Tracking the Next Killer Flu
(National Geographic - Oct. 2005)
By Tim Appenzeller
In Southeast Asia a virus that kills chickens
is now also killing people. The race is on to
keep the bird flu from ravaging the world.
Little Ngoan was buried behind her parents'
hut three weeks ago. Her grave, a bulky
concrete tomb like others dotting the
Vietnamese countryside, rests on high
ground between a fishpond and yellow-
green rice fields. At one end her family laid
out her cherished possessions: a doll's chair,
a collection of shells, plastic sandals. They
painted her tomb powder blue.
While Ngoan's parents are off helping with
the rice harvest, other relatives share their
memories. "She was so small, just 10," says
her grandmother, sitting on a hammock.
"She was very gentle and a good student.
If you look at her older sister"—the 17-year-
old hangs back shyly—"you can imagine
what she was like." Ngoan's grandfather,
silent with grief, lights a stick of incense
at her grave.
The loss of a beloved child has hit this
family hard. But ordinarily, the wider world
would pay little attention to a child's death
from infectious disease in this remote
corner of Vietnam's Mekong Delta. Old
scourges like dengue fever and typhoid
still take a toll here, & HIV/AIDS is on the rise.
Yet Ngoan's death & more than 50 others
in Southeast Asia over the past two years
have raised alarms worldwide. Affected
countries are struggling to take action;
other nations are sending aid & advisers
while stockpiling drugs and developing
vaccines at home. And scientists have
stepped up their research into the fateful
traffic of disease between animals and
people.
Why? Because Ngoan died of the flu.
To most of us, flu is a nuisance disease,
an annual hassle endured along with taxes
and dentists. Some people think a flu shot
isn't worth the bother. But flu is easy to
underestimate. The virus spreads so easily
via tiny droplets that 30 million to 60 million
Americans catch it each year. Some 36,000
die, mostly the elderly. It mutates so fast that
no one ever becomes fully immune, and a
new vaccine has to be made each year.
That's ordinary flu. But the disease that is
taking lives in Southeast Asia is no ordinary
flu. Its primary victims have been chickens,
more than a hundred million of them, killed
either by the virus or in often futile control
efforts. It's not unusual for chickens to get flu;
in fact, avian-flu viruses far outnumber human
ones. But Robert Webster of St. Jude
Children's Research Hospital in Memphis
has studied flu viruses for 40 years and has
never seen the likes of the one that killed Ngoan.
"This virus right from scratch is probably the
worst influenza virus, in terms of being highly
pathogenic, that I've ever seen or worked with,"
Webster says. Not only is it frighteningly lethal
to chickens, which can die within hours of
exposure, swollen and hemorrhaging, but it
kills mammals from lab mice to tigers with
similar efficiency. Here and there people
have come down with it too, catching it from
infected poultry like the chickens that died
on Ngoan's farm a few days before she fell ill.
Half the known cases have died.
In those deaths many public health experts
hear the distant rumblings of a catastrophe.
So far this virus—classified as H5N1 for two
proteins that stud its surface like spikes on
a mace—isn't good at passing from birds
to people, let alone from one person to the
next. "It can make that first step across, but
then it doesn't spread easily from human to
human," says Webster. "Thank God. Or else
we'd be in big trouble."
Maybe H5N1 will never learn the trick of
racing from person to person like the milder
flus that empty offices and classrooms each
year. Maybe it simply can't. Or maybe efforts
to eradicate the virus—largely fitful and under-
funded so far—will succeed. But experts are
urging the world to prepare for the worst.
What is known about flu viruses' remarkable
capacity to change and jump species has
led to a sense of inevitability, a conviction
that even if this menacing animal flu doesn't
explode into a global pandemic that kills
millions, another one will. "It's going to happen,
at some point, that a virus like this changes
to be able to transmit from one person to
another," says Jeremy Farrar, an Oxford
University doctor who works on the front
lines of avian flu at the Hospital for Tropical
Diseases in Vietnam's Ho Chi Minh City.
"It's bound to happen. And when it does,
the world is going to face a truly horrible
pandemic."
After all, it has happened before.
In 1918, the final year of the savage trench
fighting of World War I, something else
began felling the soldiers. No one knows
for sure when or where the Spanish flu
emerged, though it certainly wasn't in Spain.
As a neutral country, Spain had no wartime
censor****p, and the flu apparently got its
false pedigree from news re****ts about
outbreaks there in May 1918. In fact the
disease was already spreading on both
sides of the European front, laying low
entire divisions through the spring and
early summer. Then it seemed to subside.
