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World News
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Flesh-eating disease linked to gene differences |
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Genetic
differences between people can explain why some develop a fatal
"flesh-eating" disease following infection with a common bacterium,
while others colonised by the same strain walk away with just a sore
throat.
The study throws new light on the mechanism of Group A streptococci
(GAS) infection, and could lead to treatments better tailored to the
patient's needs.
A team led by Malak Kotb at the University of Tennessee looked at
variants in HLA-II genes, a set of genes that encode proteins on the
surface of human immune cells. Previous work has shown that these
proteins can bind to certain toxins secreted by Strep A.
The researchers identified gene variants that offered protection
against severe forms of infection. And they found others that made
patients more likely to develop potentially fatal toxic shock
syndrome or necrotising fasciitis, which causes rapid loss of flesh.
This shows you can use people's genetic make-up to predict what kind
of disease they may get if they encounter this organism, says
Patrick Schlievert, a microbiologist at the University of Iowa.
"This the way the future of medicine is going," he says.
Gene variants do not account for the whole variation in GAS risk
from person to person, however.
"We have already published work showing that if the patient does not
have antibodies against the bacteria, they are at higher risk of the
bacteria entering the bloodstream or soft tissue," Kotb told New
Scientist.
"But once bacteria make it into these normally sterile areas,
antibodies play very little role. Then, a variation in genes plays a
major role," she says.
The HLA-II genes determine the extent of the immune inflammatory
response to key proteins on the surface of GAS bacteria. The
stronger the response, the more likely the patient is to develop
very severe symptoms.
Her team compared variants - or haplotypes - of HLA-II genes in 279
patients with serious infections. Some of these people had toxic
shock syndrome or necrotising fasciitis.
The team identified one particular "risk" haplotype that was present
in one per cent of infected patients that did not have toxic shock,
but in 21 per cent of patients who did.
And they found a "protective" haplotype. This was present in 34 per
cent of infected people who did not develop severe disease, and only
10 per cent of those who did. "So not having this haplotype is a big
risk," says Kotb.
Preliminary analysis suggests these particular haplotypes do not
moderate infection with other bacteria. But previous research has
linked HLA variants with multiple sclerosis, arthritis and type 1
diabetes.
A test to analyse a person's HLA-II genes takes about one hour.
"Doctors could use this information to determine which patients
infected with Group A streptococci need more aggressive treatments,
particularly where treatments are expensive," Kotb says.
Research on the role of patient genetic variation is a "hot area of
investigation" she says. "By studying this, we can also better
understand the mechanism of the infection, in terms of which genes
are playing a role in regulating the response to infection. And this
will suggest new vaccines and therapeutics."
Source: New Scientist, 17 November 2002 |
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