04x02 - k*ller Flu

[bunniefuu]

Tonight on Secrets of the Dead:

1918... a deadly flu strain
circles the globe.

She sat down on the curb,
she spurted blood,

and she died the next day.

30 million victims
are left in its wake.

Once that virus got into humans,

there was nothing
that could stop it.

Experts warn a similar pandemic
could strike again.

There could be ten,
15 million people dying.

The race is on to crack
the genetic code of the virus.

Can they stop
the next "k*ller Flu"?

Secrets of the Dead.

Captioning sponsored
by THIRTEEN/WNET NEW YORK

Secrets of the Dead
was made possible

by contributions
to your PBS station from:

I make sure I get it

and that everybody I know
is urged to get it.

It's important.

Well, I get it
every year, you know.

No, no flu shot...
I don't believe in that.

The flu shot, I don't get it.

This year I don't get it.

Why not?

Eh... lazy.

Most years, we see the flu

as a mild inconvenience,
a winter rite of passage.

Now we check in

with that least favorite of
holiday traditions: flu season.

It can start with a sniffle.

Health officials recommend
washing your hands frequently

and keeping your hands away
from your nose, eyes and mouth.

We tend not to consider it
a real threat...

until, seemingly overnight,
it becomes one.

Flu season is off
to an early start.

According to the
Centers for Disease Control,

already more than
20 children nationwide

have died of influenza.

It's just a little pinch.

The dominant strain
of this year's virus

is not specifically covered
by this year's vaccine.

Well, later this hour
we'll check...

Influenza kills nearly
40,000 Americans each year

and ranks among
the world's deadliest viruses.

It is also one
of the least understood.

A little virus so fragile

you can destroy it
with washing-up fluid.

30,000 of them
sit on a pin's head,

and yet it's got eight genes.

And yet it can get up your nose,
get into your throat,

go down your lung,
get you into bed, and k*ll you.

Structurally
it's a simple organism...

A strand of eight genes.

But it can mutate endlessly

to circumvent our immune
system's attempts to stop it.

Every 30 years or so,

a mutation results in
the creation of a super-virus,

a pandemic strain
that renders vaccines powerless

and challenges our bodies beyond
their ability to protect us.

Three such strains have
cropped up in the past 50 years.

But no strain has ever been as
lethal as the pandemic of 1918.

That year influenza swept around
the world in three deadly waves.

It began like ordinary flu,
with aches and pains,

but it ended horribly,

its victims drowning
in their own body fluids,

their faces marked
by a strange blue cast.

It was the worst pandemic
in the world's history,

even more lethal
than the Black Death.

Through four years of battle,

World w*r I had k*lled
8½ million soldiers.

In a matter of months, the flu
claimed many millions more.

It could be 40 million,

it could be 50 million,
it could be 60 million.

People think of viruses,
they think, "Ah, HIV...

"that's an important virus,
you know.

"That's spreading
around the world.

That's k*lled
20 million people."

But I can tell you that if we
had another influenza pandemic...

And we will have another
influenza pandemic...

It will make the HIV outbreak
almost look like a picnic.

The next flu pandemic
is overdue,

and around the world,

scientists are locked
in a race against time

to answer two questions:

Where did the 1918
virus come from?

And why was it so deadly?

At an Armed Forces lab
in Washington, D.C.,

virologists are working

to crack the genetic code
of the 1918 virus

before a similar
virus strikes today.

If we can actually shed light

on why the 1918 virus
was so lethal

and we can understand
the genetic basis of that,

that information can be applied

to the emergence
of new influenza strains,

and so I think it's just
really crucial that we do that.

But what will we learn?

If a virus similar
to the 1918 flu emerged,

could we stop it?

The worry is that
because of mass transit now,

the ability of jumbo jets
to carry large numbers of people

from continent to continent
on a daily basis,

that you would find that
would such a virus emerge today,

it might spread much more
rapidly than it has in the past.

And so it's a rather
scary thought

that we may be worse off

in the ability to control
the spread of a pandemic today

than we were in 1918.

The origin of every other
20th-century flu pandemic

has been accounted for,
but 80 years later,

no one yet knows how or where
the 1918 strain got its start.

And as we look forward,

what we see is another
huge outbreak of influenza,

which could be bigger than 1918,

could have a greater
k*lling power than 1918.