In late summer, though, the Spanish flu
returned, and this time its virulence was
unmistakable. The sick took to their beds
with fever, piercing headache, and joint
pain. Many were young adults, exactly the
group that normally shrugs off the flu.
About 5 percent of the victims died, some
in just two or three days, their faces turning
a ghastly purple as they essentially suffo-
cated to death. Doctors who opened the
chests of the dead were horrified: The lungs,
normally light and elastic, were as heavy as
waterlogged sponges, clogged with bloody fluid.
After fla****ng through crowded military
camps and troop****ps in Europe and the
United States, the flu leaped out of uniform
to ****ts and industrial cities. In Philadelphia,
historian Alfred Crosby found, 12,000 people
died of flu and pneumonia in October—759
in a single day. Schools and businesses
were shut down & church services cancelled.
Morgues overflowed.
By then the sickness had spread to the far
corners of the planet, from the South Pacific
to the Arctic. "Everybody on Earth breathed
in the virus, and half of them got sick," says
Jeffery Taubenberger of the Armed Forces
Institute of Pathology in Maryland, who is
trying to learn what made it such a killer.
More than 50 million people died—at least
three times as many as in the war. The best
medical minds of the day could hardly
believe that this was flu.
It was flu all right, but with a crucial difference
that scientists are only beginning to understand.
Scattered across Taubenberger's desk are
translucent wax blocks the size of matchboxes.
Borrowed from a pathology archive, they hold
fingernail-size scraps of purplish tissue, sliced
from the lungs of flu victims in U.S. military
hospitals almost 90 years ago. In the mid-
1990s Taubenberger and his colleagues
realized that a sample from someone who
died quickly, lungs still seething with virus,
might still hold genetic traces of the killer.
They were right: In 1996 lung tissue from a
soldier who died in September 1918 at
Fort Jackson, South Carolina, yielded
pieces of the virus's genes.
The pickings soon got better. Inspired by
Taubenberger's discovery, a retired path-
ologist named Johan Hultin traveled to a
remote Alaska village and excavated a
mass grave that had been hacked into the
permafrost after the Spanish flu swept
through in November 1918. One female
body still contained intact lung tissue,
preserved by the cold and sheer luck.
Bit by bit, Taubenberger's group teased
out the entire genetic sequence of the virus.
They plan to finish publi****ng it this year.
So far this genetic blueprint hasn't revealed
exactly what made the Spanish flu so deadly.
No single gene or protein is the obvious
culprit. But comparing the 1918 sequence
to those of the flu viruses that wreak mild
havoc each winter has confirmed what was
long suspected: The Spanish flu virus had
recently crossed into people from some
unknown animal, leaving victims with little
immunity to this new threat.
One reason you generally get over the flu
after a few days' discomfort is that your
immune system has seen it before and
knows how to respond. This year's bug
won't be a carbon copy of last year's,
because the virus mutates constantly. But
it will look similar enough that your body
can almost always keep it in check.
Every so often, though, something new
comes along from the animal world—a
vast preserve of type A flu viruses, the
ones that cause the most serious illness
in humans. In far-flung studies in the late
1960s and 1970s, from Australia's Great
Barrier Reef to lakes in northern Canada,
Robert Webster and his colleagues tracked
flu to its source. "Where do flu viruses come
from?" he asks. "From the wild birds of the
world, the wild aquatic birds—the waterfowl,
the ducks, the shorebirds."
Dozens of flu subtypes inhabit the birds'
guts, mostly harmless to their hosts or to
any other creature. But occasionally one
infects domestic poultry. Even more rarely,
a bird virus or some of its genes slip into
the much smaller pool of type A viruses
that infect humans.
Normally a flu virus good at infecting birds
can't attack humans because it isn't
equipped to invade and grow in human
cells. Until recently scientists thought avian
viruses could gain that ability only by
indulging in the viral equivalent of ***.
Because flu viruses carry their genetic
information on eight separate RNA seg-
ments, it's easy for different subtypes to
swap genes if they happen to meet. The
result: offspring with new abilities.
For an avian flu and a human flu to mix it
up, they have to infect the same animal.
Scientists have long considered the pig
a likely mixing vessel, because pig cells
have surface molecules that allow entry to
both kinds of virus. A pig could conceivably
catch a human flu from a farmer and a bird
virus from, say, ducks at the same farm.
