New
research has identified a new mechanism that plays a role in controlling how
the herpes virus alternates between dormant and active stages of infection.
The
herpes virus causes cold sores and genital sores, as well as life-threatening
infections in newborns, encephalitis and corneal blindness.
Treatment
of the virus is difficult, because it hides out in nerve cells and emerges
months or years later to reactivate the infection.
When
the herpes virus enters a cell, the cell tries to protect itself by wrapping
the viral DNA tightly around spool-like proteins called histones and condensing
it into chromatin, which causes the virus to go dormant. But if the cells are
unsuccessful, the chromatin is only loosely bundled, leaving the viral DNA
accessible. The virus particles can then turn on their genes and replicate
using the cell's machinery to start a lytic infection, causing disease.
The
researchers showed that the dynamics of the chromatin regulate whether the
entire herpes virus genome is turned on, which must occur before any individual
genes can be expressed. This new mechanism represents a previously overlooked
way to regulate gene expression at the level of the entire viral chromosome.
The
discovery opens up new directions for exploring how the virus reactivates after
lying dormant. Herpes' ability to lay low has thwarted efforts to create
effective vaccines or antiviral drugs that fully prevent or cure the infection.
See:
Posted by Dr. Tim Sandle, Pharmaceutical Microbiology Resources (http://www.pharmamicroresources.com/)
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