By Will Boggs, MD
NEW YORK (Reuters
Health) - A newly discovered gene that allows immune molecules
to attach to virus-fighting cells may explain why some mice are
susceptible to infection with cytomegalovirus (CMV) and others
are not, researchers report.
CMV is the
leading cause of viral disease at birth and an important cause
of infections in people with weak immune systems. Knowing what
makes mice vulnerable to CMV infection should increase our understanding
of the disease in humans, according to Dr. Silvia M. Vidal from
University of Ottawa, Ontario, Canada and associates.
The investigators
looked for genetic differences in strains of mice that were susceptible
or resistant to infection by CMV, focusing on an area on chromosome
6 previously linked to an increased risk of CMV infection.
According
to results published in the May issue of Nature Genetics, CMV
vulnerability stems from defects or losses of Klra8, a member
of the Klra gene family. This family of genes controls the landing
sites--or receptors--on immune cells called natural killer (NK)
cells for molecules that help fight viruses and tumor cells.
When these
marker molecules bind to the landing site, the researchers suggest,
they activate a snowball effect of responses by the NK cell that
result in the death of the invading virus, thereby preventing
spread of the infection. Without a normal Klar8, susceptibility
to CMV infection results, due to the lack of these landing sites.
Humans have
genes with similar functions on chromosomes 12 and 19, the authors
note, so investigation of those genes might clarify why some people
are predisposed to CMV infection and others are not.
``In the future,
we expect this knowledge to contribute to rationale for a cure,''
Vidal told Reuters Health. ``Presently, there is neither a vaccine
nor a cure for cytomegalovirus infection.''
This is the
first genetic evidence that NK cells play such a key role in resisting
viral infection, note Dr. Jean-Laurent Casanova and associates
from University of Paris, France, in a related commentary.
Still, the
editorialists conclude, ``Whether human activating NK receptors
confer protection from human CMV and whether symptomatic patients
lack these receptors remains to be determined.''
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