The two viruses could then "reassort,"
creating a hybrid that—in the worst case—
would now be able to infect human cells
while still carrying bird-virus genes that
would make it radically new to the immune
system of the people who catch it, and
unusually virulent.
Reassortment explains the two lesser flu
pandemics of the 20th century, in 1957
and 1968. In each year a new flu subtype
appeared, combining genes from the
human virus that had been causing mild
outbreaks in prior years with new genes
from a bird virus. The new pandemic
viruses raced around the world, together
killing about two million people.
But in 1918, Taubenberger now believes
something different happened. "We think
it's pretty likely that the virus was not derived
from a previously circulating human virus,"
he says. All of its genes mark it as an
animal virus, pure and simple, that some-
how crossed to people without the help
of genes from a previous human strain.
Now H5N1 is doing the same thing. So far,
its steps across the species barrier are
tentative, which is why it has caused tens
of deaths, not millions. But as in 1918,
doctors who have seen its effects close
up are shaken.
The x-rays tell the story as Tran Tinh Hien,
a doctor at the Hospital for Tropical
Diseases in Ho Chi Minh City, clips them
to a light box. In the first image, made the
day the 18-year-old girl was admitted with
bird flu, a whitish cloud appears at the base
of her rib cage. Her lungs were partly filled
with fluid. In a second film, four days later,
the haze has spread throughout her chest.
"All the lung tissue was destroyed," Hien
says. "The process still happened when
we treated." A week later the girl was dead.
So it went for Hien and his staff throughout
January, when the latest bird-flu outbreak
reached its peak in southern Vietnam.
They cleared a 50-bed ward normally
reserved for malaria and dengue fever
and turned it into an isolation unit.
They sustained patients with oxygen masks
and ventilators and treated them with
oseltamivir, or Tamiflu, an expensive
antiviral drug that can fight H5N1. Nurses
worked 24-hour ****fts, gowned, masked,
and goggled for protection against the virus.
As Hien says: "We were pushed to the wall."
He and his staff did everything they could
for their nine bird-flu patients. "Unfortunately,"
he says, "we could not save any lives."
As an elite facility, the Hospital for Tropical
Diseases saw the bleakest face of the
disease. Only the sickest patients were
sent there, and by then they may have been
beyond help. In fact H5N1 doesn't always kill.
Some infections may even be so mild that
they go unnoticed. But every hospital that
has treated people seriously ill with avian
flu has recorded shocking death rates.
It has been that way since 1997, when an
H5N1 virus strain—a cousin of the one now
plaguing Asia—first jumped to humans.
Early that year an outbreak of the virus killed
chickens in Hong Kong's rural New Territories.
At that point, no one thought bird viruses
threatened people directly. But this one
broke the rules.
In May 1997 a three-year-old boy was
admitted to a Hong Kong hospital with a
cough and fever. His symptoms worsened
rapidly and he had trouble breathing. He
was given a flood of antibiotics and put on
a ventilator, but within six days he was dead.
Flu experts were astonished when secretions
from the boy's windpipe yielded an H5N1
virus. It turned out to be the same one that
had killed the chickens.
Still, his death looked like it might be a fluke
until late in the year, when another 17 people
checked into hospitals around Hong Kong
with similar symptoms, and tests confirmed
infection with H5N1. Five died. Many of the
victims had visited one of the island's live-
poultry markets.
Public health experts converged on Hong
Kong, fearing that a 1918-style pandemic
was about to explode. They persuaded the
Hong Kong government to kill every last bird—
1.5 million of them—in the farms and markets.
The mass slaughter worked. That particular
H5N1 virus was never seen again, and a
public health disaster had been averted.
But in 2001 another deadly strain of H5N1
cropped up in Hong Kong's markets, and
the city again began killing poultry. This time
the respite was shorter, and by the beginning
of 2002 chickens were again dying of flu. The
fact was, the drastic measures in Hong Kong
had left the source of all these viruses
untouched. They were coming from outside
Hong Kong—just across the territorial border
in southern China.
China's Guangdong Province teems with
hundreds of millions of chickens, ducks, and
geese, many wandering freely through gardens,
farms, and ponds. Flu viruses that rain into this
sea of poultry in wild-bird droppings can spread
and swap genes with abandon. The result: new
strains not found in the wild. Among them was
the H5N1 virus that gave rise to the bird flu
now plaguing Asia.