I would be very surprised

if it were not within
the next five to ten years.

More than 80 years ago,

when the pandemic first hit,
there was no warning.

Europe had endured
four years of fighting

and fresh blood was
on its way to the front.

German troops were marching in
from the east.

And from the west
came the Americans.

The United States had finally
joined the Great w*r.

People were very happy.

They just felt Americans were
going to go and win the w*r

and come back home
and live happily ever after.

Of course, it didn't
happen that way.

Though no one knows for sure,

it's long been assumed
that this flu began in America.

On March 11, 1918,
at Camp Funston in Kansas,

100 soldiers mysteriously
fell ill during training.

They complained of headaches
and sore throats,

symptoms often attributed
to the common cold.

A week later, the camp hospital
reported 522 cases.

An American origin
is entirely credible.

A large number of the recruits
that were in military camps,

including Camp Funston,
were very raw individuals...

People that came
from a rural background

that had not been exposed
to urban diseases

and had not acquired
the level of immunity

as their urban counterparts.

Suddenly the young men
began to die.

That spring,
48 soldiers would succumb

to what camp doctors
termed pneumonia

but which was, in fact,
the first wave

of the worst influenza outbreak
the world had ever seen.

80,000 Americans crossed
the Atlantic in March

with nearly 120,000 more
to follow in April.

Was it coincidence that
when they arrived in Britain,

so did the flu?

The large-scale rise

in influenza incidence
in the British Isles

occurred when it was
clearly on the wane in America.

It was a three-day flu.

I had it.

I remember laying
on two kitchen chairs

not caring whether
I lived or died.

Now deemed
the "three-day fever,"

the flu spread around the world.

But it soon got a more exotic
if somewhat misleading name:

the Spanish flu.

In Spain, eight million were
sick, including the king.

In this neutral country,
there was no censorship.

News traveled fast.

This was a wartime situation

in which all of the presses
of the combatants

were heavily censored...
The British press included...

But the Spanish press was not.

And many of the stories

that were originating
during the first wave

were coming from Spain

of this catastrophic new disease

that was sudden in its onset and
that was very, very dangerous.

Just where the flu came from

was quickly lost
in the turmoil of w*r.

A German offensive had smashed
through the French lines.

As the Allies fought back,
influenza moved freely

between the Americans,
French and British.

On the British home front,

the flu was having
a crippling effect.

Phone networks broke down.

Transit all but came to a stop.

Munitions factories
were hard hit.

In Manchester, England,
the city's medical officer,

James Niven, was overwhelmed
by the outbreak.

He had rid the city
of tuberculosis,

cutting its death rate in half.

But faced with
this new infection,

he was suddenly bewildered.

"The epidemic
is increasing rapidly...

The worst I have seen
in my long experience."

There were some
who simply blamed the enemy.

There were a number of arguments

that this was somehow German
biological or chemical warfare

that had been imported into the
British Isles by German spies

and it had been unleashed
into the atmosphere.

This was seen as another aspect
of German barbarism

and yet another weapon
in the German arsenal.

But the Germans
were also suffering.

By June, the flu had reached
epidemic proportions

among their ranks.

In Britain,
the disease seemed to follow

the lines of the railways,
appearing first in the seaports,

going on to peak in London

and then spreading out to
neighboring cities and beyond.

Those in the country
were especially hard hit.

- "July the 19th, 1918...
- death of another Flint soldier.

"Sergeant Barratt, aged 28,
of Lake Villas, Gresford,

died of pneumonia
whilst on leave."

In rural Flintshire, England,

amateur historian Mary Moore has
charted the disease's progress.

Among the dead
were Mary's own family.

My mother's first husband died
just after they'd been married.

He was very strong physically.

He was cultured.

I don't think
he'd ever had an illness,

and yet he was the one
that developed the flu.

I think there was
a feeling of great frustration

that men who'd actually
survived the w*r

should then die of the flu.

It went like a scourge through
these rural areas around here.

There are cases of small boys

that were playing
football on Sunday

who were dead on Wednesday.

There are reports
of a brother dying today

and a sister dying on Thursday
and a child dying on Friday.

In Manchester, James Niven
was horrified and helpless.

"At one school I observed
the children falling ill.

