杏吧原创

IN THE film Outbreak, US Army doctor Sam Daniels, played by Dustin
Hoffman, saves the town of Cedar Creek and the entire US from certain death by
an Ebola-like virus. The dynamic Daniels finds a monkey carrying the virus,
draws off some serum, then makes enough of the stuff to treat the town and save
his ex-wife鈥攁ll in the space of a day.

While the method behind Daniels鈥檚 frenzied activity may have been true to
life, the timeframe certainly was not. Researchers searching for what triggers
childhood diabetes can only dream of such powers. The notion of a virus
prompting the immune system to destroy the insulin-producing beta cells in the
pancreas has been around for more than 20 years. But identifying the viruses
with any certainty is proving very tough indeed.

So a paper from scientists at the Walter and Eliza Hall Institute in
Melbourne, Australia, is causing great excitement. The researchers have found
that rotaviruses, the most common childhood stomach bugs, may trigger diabetes
in susceptible children
(see p 4). The immune systems of children who later
developed diabetes appeared to attack their own beta cells whenever they
contracted a rotavirus.

Rotaviruses fit well with the epidemiology of diabetes. New cases tend to
peak in the cold, dark months, which is just when rotaviruses go to work.
Several studies have also found that diabetes is on the increase in areas where
parents send young children to day-care centres, which are hotbeds of
infection.

So, could a rotavirus vaccine stop children developing diabetes? At first
glance the answer looks like 鈥測es鈥�. But the Australian research questions this.
One theory suggests that amino acid sequences carried by beta cells and the
virus are very similar. The argument goes that this molecular mimicry triggers
diabetes鈥� immune cells attacking the virus also take out beta cells. So a
鈥渄iabetes vaccine鈥� with these amino acids could trigger the disease instead.

One other hope is that a vaccine could be made with amino acids from the
virus that are different from those found in beta cells. This would sidestep
molecular mimicry. Repeating the Australian study with children who have
received such a vaccine could prove whether rotaviruses really spark off
diabetes.

So it鈥檚 all clear then? Unfortunately not. The Melbourne team looked at
children with only two of the 16 or so gene variations thought to increase the
risk of diabetes. Other viruses are also implicated. Children who contract
rubella in the womb have a raised risk of diabetes, and there is evidence
against other viruses, such as Coxsackie B. Then there鈥檚 the mechanism:
molecular mimicry is only one theory. Perhaps viruses infiltrate beta cells, and
the immune system mops them up as it does other infected cells.

At the molecular level, childhood diabetes looks nothing like a single
disease. This is not the sort of message that Sam Daniels would have wanted to
hear, but life is rarely as cut and dried as Hollywood portrays it. What the
Australians show is the power of combining genetics, virology and immunology.
And as we plumb the genomes of humans, viruses and other pathogens, you can bet
there鈥檚 more to come.