918 believes there is good evidence the 1918 virus was responsible for the outbreaks of the herald wave.
Dr. Lone Simonsen, an influenza epidemiologist at George Washington University in Washington, D.C., has studied medical data for a number of centres that reported outbreaks in the spring of 1918 - New York and Denmark among them.
"There's always this discussion about 'If you don't have a virus, can you say anything about something?"' she said.
Simonsen argued the answer is yes, if the pattern of disease bears the signature of flu pandemic - things like a shift in the age group in which severe disease is seen. That was observed in the spring of 1918 and in the spring of 2009 as well, she noted.
"Absolutely there was a first wave that was milder. There's no doubt about it," she said.
Simonsen said accepting that there was a herald wave of illness doesn't mean that the change in severity in the fall has to have been the result of viral mutations. There could be other explanations, she said, including concurrent spread of bacterial illness that combined to make the flu cases more dangerous.
As to the path of the current pandemic, Simonsen suggested the best approach is a prudent one.
"I just think we should keep our guards up. That's really my prediction."
That is a point on which Taubenberger and Simonsen agree.
"It's worth going through all of the effort to plan for a serious recurrence and to make vaccine and try to distribute vaccine as soon as possible," he said.
"But we don't know what's going to happen."
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