"They simply dropped
on the desk like a plant

"whose roots have been poisoned,
the attack being quite sudden

and drowsiness
a prominent feature."

And then just when they seemed
to be at the breaking point,

the first influenza wave
fell back.

It was high summer.

Like a reaper, the disease
had circled the globe,

cut a swath through humanity
and retreated.

For the moment,
the w*r effort could resume,

and the k*lling on
the front lines could continue.

What no one could know was that
this was just the beginning,

that the w*r
would enable the flu

to return
in a far deadlier form.

There was a kind of symbiotic
relationship that developed

between the w*r
and the pandemic.

It certainly created a
epidemic-conducive environment.

After years of food shortages
and anxiety and strain

and shortage
of medical personnel

and overcrowding and vast
movements of populations

on an unprecedented level,

it's clear that the environment
was very much conducive

to the flourishing
of a pandemic.

Within weeks of the first wave
of influenza receding,

the second one hit.

Overnight it appeared
in three continents:

in Boston, Massachusetts;

in France at Brest;

and in Africa at Freetown,
the capital of Sierra Leone.

And now the disease had become
even more devastating.

In September
near Boston at Camp Devens,

the death toll reached
100 soldiers per day.

The camp's medical staff
was overwhelmed.

Every morning the bodies,

the corpses were stacked up
like cordwood in the morgue

and in the hallway
outside of the morgue.

They did thousands of autopsies
just in this one camp.

It's hard to imagine
the conditions

under which these
pathologists had to work.

They had never seen
anything like this.

People described that this
must be some sort of plague,

was a term
that was used, that...

harking back to the Black Death
of the medieval ages,

that that was the only
analogy one could use

for something so devastating,

so that it was really
an unbelievable situation.

Doctors recognized
there was something new.

They'd seen influenza before,

but here there was
something extra.

It was like a virus
with extra punch.

And then they picked out

what seems to be a unique
feature of that outbreak...

This what was called
this "heliotrope cyanosis,"

this discoloration
of the face, the ears.

Cyanosis happens when the lungs
are so desperate for air

that they sap oxygen
from blood vessels in the face.

"Heliotrope cyanosis" was coined
to describe the precise coloring

on the faces of those who died
in this second wave of flu...

Bluish tones so distinctive

that the British army employed
an artist to depict them.

And doctors
like James Niven noticed

another disturbing trend:

This flu was targeting
the young and the healthy.

"Frequency of death
presents a striking peak

"at ages 25 to 34.

"This is totally unlike
the behavior of flu

in previous pandemics,
and requires special study."

Young adults and children seem

to be much more susceptible
to be infected with the virus,

and then for whatever reason,

young adults
rather than children

were highly susceptible to die.

We don't know what influenza
viruses circulated before 1918.

We don't know

what the immune status
of the population by age was

to different kinds
of influenza viruses,

including the kind that emerged
in 1918 as the Spanish flu.

But I think there's
pretty good evidence to allow us

to conclude that there must
have been an influenza virus

of a similar nature that
circulated in the mid-1800s,

so that people who were
middle-aged and elderly

probably had
at least some protection

against the 1918 virus.

In four years of w*r,

death had become
commonplace among soldiers.

Now it was an everyday
occurrence among civilians.

I was out with me mum shopping,

and I said to her, "That lady
doesn't seem well there."

She said, "Don't watch her."

And I said, "But she's swaying."

She sat down on the curb
because she was poorly.

And as she coughed,
so she spurted blood.

And she died the next day.

Well, I was very upset,

because she was
only a young woman.

As things got worse,
there were calls

for doctors to be released
from active service

to deal with the crisis.

"The shortage of medical men
is scandalous and disgraceful.

"It is time more doctors
were sent home from the front.

"They are fighting a foe at home
as deadly as the Hun.

People are dying off
like sheep."

In the United States,

the situation
had turned desperate.

Even though 200,000 recruits
had been hit by the flu,

moves to quarantine the camps
were rejected.

The w*r demanded reinforcements
no matter what the cost.

Part of the tragedy
of the pandemic

as far as America was concerned

was that it raised
this enormous army.

And many of their troops
never even saw the front line

in the First World w*r
because so many of them died

on their way over.

You were more apt to die
aboard a U.S. transport

or in a U.S. base camp

than you were
in the actual firing line.