Year after year it swapped genes with other
avian-flu viruses, generating a plethora of new
H5N1 variants. Year after year they besieged
Hong Kong, which im****ts poultry from the
mainland. By the end of 2003, they were
infecting and killing birds across half of Asia.
Radiating from China, H5N1 strains reached
South Korea and Japan in the north; they
swept through Southeast Asia as far as
Indonesia. Some experts and officials have
suggested that the viruses traveled in the guts
of wild waterbirds—geese, ducks, herons—
which might have picked up the infection from
farms. Governments embarrassed by their
failure to halt the flu's spread welcome that
idea. "They get a free lunch," says Yi Guan,
a virologist at the University of Hong Kong.
"Each time there's an outbreak, they say, 'It's
migratory birds. I cannot control them. I cannot
lock my sky!'"
This summer the virus killed thousands of wild
geese and gulls at a nature reserve in western
China. It was the largest known outbreak in wild
birds and a warning that in the future they might
spread the disease far and wide. But Guan isn't
ready to blame migratory birds for the spread
so far. He thinks the virus has killed infected
birds too quickly for them to fly long distances.
Instead H5N1 probably hitchhiked across
Asia in ****pments of live poultry, in a disaster
of our own making.
As it advanced, the virus began killing people
again—by August the count stood at 40 in
Vietnam, 12 in Thailand, 4 in Cambodia, and
at least 1 in Indonesia. And it inflicted economic
losses that, by one estimate, amounted to
more than ten billion dollars in 2004 alone.
Ex****ts from Thailand's industrial chicken
farms collapsed when the world learned of
the outbreak there. In areas of Indonesia hit
hard by the virus, more than 20 percent of
the workers on commercial poultry operations
lost their jobs.
Small farmers are suffering too. As one
animal health official in Vietnam explains,
"The birds are big treasures for the farmers."
They scavenge for themselves, costing next
to nothing to raise and putting good meat on
the table. Vietnamese farmers lost some 40
million of these treasures in 2004, dead of flu
or killed in control efforts. Even farms
untouched by the disease were hit as fearful
shoppers began avoiding poultry.
It may take a long time for Vietnam to
regain its taste for chicken. At a riverside
restaurant in the southern city of Can Tho,
six veterinary officials—men responsible
for keeping the district's poultry healthy—
order prawns and a fish stew for lunch.
They admit it: Not one of them will touch
chicken these days.
H5N1 is all the more frightening because
so much is unknown, starting with how it
kills people. In a chicken, the virus spreads
everywhere—gut, lungs, brain, muscle. In
humans, like the 1918 flu, it devastates
the lungs first and foremost.
Researchers at the Univ. of Hong Kong
have found that a victim's own immune
system may be part of the problem. It
reacts to the virus with a flood of chemical
messengers that draw white blood cells
into the lungs, where they trigger a massive
inflammatory reaction. "It's kind of like
inviting in trucks full of dynamite," says
Malik Peiris, who led the work. Healthy
tissue dies and blood vessels leak, filling
the lungs with fluid.
But H5N1 may have more than one way
to kill. This year researchers in Ho Chi Minh
City, including Jeremy Farrar, detected
H5N1 in a little boy who died in a coma,
his brain inflamed but his lungs healthy
until the very end. To Farrar it suggests
that the virus can spread throughout the
body. Others aren't sure.
It's one more bird-flu mystery.
Ask Keiji Fukuda and Tim Uyeki, flu
epidemiologists at the CDC in Atlanta,
what they would most like to know about
the disease, and the questions come
tumbling out. "How many people are
infected? How many animals are infected?"
Asks Fukuda. Since 2004 only four countries
have re****ted human illnesses. "Have there
been no others?" Uyeki asks. "It's pretty
likely there have been, but we have no
information about that."
Then there's the mystery of exactly how
people get infected. "Right now we
believe that most cases are related to
people somehow being exposed to sick
or dying or dead poultry," says Fukuda.
"Well, what does that mean?" He asks,
ticking off possibilities. Does that mean
people touched it? Did they eat it? Did
they breathe in dust containing chicken
feces? He's frustrated at the often sketchy
re****ts from Asia. "What is really going on?"
He asks. "This has very practical implications"
for fighting the disease.
The biggest question is whether the virus
will start spreading like ordinary human flu.
"Human to human—that's the one that we
don't want to see," says Robert Webster.
But already, H5N1 has given experts a
few scares.
