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Argentines
Report Advance
Against Chagas' Disease
BUENOS
AIRES, Argentina (Reuters) - Argentine scientists said on Thursday
they had made a breakthrough in efforts to combat a deadly parasitic
infection that is believed to have killed Charles Darwin and is
endemic in Latin America, affecting millions of mainly poor, rural
families.
Researchers
at the Institute of BioTechnological Investigations at San Martin
University said they had unraveled the genetic makeup and structure
of the enzyme that allows the parasite responsible for Chagas'
disease to defeat the body's immune system.
The disease
causes swelling of the internal organs, such as the brain and
intestines, and can damage the heart. It is caused by the parasite
Trypanosoma cruzi and transmitted to humans by bloodsucking reduviid
bugs, or ``kissing bugs,'' that live in the cracks and holes of
homes in South and Central America.
Carlos Frasch,
head of the research institute, told Reuters the scientists had
identified the part of the molecule to which ''we have to direct
antibodies or a drug so that this molecule no longer works.''
``We now know
what to attack. Now it remains simply to do the job of making
sure the molecule does not operate,'' he added.
Darwin is
believed to have contracted the disease in Latin America while
conducting the research that led to his 19th century work ``The
Origin of Species.'' He died at age 73 after a long illness that
included symptoms similar to those experienced by people with
Chagas' disease.
Infected people
will often die 10 to 20 years after being bitten, frequently from
heart failure. Some 16 million to 18 million people around the
world are infected with Chagas' disease and about 50,000 die each
year, according to the US Centers for Disease Control and Prevention.
The parasite
is spread to humans when an infected bug bites a person and deposits
feces on the person's skin, usually at night while the person
is sleeping. The person often accidentally rubs the feces into
the bite wound, an open cut, the eyes or mouth.
Reference
Source 89
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