By August, a quarter
of a million Americans a month

were on their way to Europe.

But by the time the troops from
the Tennessee National Guard

arrived in
the French port of Brest,

there were already casualties.

When many of these
transports reached Brest,

which was the main
port of disembarkation,

invariably there was a convoy
of ambulances there to meet them

to take off the dead and the
suffering from the pandemic.

Those who survived were sent
into battle,

The Germans would later claim

that the flu came with them
as an unwitting ally.

By then the Germans
had retreated

to the Riqueval Tunnel,

part of the system of
strongholds in northern France

known as the Hindenburg Line.

They had transformed the tunnel

into a vast
underground fortress.

Losing to the Americans here
could lose them the w*r.

The very nature of the site
has led Robert Brown

to consider whether
the flu-addled Americans

might have infected the Germans
in the midst of battle.

Just being here,

we get the sense
of confinement and enclosure.

We don't feel a gust of air
or the free circulation of air.

And once a disease is
introduced in that environment,

you can imagine it would sweep
through here like wildfire.

To seize the tunnel,

the Americans had to fight
their enemy hand to hand.

It was a desperate battle,
and for the Germans,

defeat was doubly catastrophic.

The Hindenburg Line collapsed,

and the new wave of influenza
took Germany in its grip.

At least one German medical
officer is noted as saying

that it was the American army

that introduced the epidemic
in this tunnel,

and the German troops
that contracted it

ultimately brought it back
to the German homeland.

Wherever it came from,

within a month, flu was k*lling
500 people a week in Berlin.

The German high command
had to accept

that the w*r was lost.

When the armistice came on
November 11, the world rejoiced.

At 11:00 we heard
a great big bang,

and I said to my mother,
"What's that?"

She said, "Keep calm."

And then we heard the town crier
telling us the w*r was over.

"Hurrah!"

You know... oh, yeah!

"The w*r's over, hurrah!"

The relief of knowing
the w*r was over and finished

was absolutely terrific.

People went wild in the streets,
in apartments or whatever.

But relief was mixed
with foreboding.

The specter of influenza
still hung in the air.

For many, the peace
brought no release

from the pain
of losing loved ones.

I do remember very clearly
being with Mother,

and saying, "It's over.

"The w*r's finished.

"Your daddy
won't be going away again."

Ada Darwin's father
had served throughout the w*r

as a medical orderly.

Now he was back home
in Manchester.

Ada was one of six children and,
shortly after the armistice,

the first to become ill.

I remember...

crying to tell my mother
to stop the others

making a noise
and making my head ache.

And she put me to bed,

and I wondered why
she put me in her bed

and not where I usually slept
with my sister.

Within hours,

Ada's mother and baby brother
also came down with the flu.

To try to isolate the infection,

the family doctor moved Ada
from the house.

It would be the last time
she would see her mother.

She looked very sad
when I was being dressed to go,

and I thought perhaps she was
sad because I was leaving her...

A childish thought.

By the next morning,
Ada's mother was dead.

I remember being on Auntie's
knee crying for my mother.

And she said
she'd gone to Jesus.

I remember saying, well, Jesus
had lots of other people...

"I want my mama."

And there was worse to come;
her father had also fallen ill.

A medical orderly,

he knew the disease's symptoms
and what would follow.

I remember him going round
the bedroom saying good-bye.

I'm sure he must
have been brokenhearted.

The funeral, when it came,
was for three people:

Ada's father, her mother
and her baby brother.

They were buried
with military honors.

I remember the band and
the body of soldiers marching,

my dad's coffin
and the Union flag over it

and his cap on the top

and the big glass hearse
with the black horses.

It's like a film in my head,
you know, I can always see it.

Almost every day

I get a letter from someone

describing how
their grandparents died

or their favorite cousin.

You know, 80 years later
they're remembering it.

So... fantastic impact
at the time

in a country, in a world
that was just reeling

from the First World w*r.

And they took it quietly,
they really did.

"Seventh of November, 1918.

"In the 96 great towns
in England and Wales,

"there were 7,417 deaths,

compared to 4,482
the previous week."

The death toll was mounting,
and science had no answers.

The reaction to the outbreak

from the medical community
in general...

The clinicians
and the pathologists...

Was just one of total loss.