Nguyen Thanh Hung, a cement trader in
Hanoi, says he feels well these days. He
works, tends a small forest of potted plants,
and spends hours a day jogging & doing
breathing exercises. In his living room one
day in February he shows off his hospital
discharge papers as if they were his new
lease on life. It's been just a month since
Hung got over a serious bout of avian flu.
"The doctor told me if I had been taken to
the hospital one or two days later—no way,"
he says. His older brother, also infected,
was not so lucky.
If Hung's survival is remarkable, so is the
way he seems to have caught the disease.
On a visit to their home village outside
Hanoi he and his brother had shared a
pudding made of raw duck blood, a
Vietnamese delicacy. The duck must
have been infected with H5N1, because
Hung's brother came down with the flu a
few days later. But Hung did not get sick
for more than two weeks—not until the day
after his brother died.
That's too late for the pudding to be the
cause, Tim Uyeki believes. Hung probably
got infected while caring for his brother in
his final days.
H5N1 is also thought to have jumped
from a girl dying of avian flu in Thailand
to her mother and aunt, who nursed her.
Several other cases of human-to-human
transmission are suspected. But one step
beyond the initial victim is all the virus
seems to have managed. So far, sustained
transmission—the chain-reaction spread
of ordinary flu—is not in its repertoire.
It might gain that ability on its own, by mutating.
Or it might swap genes with a human-flu virus.
That could take place in an infected person
who also catches ordinary flu, or in the classic
flu mixing vessel, the pig. Still, no one knows
whether the exchange would yield a nightmare
virus or a dud.
Flu researchers at the CDC and in the
Netherlands hope to find out in advance,
by artificially breeding new viruses. In high-
containment labs they are deliberately mixing
and matching genes from H5N1 and human-
flu viruses. Then they will test the hybrids to
see whether any have inherited both the bird
virus's virulence and the human virus's ability
to spread. In effect, they are trying to create
a pandemic flu strain in the lab.
Some critics think that's reckless, but Erich
Hoffmann, a St. Jude researcher who helped
develop a genetic engineering technique for
flu, says the experiments are key to learning
what we may eventually face. "It's basically
the best simulation one could have in the lab
of what possibly could happen in nature."
If we're lucky, he says, all the hybrid viruses
will be harmless or won't thrive, suggesting
that H5N1 may never spawn a pandemic.
"That of course would be good news," says
Hoffmann. And if the news is less reassuring?
Then scientists monitoring H5N1 in Asia
would have a clue about what to watch for—
what genetic changes in the virus might
signal big trouble ahead.
That knowledge might buy some warning
time, but no one wants to sit and wait for
H5N1 to make its move. And everyone
agrees on the best way to head it off:
Eradicate H5N1 in poultry, so people can't
catch it. It's simple—but not easy.
Howard Wong, a senior veterinary officer
in Hong Kong, knows what it takes. Since
2003, after multiple outbreaks and two
wholesale poultry slaughters, the territory
has kept its farms and markets free of
H5N1. Wong is proud of his success.
"We were very happy in 2004, when it
was everywhere else, and we managed
to hold it back."
Here are some steps Wong and other
officials took: vaccinating every chicken
in Hong Kong against H5N1; regularly
testing chickens, pet birds, even wild birds;
shutting down the hundreds of live-poultry
stalls twice a month to disinfect them; and
inspecting farms and markets obsessively.
"We're almost at the limit of what we can
do," says Wong. "It's like holding up this
wall, & this wall just gets heavier all the time."
And as one aid official in Vietnam puts it,
Hong Kong is rich, and an island. Vietnam
is neither. In the winter of 2003-04, H5N1
broke out in most of the country's 64
provinces. To fight it, the country slaughtered
tens of millions of chickens. The epidemic
seemed to decline, and in March the
government declared victory.
But in late 2004 avian flu roared back,
infecting birds and people along the
length of the country. Cooler weather,
which favors the survival and spread of
the virus, had apparently brought it out
of hiding. By February of this year Anton
Rychener, the representative of the United
Nations Food and Agriculture Organization
(FAO) in Hanoi, was beside himself. "Why
the hell are we sitting here a year later with
literally the same pattern of outbreak?" he
asked a roomful of officials. A year of
meetings and emergency initiatives had
done little to change the conditions that
made Vietnam ripe for viral spread.
In the countryside, chickens peck in yards
and stalk through underbrush, mingling
with birds from other farms. Poultry markets
act as viral swap meets, and unsold birds
are taken back home with any viruses they
picked up. Farmers with sick birds have
little incentive to speak up and see their
flocks destroyed: The government can
afford to pay less than half of a bird's market
value as compensation. And then there are
the ducks.
