Published Date: 2009-08-13 03:00:07
Subject: PRO> Influenza pandemic (H1N1) 2009 (30): assumptions
Archive Number: 20090813.2879
INFLUENZA PANDEMIC (H1N1) 2009 (30): ASSUMPTIONS
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A ProMED-mail post
<http://www.promedmail.org>
ProMED-mail is a program of the
International Society for Infectious Diseases
<http://www.isid.org>
Date: Tue 11 Aug 2009
Source: News 1130, the Canadian Press [edited]
<http://www.news1130.com/news/national/more.jsp?content=n115289529>
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 ratcheted up in
virulence in a fall wave, because there is no solid proof outbreaks of
illness in the US 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, Maryland, where he and Morens work at the US 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 were 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 US 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 US 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 DC, 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 1st 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."
[byline: Helen Branswell]
--
communicated by:
ProMED-mail rapporteur Mary Marshall
[The article referred to above in the Journal of the American Medical
Association (JAMA) is entitled "Understanding influenza backward", by DM
Morens, JK Taubenberger. The reference is: JAMA 2009; 302(6): 679-80.
(<http://jama.ama-assn.org/cgi/content/extract/302/6/679 >). The 1st
paragraph reads:
"The novel pandemic influenza A(H1N1) 2009 virus has been an unexpected
trigger for pandemic preparedness plans in the United States and elsewhere.
It is appropriate to ask how the novel virus might behave epidemiologically
in coming months, including the possibility of multiple recurrences or
"waves." Spring circulation of the novel virus in the Northern Hemisphere
at the end of the 2008-2009 influenza season inevitably has led to
comparisons with events in 1918-1919, which in some settings were preceded
and followed by outbreaks of respiratory illnesses. Some also believe that
the 1918 pandemic began with a premonitory "herald wave," a term related to
an old hypothesis, which influenza and dengue fever appeared to have
supported, that as new viruses begin to circulate in human populations,
they inevitably acquire mutations that increase transmissibility and
virulence."
The full text should be compulsory reading for all crystal gazers (and
others). - Mod.CP]