If you put this into context,

you can understand why it was
so particularly frustrating.

By 1918, people felt that
great strides had been made

in fighting off
infectious diseases,

and so it was a really huge blow

to the morale
of the medical community

that the advances
of the last 50 years

had all been
seemingly worthless,

that they were not able
to do anything about this.

It was not unheard of to find
large numbers of unburied dead...

Even in the streets...

That had been uncollected
by sanitation officials.

The public services broke down
in many communities

because of the number of people
that were ill.

There was very much
a climate of fear.

And fear turned to panic.

I remember at times
my mother would wear a mask

and you could see her fright.

You don't soon forget that.

It stays deep within you.

When things got very bad,

they would run out of the city
into the country,

but the country air wasn't
any better than the city air.

They didn't know
where the bug was coming from.

"Recent deaths..."

"Lieutenant John..."

"Bernard
Bakewell..."

"Aged 26..."

Doctors are dying,
nurses are dying,

everyone is ill.

"Harry, aged 27,
died..."

Schools are closing,

factories are closing.

The whole modern society
finds itself grinding to a halt.

You can't buy coffins.

You can't get your parents
or your children buried.

In 1918, flu was thought to be
produced by bacteria,

which can easily be seen
through a microscope.

It was not until 15 years later

that the disease was first
identified as a virus,

thousands of times smaller.

And we now know that the virus
didn't originate in humans.

Influenza originated
as a bird virus.

It still is
a particular virus of birds.

Sometimes it kills them...

They drop out of the sky
like lead balloons.

Sometimes it has no effect
whatsoever in them,

but they're excreting virus
in large quantities

in their droppings
and through their upper airways.

Flu strains rarely jump directly
from wild birds to people.

Typically they must first infect
domestic birds, like chickens,

then cross the species barrier
into mammals, such as pigs,

before they are capable
of human infection.

In the Far East,

where known recent flu pandemics
have originated,

food markets regularly bring
humans, birds and other animals

cheek by jowl...

Ideal circumstances
for the virus to exploit.

Influenza is fully dependent
on its host.

It survives and thrives

only by invading cells and
reproducing itself inside them.

Without cells to infect,
it would die within hours.

What the virus does is it acts
like a little t*rror1st.

It gets inside the cell,

and then it takes over
the machinery of the cell.

It redirects the cell to change
from its normal function

to become
a little virus factory.

And as it reproduces itself
in humans,

the virus continues to mutate,
each time maximizing its chances

of defeating
the body's immune system.

Its genetic structure makes it
uniquely well-equipped to do so.

The virus has only eight genes,

but they are not locked
in a fixed structure.

They exist
as separate fragments,

so the virus can change
its permutations endlessly

and, some scientists argue,
even cyclically.

This means that a new strain

with similar genetic
characteristics
to the 1918 strain

could therefore emerge.

And since scientists
do not yet know

what the 1918 virus looks like,

the world would be unprepared
for its present-day equivalent.

From his lab at the U.S. Armed
Forces Pathology Institute,

Jeffrey Taubenberger knew that
to head off a repeat of 1918,

he would have to find
the genetic code

of the k*ller virus.

For the past 150 years,

U.S. Army doctors have stored
samples of diseased tissue

in the Pathology
Institute's archive,

especially when a disease tests
the limits of their knowledge.

Among the 70 million samples
are 100 slivers of lung tissue

taken during autopsies of
U.S. soldiers who died in 1918.

Finding them gave
Taubenberger hope.

I was really surprised

to find that there were

approximately a hundred
autopsy cases

of U.S. soldiers that died of
influenza in 1918 in the files.

So I had no idea that
there would be so many.

Most of the samples came up
negative for the virus.

It had escaped its victims

before they died
of secondary infections.

But Taubenberger was undaunted.

We were just...

so convinced that this was
such an important tack

that we just really kept at it,

even though we kept getting
negative results.

Finally, after
months of searching,

Taubenberger found fragments
of the virus in a tissue sample

taken from the body of
U.S. Army private Roscoe Vaughn.

When we got the first
positive case,

it was just really
a fantastic moment.

It's one of these rare things
that happen in science...

To be able to read
a very tiny fragment

of this virus that k*lled
50 million people

and knowing that we were
the first people on earth

ever to have come close
to identifying this virus

and actually seeing
this virus up close.

