polio (DOC) by stariya


									Polio: don't let eradication slip away again
     23 March 2011 by Debora MacKenzie
     Magazine issue 2805.

After years of frustration, polio is on the ropes. But we could still miss the historic opportunity to
wipe it out for good
IT IS the disease that's always down, but never quite out. In 1998 the World Health Organization
claimed it was going to eradicate by 2000. In 2000 it revised the target to 2005. Then it stopped
setting deadlines - and the virus is still out there. Last year polio afflicted nearly 1300 people, and
the virus has been making a comeback in countries where it had been stamped out. Senior public
health experts have railed for years that attempts at polio eradication are a grandiose waste of
Until now. A sea change is taking place. Even the most outspoken former pessimists - including D.
A. Henderson, who led smallpox eradication - are now talking about the post-polio era. For an
observer like me, it is wonderful to watch. Yet the whole grand effort could still fall at the final
The Polio Eradication Initiative's recent results are spectacular. In 2009 there were 741 polio cases
in India. Last year there were just 42. One of the three families of wild poliovirus is no longer
circulating; another should be gone soon. In Nigeria, the number of genetically distinct kinds of
polio has fallen from 26 in 2008 to four. Bill Gates, who has a nose for winners, made tackling
polio his flagship campaign in January.
But amid all the good news the main obstacle to eradication - revealed by this magazine in 2000 -
remains: we have been fighting fire with fire. The oral polio vaccine (OPV) used by the eradication
initiative contains poliovirus itself, weakened but very much alive. The weakened virus sometimes
sticks around in people and the environment, and can circulate and mutate back into a killer.
A study in Nigeria last year confirmed the fears of some virologists that the OPV virus can mutate
to be as nasty as wild polio (The New EnglandJournal of Medicine, vol 362, p 2360). And because
only one polio infection in 200 causes disease, the virus can spread undetected until there's a lot of
it about.
The eradication initiative chose OPV, rather than the original Salk vaccine made of killed virus
(inactivated, or IPV), for good reason: it's cheap and effective. You need less virus in a live vaccine
because it replicates in the body, induces immunity in the gut where it is needed, and vaccinated
children shed it in faeces and "vaccinate" their friends.
For now, the advantages of OPV outweigh the risks. The wild virus is still circulating and the
priority remains to stamp it out as efficiently as possible. But once the wild virus stops circulating -
as officials hope will happen in a few years - OPV is left as the only source of infection.
So to genuinely eradicate polio we must stop using the live vaccine. But therein lies a problem:
children born after OPV is phased out will be vulnerable to any vaccine virus still lurking, so polio
could stage a very nasty comeback unless we protect them some other way.
The best way to do this is to vaccinate people with IPV while the OPV viruses die out. Rich
countries have already made the switch, but IPV has always been unaffordable in the poor countries
that need it most. It costs 20 times as much as OPV and requires expensive needles.
IPV is also in short supply. The vaccine industry can make 120 million doses a year, but a report for
the Gates Foundation calculates that if the world switched to IPV tomorrow, we'd need 450 million.
Yet vaccine companies have little incentive to build expensive new factories to make a product that
will mostly be used once wild polio is gone - maybe in three years, maybe 10 - and then only for
another five years or so.
Despite these obstacles, things are changing. Mexico and the Indonesian province of Yogjakarta
have successfully used IPV. Companies in China and India that had no plans to add IPV to routine
childhood vaccines two years ago now do. And research has revealed tricks to make IPV go further
for less.
For example, a study in Oman found that very small doses injected into the skin work almost as
well as the usual, larger dose injected into muscle, because skin is teeming with immune cells (The
New England Journal of Medicine, vol 351, p 2286). There is also evidence that babies might need
only two shots instead of the usual three or four (The New England Journal of Medicine, vol 351, p
Adjuvants - chemicals added to vaccines that boost immunity - might also stretch the supplies. And
Indian vaccine companies, which can produce vaccine more cheaply, hope to make their own IPV
not from wild polio, which is risky to handle, but from the weakened virus used in OPV.
Uncertainties remain, however. Will reduced-dosage IPV work against a revived vaccine virus even
as we cut corners on dosage? What if the comeback virus has changed its genes, as they can? Will
poor countries fork out for a vaccine against a disease that has supposedly been wiped out?
There are also worries that IPV-lite will stop people getting sick but not prevent them from catching
and spreading the virus without symptoms. When you're trying to stamp out every last virus
particle, that's not good enough.
More research on IPV will help solve these problems, and that has been increasing since 2008. But
research budgets everywhere are being slashed, and even with Bill Gates's deep pockets the World
Health Organization has barely enough money to do its main job of wiping out wild polio.
Right now, despite past setbacks, that is really looking likely. It will be a crime if we get the
endgame wrong because making IPV wasn't profitable enough, because the research money ran out,
or because impoverished governments couldn't justify the expense. Polio eradication is in sight. We
must not drop the ball just as we reach the final, agonising inch.
Debora MacKenzie is New Scientist's Brussels correspondent

     From issue 2805 of New Scientist magazine, page 32-33.

To top