The duck, says Webster, is "the Trojan
horse of this outbreak." His group has
found that unlike chickens, infected ducks
often seem healthy, able to waddle, swim—
and spread the virus in their droppings. In
Vietnam and other parts of Southeast
Asia, they spread it far and wide because
duck herders drive their flocks from one
rice field to the next, following the harvest,
so the birds can fatten on leftover grains.
Inefficiency, tradition, and scarce funds
have all slowed Vietnam's efforts to
change such practices. And although
officials gamely declare that they are
making progress, last year's confidence
has faded. When asked whether he
expects his district to be hit by bird flu
again next year, a veterinary officer in
Can Tho says, "It's not my expectation,
but I think it will happen."
Thailand has made more headway.
Wealthier and more developed than
Vietnam, it reimburses farmers more
generously when birds are slaughtered.
It tests ducks for H5N1 and allows only
virus-free flocks to move around the
countryside. And it has enlisted nearly
a million village volunteers to watch for
unusual chicken die-offs. By early this
year it had driven the virus back into just
a handful of provinces.
Even so, Wantanee Kalpravidh, the
FAO's regional coordinator for avian
influenza in Southeast Asia, says the
country cannot rest easy. It has long
borders with Laos and Cambodia,
destitute lands struggling with their
own avian-flu outbreaks. Thailand's
efforts could quickly be undone if a
crate or two of infected poultry slipped
in. As Kalpravidh points out, "Birds
need no visa or pass****t."
Nor do viruses. Suppose H5N1 lives
up to the fears and picks up a new talent
for contagion. Somewhere, probably
deep in the countryside, a pandemic
spark would ignite. A person sick with
bird flu would infect his family, who would
pass the disease to friends and neighbors.
Exponential spread might follow.
Computer simulations suggest that public
health officials just might be able to douse
the spark by flooding the region with anti-
viral drugs, treating the 100s of thousands
of people who are at highest risk for
infection. But the strategy could succeed
only if the outbreak were detected within a
few weeks and the virus spread slowly at
first. And the infrastructure and skills
required are lacking in much of Asia.
If containment failed, in a few more weeks
the newborn pandemic would hit major cities.
There it would infect people with pass****ts
and plane tickets. The rest of the world
would be hours away.
Richer countries are scrambling to prepare.
Because Tamiflu can protect against H5N1
as well as treat it, governments are building
up stockpiles, and drugmaker Roche is hard-
pressed to keep up with demand. The U.K.
has ordered enough for 15 million people,
a quarter of its population, and France
almost as much. The U.S. has opted for a
smaller stockpile—just 2.3 million treatments
so far. It is also pinning its hopes on a vaccine.
Ordinary flu vaccines contain flu virus, grown
in fertilized chicken eggs, then killed and
split into pieces. But because it's so deadly,
H5N1 requires expensive safety measures
and tends to kill the eggs needed to grow it.
So Webster's group turned to genetic
engineering, altering one gene to tame the
virus and splicing in others to speed its
growth. By August human tests of a vaccine
made from the altered virus showed early
signs of success. The U.S. government
has already ordered two million doses.
Two million doses would be scant protection
for a country of nearly 300 million. But
officials hope the vaccine formula will be
fully tested and ready before it is ever
needed. Makers would know how to
produce it and could boost production fast,
says Anthony S. Fauci, director of the
National Institute of Allergy and Infectious
Diseases. At the first sign of a pandemic,
"We'll be able to say: Go, take off the brakes
and make millions and millions of doses."
But again comes the refrain, no one knows.
No one knows whether an H5N1 pandemic
strain—if it ever emerges—will be similar
enough to the virus now stalking Asia for
this vaccine to offer full protection. No one
can even be sure H5N1 is the right threat
to focus on. Several other bird-flu viruses
have recently shown signs of infecting
humans, though none has proved as deadly
as H5N1.
Here is what we know for sure. One day a
new flu pandemic will come, and one day
it will pass. And then the killer strain, tamed
by our immune systems and the passage
of time, will fade into the background of
nuisance flus.
It even happened to the worst of them all.
Did you catch the flu last winter? There's
a chance it was a direct descendant of the
Spanish flu. If so, you were lucky. The heir
to 1918 is one of the milder flu strains
around today.
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"Endeavor to persevere"
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