To boost the limited size
of his sample,

he used a new scientific
technique called

polymerase chain reaction,
or PCR.

You can theoretically start
with just one copy,

one piece of genetic material,
and make multiple copies...

In a sense,
like making multiple copies

of a piece of paper
on a photocopy machine.

And it allows you to go from
material that is so limiting

that you wouldn't be able
to study it at all

to having enough material

that you can actually manipulate
in a laboratory.

Taubenberger's team has since
examined tissue samples

from other parts of the world
that contained the 1918 virus.

Amazingly, the exact same strain
cropped up in each sample,

indicating to Taubenberger

that the virus had
not needed to mutate

as it jumped from
population to population.

What it suggests to me is
that this new virus emerged

with all the features necessary

to allow it to spread
efficiently in humans...

That is, that large sections
of population

didn't have immunity to it,

that it was supremely
human-adapted,

that it replicated well

and transmitted well
from person to person,

and that once that virus
got into humans

there was nothing
that could stop it.

There were outbreaks...
simultaneous outbreaks...

In India, Africa, New Zealand,
the United States,

Alaska, Norway, England.

People were dying
left, right and center.

Now, how could this happen in
a community with no airplanes,

where it took weeks and weeks
and months to move around?

All that pointed,
at least to me,

towards the fact that there must
have been some precursor waves,

some herald waves of outbreak
long before 1918,

and the virus had seeded itself
during that period.

Many experts believed
the pandemic erupted overnight

in the American training camps
in March 1918.

John Oxford thinks
they're wrong.

He wondered if there was
any evidence

of the disease emerging in
the more crowded European camps

perhaps even earlier than 1918.

He narrowed his search
to northern France.

The British Army had
two million soldiers

on that little stretch of the
Western Front, which was what?

17 miles long, ten miles wide?

Fantastic concentration
of young people and movement.

So I can see why it could
very well be a focus there

for a virus like influenza
in the British sector.

Scanning old records,
Oxford came across a 1917 report

published in
The Lancet medical journal.

It described a strange
respiratory disease

which in 1916 had struck

the British Army's largest
transit camp, Étaples.

I remember perfectly
the day we found it

and this student came to me
and said,

"This place is called Étaples."

Never heard of it.

Étaples... can't even find it
on the map.

Today, Étaples is
a quiet backwater.

But during World w*r I,

the railway brought through
a torrent of humanity.

The camp was the size
of a small city

with a dozen hospitals,
20,000 hospital beds

and a constantly shifting
population of 100,000.

Étaples was a melting pot.

Every infantry division in the
British army had a depot there,

so you had
the Highland Division,

you had the Tyne Tees Division,

you had the Welsh Divisions,
you had the Irish Divisions,

to which was added four-fifths
of the Australian Divisions

and the New Zealand Division.

They brought labor units
from South Africa,

they brought in
West Indian soldiers.

There was an almost unlimited
supply of foreign nationals.

With its endless
troop movements,

Étaples in 1916 seemed
the perfect breeding ground

for a virus.

But knowing how influenza
finds its way

into the human population,
Oxford still had questions.

This new pandemic virus
is going to come

either from an animal
or from a bird,

so were there any animals
in the camp at Étaples?

In particular,
were there any pigs?

Because we still think that
a pig can act as a mixing bowl

between the bird,
an influenza virus in a bird

and influenza virus in a human.

Remarkably, the answer is yes.

With a hundred thousand troops
at any one day in that camp,

they had to feed them
all something,

and so the British army
instigated a new experiment;

that is, get piggeries
into a camp.

And we've got photographic
evidence of big piggeries

in the camp at Étaples itself.

Now, the next question is,
is there any contact of soldiers

with live birds...
Chickens, geese, ducks?

And the answer again is yes.

In other words, lots
of opportunities

for a virus to move
from a bird to a soldier.

Now, you need a third factor:

lots and lots of people.

A hundred thousand soldiers
in any one day,

all of them on the move.

So, from my point of view,

from the point of view
of a virologist,

it had everything,
I think, and more.

The Lancet report

of a fatal respiratory ailment
hitting Étaples in 1916

added weight to Oxford's theory

that the camp could
in fact be the birthplace

of what would become
the 1918 flu pandemic.

