Why was 1918 flu pandemic so deadly?

Research
offers new clue
Last updated: 29 April 2014 at 3am PST

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In 1918, as one global devastation in the shape of World War I came to an end, people
around the world found themselves facing another deadly enemy, pandemic flu. The virus
killed more than 50 million people, three times the number that fell in the Great War, and
did this so much faster than any other illness in recorded history.
But why was that particular pandemic so deadly? Where did the virus come from and why was it
so severe? These questions have dogged scientists ever since. Now, a new study led by the
University of Arizona (UA) may have solved the mystery.
Michael Worobey, a professor in UA College of Science's Department of Ecology and
Evolutionary Biology, and colleagues describe their findings in the Proceedings of the National
Academy of Sciences.

They hope the study not only offers some new clues about the deadliness of the 1918 pandemic,
but will also help improve strategies for vaccination and pandemic prevention, as Prof. Worobey
explains:
"If our model is correct, then current medical interventions, especially antibiotics and vaccines,
against several pneumonia-causing bacteria, could be expected to dramatically reduce mortality,
if we were faced today with a similar set of pandemic ingredients."

The 1918 pandemic killed predominantly young adults

One of the questions that has been particularly vexing is why the 1918 pandemic
human influenza A virus killed so many young adults in the prime of life, he says, adding: "It
has been a huge question whether there was something special about that situation, and whether
we should expect the same thing to happen tomorrow."

Researchers reconstructed the origins of the 1918 pandemic virus, the classic swine flu and the postpandemic

seasonal H1N1flu virus lineage that circulated between 1918 and 1957, to find out why the 1918 pandemic was so
deadly.

Usually, the human influenza A virus is deadlier to infants and the elderly. But the 1918 strain
killed many people in their 20s and 30s, who mainly died from secondary bacterial infections,
especially pneumonia.
For their investigation, the researchers developed an unprecedentedly accurate "molecular
clock," a technique that looks at the rate at which mutations build up in given stretches of DNA
over time.
Evolutionary biologists use molecular clocks to reconstruct family trees, follow lineage splitting
and find common ancestors of different strains of viruses and other organisms.
Prof. Worobey and his team used their molecular clock to reconstruct the origins of the 1918
pandemic virus, the classic swine flu and the postpandemic seasonal H1N1 flu virus lineage that
circulated between 1918 and 1957.

Genetic material from bird flu virus picked up just before 1918
They found that a human H1 virus that had been circulating among humans since around
1900 picked up genetic material from a bird flu virus just before 1918 and this became the
deadly pandemic strain.
Exposure to previous strains of flu virus does offer some protection to new strains. This is
because the immune system reacts to proteins on the surface of the virus and makes antibodies
that are summoned the next time a similar virus tries to infect the body.
But the further away the new strain is genetically from the ones the body has previously been
exposed to, the more different the surface proteins, the less effective the antibodies and the more
likely that infection will take hold.
This is what the authors suggest happened to the young adults in the 1918 pandemic. In
their childhood around 1880 to 1900, they were exposed to a supposed H3N8 virus that was
circulating in the population. This virus had surface proteins that were very different from
those of the H1N1 pandemic strain. Their immune system would have made antibodies, but
they would have been ineffective against the H1N1 virus.
But people born either before or after those decades would have been exposed to a virus much
more like the 1918 one and their immune systems were thus better equipped to fight it.

Prof. Worobey notes:

"We believe that the mismatch between antibodies trained to H3 virus protein and the H1
protein of the 1918 virus may have resulted in the heightened mortality in the age group that
happened to be in their late 20s during the pandemic."
He says their finding may also help explain differences in patterns of mortality between seasonal
flu and the deadly H5N1 and H7N9 bird flu viruses.
The authors suggest perhaps immunization strategies that mimic the often impressive
protection that early childhood exposure provides could dramatically reduce deaths from
seasonal and new flu strains.
In February 2014, Prof. Worobey and colleagues began challenging conventional wisdom
about flu outbreaks, when in the journal Nature, they reported the most comprehensive analysis
to date of the evolutionary relationships of flu virus across different host species over time.
Among other things, they challenged the view that wild birds are the major reservoir for the bird
flu virus. Instead of spilling over from wild birds to domestic birds, they say the more likely
scenario is the other way around - that new strains jump from domestic to wild birds.
Written by Catharine Paddock PhD
Copyright: Medical News Today
Not to be reproduced without permission.