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nce the virus began spreading
within the NewOrleans popula-
tion, the epidemic erupted, leav-
ing no one unaffected. In spite
fatality in previously healthy, young adults.
The emergence of such a virulent virus from
the backdrop of milder strains lies in the flu
virus’ dramatic, built-in ability to reinvent
itself. Influenza accelerates genetic change
through mixing genetic material from two
or more viruses in a process called reas-
sortment. The genome is divided into eight
separate segments, and whenever natural
hosts (primarily wild birds) are infected with
more than one virus, segments from one
viral strain can be packaged together with
segments from another strain, essentially
creating a new virus. That’s why seasonal flu
vaccination is required each year.
Public health virologists monitor newly
emerging viruses and make their best judg-
ment of which viruses will be the most prob-
lematic for humans. They then create a vac-
cine that protects against the top 3 or 4 of
these. (In the future, this may not be neces-
sary. Sridhar et al., in this September’s
Nature
Medicine
, unveiled a theoretical framework
for a “universal influenza vaccine” based
on T-cell responses to the core of the virus
rather than antibody responses to surface
proteins. The development of a real-world
universal vaccine, however, will require
years, if not decades, of development. Until
O
of a massive response on multiple levels—
from the arrival of hundreds of volunteer
Red Cross nurses to impressive coopera-
tion between government agencies—one
month after the first ship had arrived, over
2,000 cases per day were being reported. By
the time it had run its course, almost 3,500
New Orleanians had died from the disease
and countless others were severely affected.
(A staggering 54,089 cases were reported
in New Orleans between October 1918 and
April 1919). Worldwide, mortality estimates
range from 20 million to 100 million dead
by the end of the pandemic, about a twen-
tieth of the world’s population at the time.
How could influenza, the same virus
responsible for the humble seasonal flu,
cause such a deadly epidemic? While the
answer lies partly in the resources available
in 1918 vs. today (such as antibiotics to fight
secondary, bacterial infections), the virus
itself was extremely aggressive, inducing an
over-reaction of the immune system that led
to acute respiratory distress syndrome, mas-
sive hemorrhaging of the lungs, and rapid
A magnifired view of the
H1N1 virus.