influenzas. “Immunity is complicated,”
Donis says. “How all these mechanisms
play out in the guy that is shedding virus,
or the person that is shaking hands or
breathing in droplets after someone
sneezes or coughs, is still a very complicated biological process that we don’t
understand completely.” Younger folks
are more susceptible than older people
to getting the new H1N1 virus, but its
overall threat to a young person is still
proportionally similar to that of any
seasonal flu, Palese says.
The number of deaths from pandemic
H1N1 are estimated to be much lower
than that of seasonal flus: On average,
about 36,000 Americans die from flu-related causes each year, according to
the CDC, while the current pandemic
is responsible for an estimated 11,000
deaths from April through December.
“It’s the same rate,” Palese says. “That
has been really overlooked. It is not more
virulent per 18-year-old, or per 25-year-
old, than the seasonal one.”
The inside counts
Another study finds that the virus isn’t as
unrecognizable as its outer proteins had
led scientists to believe. A hidden familiarity might help people fight the virus
once they’ve been infected.
Antibodies latch on to proteins on the
outside of virus particles but are unable
to detect what’s on the inside of the virus.
A different faction of the human immune
system is formed by cells that recognize
foreign proteins on the outside and on
the inside of viruses. These cells, a type of
T cell, are an underappreciated arm of the
immune system and might be doing some
of the immune system’s heavy lifting, says
Bjoern Peters of the La Jolla Institute for
Allergy & Immunology in California.
In a study published December 1 in
Proceedings of the National Academy
of Sciences, Peters and his colleagues
addressed how familiar the virus is to the
immune system. “We were essentially
asking, how is this virus different, from
the immune system’s point of view?”
Peters says.
As expected, proteins such as hemagglutinin and neuraminidase that decorate
the outside of the H1N1 virus differed
from proteins in earlier seasonal viruses,
and as a result, were unfamiliar to most
people’s antibodies. But proteins on the
inside of the virus were quite similar to
past influenzas, Peters and colleagues
found. Because of this similarity, T cells
might be able to quickly begin neutralizing cells once they are infected. “While
there’s no immunity against the surface,
there’s plenty of immunity against the
internal proteins,” Peters says. The same
study found that blood samples taken in
2007 from the general U.S. population
had some immunity against the pandemic strain, thanks to T cell immunity.
“We believe we have a reason why
the incidence of severe disease isn’t
that high, based on the fact that people
have T cell immunity,” Peters says. “You
would expect that this is going to be a
very severe, deadly pandemic if you have
no immunity. Obviously, as we know,
that’s not how it turned out.” A strong
T cell reaction probably reduces the sever-
ity of influenza infections, clearing virus-
laden cells before symptoms get bad.
Not out of the woods
Influenzas are notorious for playing fast
and loose with their genomes— mutations are introduced as the virus replicates and gene segments are swapped
with other viruses in a process called
reassortment. Reassortment is responsible for the repackaging errors that, in
part, created the H1N1 pandemic influenza. This genetic recklessness confounds immune systems and worries
public health officials.
Early results from animal studies suggest that pandemic H1N1 isn’t eager to
reshuffle its genetic deck, even when
the influenza is infecting the same cell
as another virus at the same time —a
prime opportunity for gene segments
to get combined in new ways. Perez
and his colleagues infected ferrets with
Anatomy of influenza
some aspects of the current
h1n1 virus differ from earlier
type a influenzas, possibly confounding immune systems. But
all influenza a virus particles
(generic version shown) share
some features.
Hemagglutinin helps
a virus break into
cells. Changes in the
protein may dictate
what organisms a
virus can infect.
Neuraminidase
helps a newly formed
virus particle escape
from an infected cell
and is a target for
antiviral drugs.
M2 ion channels
allow protons to
enter the virus particle, leading to the
release of genetic
material in the cell.
RNA (with associ-
ated proteins) is held
on the inside of the
virus and carries
the virus’s genetic
instructions.