Once you've seen that article,

then a lot of things
which were puzzling

to do with the mortality rate
in the camp

suddenly fell into place,

because I'd noticed in the
records of certain hospitals

that they were handling
far more sick than wounded

during that 2½-month period.

The staff reported

that six times as many men died
of disease than died of wounds,

and that was something
highly unusual

in the history of the camp.

They thought they'd
encountered a new disease.

It wasn't exactly pneumonia.

It wasn't pure bronchitis.

They called it in their article
"purulent bronchitis."

Men got fevers,
men got heightened pulse rates,

the lungs were afflicted,

and plenty of these men
died of asphyxiation

and getting this
heliotrope cyanosis.

But was the purulent bronchitis

that swept through Étaples
in 1916

caused by the same virus
as the 1918 flu?

Oxford found tantalizing
evidence in The Lancet

suggesting the two diseases
shared similar symptoms.

According to
Captain William Rolland,

one of the article's authors,

the Étaples bronchitis was
extremely infectious

and unusually fatal.

Within a month, he said,

"The disease assumed
such proportions

as to constitute almost
a small epidemic."

Rolland listed 20 patients
at Étaples

with symptoms
of purulent bronchitis.

13 of them had died.

He concealed identities
by using initials.

But from British army records,

Oxford believes his team
can identify at least one

and establish what led
to his death.

The service records are charred
from b*mb damage,

but to Oxford,
the story they tell is clear.

"Private U" was Harry Underdown,

a soldier
in England's Surrey Regiment.

He was a farmer's son from Kent,
not a big man, but fit,

five-six and less
than 140 pounds.

He said his job on the farm
was a hay trusser.

Underdown volunteered
in December 1915

and gave his age
as 20 years and 57 days.

There...

Here, this is him.

To my way of thinking,
he, Harry,

would be one
of the first cases...

Maybe even the first...

To die of what
was going to be known

within a year
or a year and a half

as the great Spanish
influenza outbreak.

In the summer of 1916,

Harry Underdown was stationed
in France.

His training had been short...

He was needed in the ranks
for the Battle of the Somme,

one of the bloodiest battles
of World w*r I.

In October,
he was wounded in action

and suffered shell shock.

His symptoms
included memory loss

and the inability to speak.

Harry was shipped back
to England to rest and recover.

Then, after one month,

Harry Underdown
was sent back to France

and he and his fellow
soldiers returned

to the mire of trench warfare.

This was December 1916, one of
the coldest winters on record.

In conditions of stress, all
resistance to infection drops.

Within weeks,
Harry was struck down

by the mystery disease,
purulent bronchitis.

He was taken to the base
hospital in Étaples.

His symptoms included
a temperature of 103,

blood in his saliva,
breathlessness

and heliotrope cyanosis,

the same bluish discoloration
of the skin

that is caused by influenza.

On February 21, 1917,
Harry Underdown died,

barely six months
after joining his regiment.

He was 21 years old.

The autopsy showed his lungs
were choked with blood.

Was the respiratory disease that
k*lled Harry Underdown in 1916

the same ailment that
would strike down millions

two years later?

After the 1918 virus
had run its course,

Captain Rolland's superior,
Dr. William Leishman,

did make that connection.

"The dominant symptoms of the
two outbreaks were so similar,"

he wrote, "it is difficult
not to conclude

that one common agent
was responsible."

John Oxford is
more convinced than ever

that the origin of the 1918 flu

lies in
the k*lling fields of 1916.

There were particular
circumstances

after that Battle of the Somme...

So many young people,
so much distress...

Which would lead
to the transmission

of a virus like influenza.

The soldiers
all crowded together

would have enabled the virus
to move rapidly

from person to person
to person to person

much more rapidly than
in the civilian population.

Normally that enhances
the virulence of a virus,

so the circumstances
would have been there,

and then it did the final leap

from those camps
into the civilian population.

If Oxford has found
the birthplace

of the 1918 virus's
precursor strain,

it would mark
a significant discovery.

Scientists could begin charting
the virus's evolution,

and it would confirm that, given
the right set of conditions,

a pandemic flu strain
could get its start

anywhere in the world.

But Jeffrey Taubenberger
believed

that for Oxford's claim
to be substantiated,

they must uncover
pre-1918 tissue samples

of patients like Harry Underdown

that test positive
for influenza.

