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| Archive : Spring 2006 |
POLIO IS ALMOST GONE, BUT WILL IT
EVER BE?
Eradication plans have been in place
for decades // Two vaccines have saved millions of
lives // More countries become virus-free each year
// But several doors to infection remain wide
open.
Still a Scourge [page 2]
 By Wendy Orent
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But whatever the cause of the outbreaks of epidemic
polio in the first half of the twentieth century, it mystified physicians
and petrified parents. Summer was an especially terrifying time: Swimming
pools and even parks were off-limits, and many parents kept their children
indoors and away from crowds; you never knew where, or how, the virus
might strike. One of the most frightening aspects of polio was its stealth.
Unlike smallpox, for example, which left its unmistakable mark on everyone
it touched, polio infects as many as 1,000 people for every one who is
felled by paralysis.
Poliovirus is an Enterovirus, a genus in the picornavirus
family of very small, single-stranded RNA viruses. Enteroviruses inhabit
the intestines and circulate largely through fecal-oral transmission or
in polluted water. Though many cause little disease, a few, such as Enterovirus
71, or several of the Coxsackie viruses, may cause meningitis and occasionally
paralysis. But poliovirus is among the most dangerous.
Under an electron microscope, a polio virion (virus
particle) appears as a bumpy sphere. Each of the three immunologically
unrelated serotypes consists of an RNA genome enclosed in a capsid, or
outer shell, by which the virion adheres to human cells via so-called
polio receptors. These are found, among other places, on cells of lymphoid
tissue lining the digestive tract. According to Harvard virologist James
Hogle, the virion uses the receptor as a portal into the cell. There it
hijacks the cell’s machinery to replicate itself. As long as the
infection remains in the gut, however, it’s unlikely to harm its
human host.
Sometimes, though, this intestinal virus produces
paralysis. That, says Hogle, is because poliovirus receptors also exist
in nervous tissue, including the anterior horn motor neurons of the brain
stem and spinal cord. After it replicates in intestinal cells, the virus
can enter the bloodstream, where it causes a mild but noticeable infection.
Then it may cross the blood-brain barrier to reach the spinal cord.
Other times, circulating poliovirus finds a break
in muscle tissue, makes its way to nerve cell endings and then shoots
up the axons to the motor neurons in the spinal cord or brain stem. According
to one theory experimentally proven by Wimmer, injections may sometimes
be to blame, giving blood-borne poliovirus increased opportunity to ascend
to the motor neurons. Kew believes that tonsillectomies may play a role;
these operations, once very common, have been associated with bulbar polio,
the most serious form of paralytic disease. Whichever way it gets to the
anterior horn motor neurons, the poliovirus destroys them and may cause
paralysis or death.
As devastating as the poliovirus can be, for half
a century there have been two effective vaccines. The Salk version, approved
in 1955, is known as inactivated polio vaccine (IPV). Consisting of a
killed strain of the virus, it produces antibodies that circulate in the
blood. Children vaccinated with IPV won’t get paralytic disease,
though they could develop - and unknowingly pass along - polio-related
intestinal infections if exposed to the live poliovirus.
In contrast, the oral polio vaccine (OPV), developed
by Albert Sabin and approved in 1961, is made of live, weakened strains
of the virus and is designed to produce a mild intestinal infection and
induce long-lasting immunity. OPV has been the vaccine of choice for the
eradication campaign. Volunteers can drop OPV in a child’s mouth
and the infection it produces can spread beyond the vaccinated child to
others in the community, widening the impact of a vaccination initiative.
As those on the front lines of the eradication campaign
well understand, children in high-risk areas often need more than the
usual three doses of oral vaccine to acquire immunity. Even then it doesn’t
always work, Kew notes, especially during summer and autumn, polio’s
high season. (Cold weather slows transmission of the virus.) Moreover,
if a child has diarrhea, the vaccine can pass through the intestines before
the live virus strain has a chance to replicate, and malnutrition can
prevent antibodies from developing. Both diarrhea and malnutrition are
common in Afghanistan, India, Nigeria and Pakistan, where polio has found
its last redoubt. What’s more, these countries have high birth rates,
continually providing a fresh supply of susceptible potential hosts. |
Next page | Pages: 1 2 3
Photo by Giocomo Pirozzi/UNICEF |
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