A key protein previously implicated in Lou Gehrig's disease and other
neurological diseases plays an important role in the response to viral
infection, according to a study led by scientists from the Icahn School
of Medicine at Mount Sinai published today in Nature Immunology.
Neurological diseases have long been associated with inflammation,
part of the body's response to injury or infection that occurs when
immune cells home in to attack invaders like bacteria and viruses, and
to drive healing, but the link between them has not been understood.
This new study result suggests that genetic changes take away the
ability of a protein called senataxin to moderate the inflammatory
response to certain viral infections, possibly leading to persistent
inflammation that could aggravate disease progression.
Using cutting-edge genomic tools, the scientists found that
senataxin is deployed to quench the body's natural antiviral response at
a specific point; without such control, prolonged exposure to the
antiviral response can lead to inflammation. People with
senataxin-related forms of ALS and ataxia have a defective SETX gene
that leads to a dysfunctional form of the protein.
neurological diseases plays an important role in the response to viral
infection, according to a study led by scientists from the Icahn School
of Medicine at Mount Sinai published today in Nature Immunology.
Neurological diseases have long been associated with inflammation,
part of the body's response to injury or infection that occurs when
immune cells home in to attack invaders like bacteria and viruses, and
to drive healing, but the link between them has not been understood.
This new study result suggests that genetic changes take away the
ability of a protein called senataxin to moderate the inflammatory
response to certain viral infections, possibly leading to persistent
inflammation that could aggravate disease progression.
Using cutting-edge genomic tools, the scientists found that
senataxin is deployed to quench the body's natural antiviral response at
a specific point; without such control, prolonged exposure to the
antiviral response can lead to inflammation. People with
senataxin-related forms of ALS and ataxia have a defective SETX gene
that leads to a dysfunctional form of the protein.
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