the impact of Tamilflu.
Age of Flu Victims Has Big Implications
Scientists Say Relative Youth of Ill People Is Evidence of Pandemic
Potential
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By David Brown
Washington Post Staff Writer
Sunday, May 17, 2009
The swine-origin influenza A (H1N1) virus that burst into public
consciousness a month ago is starting to behave like a mixture of its
infamous, pandemic-causing predecessors.
It seems to have a predilection for young adults, as did its notorious
ancestor, the 1918 Spanish influenza. Many of the young victims who
have become deathly ill turned out to have other medical problems -- a
phenomenon first clearly seen with the1957 Asian flu. H 1N1 is
spreading easily in North America but sputtering in Europe, just as
Hong Kong flu did in 1968. And as in the mini-pandemic of Russian flu
in 1977, some people appear to have a degree of immunity.
Exactly how swine flu fits into the pantheon of flu pandemics will not
be known for a while. It will take months -- and many more victims --
for its full personality and behavior to emerge. But one thing is
clear: This is a lot more than just seasonal flu out of season.
After a brief moment when news of the outbreak in Mexico made swine
flu look like a horseman of the apocalypse, public health officials
have spent much effort reassuring people that most of the time, the
virus causes a mild illness that can be ridden out at home. Yet,
officials at the World Health Organization, the Centers for Disease
Control and Prevention and elsewhere do not want the public to get
blase.
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Pandemic flu strains -- and this new H1N1 strain is all but certain to
cause the 21st century's first pandemic -- are unpredictable. Any
contagious disease that most of the world's 6.8 billion people can
catch is inherently dangerous.
"Our message to everybody is, of course, do not over-worry about these
things, [but] it is important to know it is serious," the WHO's Keiji
Fukuda said last week.
Perhaps the most worrisome features so far are the number and severity
of cases in teenagers and young adults. This was noticed early, and
the pattern has not changed much now that there are 5,000 laboratory-
confirmed infections and probably more than 100,000 overall. The
average age of the confirmed and probable cases is 15 years. Two-
thirds are younger than 18.
There are two theories for what is happening.
One is that students visiting Mexico on spring break were the chief
"vectors" bringing the virus to the United States, where they then
infected schoolmates and friends. The other is that young people are
especially vulnerable for some reason.
"As we get farther and farther in, are we going to be able to choose
between these two hypotheses? Sure we are," Joseph Bresee, the CDC's
chief flu epidemiologist, said late last week. But, he added, it may
take two or three months.
Determining the true age distribution is crucial, as it will help set
the policy for who should be first in line for vaccines and how to
ration antiviral drugs if they are in short supply. "It really does
have big implications," Bresee said.
A closely related question is whether the illness tends to be more
serious in younger age groups as well as more common.
In the United States, the familiar seasonal influenza causes about
8,100 deaths a year directly and contributes to about 36,000 more in
people with lung or heart problems. Ninety percent of those deaths
occur in people 65 and older. The risk of a healthy person older than
65 dying directly from flu is about 100 times that of a healthy person
5 to 49 years old.
Compared with seasonal outbreaks, all flu pandemics cause a higher
percentage of severe cases and deaths in younger groups. Although the
overall mortality rate from the current swine flu is low, this trend
is already apparent.
Last Thursday, when Fukuda announced that the global death total was
65, he noted that "half of them are healthy people who have no
predisposing conditions. This is a pattern different from what we see
with normal influenza."
There have been too few deaths in the United States to draw any
conclusions. But of the 173 people who have been sick enough to be
hospitalized, more than half are in the 5-to-24 age group.
In the 1918 pandemic, which killed at least 50 million people, nearly
half the deaths were of people 20 to 40 years old. More than 95
percent were of people younger than 65. In comparison, 36 percent of
the deaths in the 1957 pandemic were of people younger than 65, and 48
percent in the 1968 pandemic.
The 1918 pattern has led many experts to speculate that older people
may have had immunity from a "Spanish-like" virus that circulated in
their youth, sometime before about 1885. Something similar may be
happening this time.
The H1 and N1 in the name of the new strain refer to proteins on the
virus's surface. The human immune system "sees" them and tailor-makes
antibodies to attack the bug. Flu vaccines work by priming the immune
system with harmless versions of the same H and N proteins.
A variety of H1N1 strains circulated from 1918 to 1957, then
disappeared for two decades. In 1977, however, an H1N1 strain surfaced
that was nearly identical to the previous one, so much so that
scientists suspect it was an accidental release from a lab freezer. It
caused a pandemic -- Russian flu -- that was largely limited to people
younger than 25, whose immune systems had never experienced H1N1.
Strains of H1N1 have continuously circulated since then. While the new
one is very different -- the H and N proteins are from pig, not human,
viruses -- decades of exposure to H1N1s may be providing older people
with some protection. Some young people may have had essentially no
exposure.
"My first speculation is that this younger population has somehow
missed contact with H1N1 or with vaccine," said Edwin D. Kilbourne, an
emeritus professor at New York Medical College and, at 88, flu
virology's elder statesman in the United States.
Differences in background immunity may also exist across geographical
areas. This is the reason for the big difference in North America's
and Europe's experience with the 1968 Hong Kong flu, a pandemic that
spanned two winters.
In the United States, nearly three-quarters of all deaths that were
ultimately attributed to that flu came in the first winter
(1968-1969). In England and France, more than three-quarters were in
the second winter (1969-1970).
In that virus, one old surface protein, the H, was switched out for a
new one in a process called reassortment. The strain went from H2N2 to
H3N2. Epidemiologists now believe that Europeans had had more recent
and intense exposure to H2N2 viruses than North Americans.
Consequently, Europeans had developed antibodies and were partially
protected when the "half-new" H3N2 strain arrived.
By the second winter, however, the N2 part of the virus had also
changed somewhat through mutations and was no longer very recognizable
to the immune system. The antibodies that had protected a lot of
Europeans the previous winter no longer worked against this "drifted"
strain of H3N2. Cases of flu -- and deaths -- went way up.
Whether a similar difference in continent-wide susceptibility explains
why swine flu is spreading in the United States but standing still in
Europe will take a while to figure out.
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