He and Oxford have been trying
to locate bodies

buried in permafrost that might
still contain such samples.

So far, they have had no luck.

If these tissues could be found,

then obviously rescreening
of the pathology itself

could be done,

but more importantly
we could do examination

to see if they still contained
influenza genetic material.

But in the absence
of this material,

unfortunately this all ends up
being entirely speculative.

Until we get that evidence,
we cannot be 100% sure.

But on the other hand,

I think you work with
the information to hand.

You don't just discard it.

You don't discard three detailed
papers from pathologists

working at Étaples, Aldershot
barracks and whatever.

You don't just say,
"Well, forget all that;

they don't know
what they're talking about."

They are telling us
over these years

that the new disease
that they described at Étaples

was just the same as the disease
they saw in the fall of 1918.

I don't think
we can just discard that

and say, "Oh, no, you made
a mistake, you got it all wrong.

"You were there,
you did the pathology,

"you did everything else,

but I'm sorry, you made
the wrong conclusions."

I think we should take a view

that at the moment,
the weight of evidence...

Not proven,
but the weight of evidence...

Points towards
northern France and Étaples.

I think that all you can say

is that there is really
no solid evidence

that would pinpoint an origin,

that there's nothing we can do
to test this hypothesis.

It's just not clear.

So obtaining
the sequence of the virus

is the thing that we can do now,

and so that's what
we're going to go for first.

Taubenberger
and his team identified

six of the eight 1918 flu genes.

But they saw the limitations

of only having
the genetic sequence on paper.

They could neither determine
how the virus attacks its host,

nor predict its resistance
to vaccines.

They decided they needed
to see the virus in action.

We need to try to develop models

to help us understand
where those changes are

that would lead to virulence,
and the only thing we can do

is to do that in tissue culture
or animal models.

Knowing that there may not be
suitable animal models

for what is ultimately
a human-adapted virus,

one would hope that we could
learn something about virulence

by studying animal models
that would lead us

to an understanding
of what happened in people.

That's really
the best thing one could do.

As controversial as it is
to bring the virus that caused

the deadliest pandemic
in history back to life,

Taubenberger's team
is doing just that.

In an extremely
high security lab in Atlanta,

Taubenberger's colleague,
Terrence Tumpey, combined

two 1918 flu genes with genes
from a modern flu strain.

This virus went directly
into mouse lungs,

and it was lethal to mice.

And when we looked
at the lung tissue,

they developed
this purple discoloration

that's often seen with highly
pathogenic influenza viruses.

You have this tremendous
purple discoloration.

So it was
a very striking finding.

However, once the mice received
a modern vaccine

for the hybrid virus,

they formed
the necessary antibodies

to ensure their survival.

Perhaps most importantly,

modern antiviral drugs were
successful in treating the mice

once the virus took hold.

From Tumpey's
experiments with mice,

can one draw conclusions

about human susceptibility
to a 1918-like virus?

Taubenberger advocates that
future tests with 1918 flu genes

be done on primates,

who have a much greater
genetic similarity to humans.

But Tumpey feels his initial
study is an early indicator

that modern medicines would
indeed provide protection

from such a virus.

So, I think that we may see
a new influenza virus

that will jump into humans.

And it might jump into us
in a situation where we just...

um... we don't have
the immune responses

to a new particular virus.

But I think
with the surveillance

that we have nowadays
and the antiviral drugs

and the potential vaccines,
that we'll never have a pandemic

as severe
as the 1918 Spanish influenza.

Despite encouraging evidence

that those with access
to antiviral drugs

might be protected
from an emerging pandemic,

John Oxford feels
we cannot yet write off

the possibility
of a repeat of 1918.

On the one hand,
if you're an optimist,

you could say there's
new antiflu drugs,

there's the capability of making
vaccine more now than there was.

On the other hand,
there's many more people around.

There's terrific movement of
population... around the world.

There's 30 million people
affected with HIV

who are immunosuppressed.

So when you begin
to put those factors

against the other factors,
you weigh the thing up,

you can come up
with a good-case scenario

and a bad-case scenario.

The bad-case scenario tells you

that this situation
could be worse than 1918.

And I think the best-case
scenario tells you

that there could be ten
or 15 million people dying.

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