WEDNESDAY, July 7 (HealthDay News) -- U.S. scientists believe
they are getting closer to understanding how the herpes simplex
virus invades cells, potentially providing a target for new drugs
to fight the virus, researchers say.
The scientists used advanced imaging technologies to learn more
about the structure and function of the cell-entry protein complex
used by the herpes simplex virus type 2 (HSV-2), which causes
Complications of this sexually transmitted disease include
recurrent painful genital sores, mental distress and, if
transmitted from mother to child, potentially fatal infections in
The new research may "help us answer some of the many questions
about how herpes virus initiates infection," first author Tirumala
K. Chowdary, a postdoctoral associate at Tufts University School of
Medicine, explained in a university news release. "Knowing the
structures of cell-entry proteins will help us find the best
strategy for interfering with this pervasive family of viruses,"
The study was released online July 4 in advance of publication
in an upcoming print issue of the journal
Nature Structural & Molecular Biology.
"Most viruses need cell-entry proteins called fusogens in order to invade cells," explained senior author Ekaterina Heldwein, an assistant professor in the molecular biology and microbiology department at Tufts.
But the herpes virus also requires a complex of two other
proteins to aid its entry into the human cell. It was thought that
these proteins were also fusogens, but the new research shows that
they are not, Heldwein said.
This unexpected finding suggests that these proteins may help
regulate the fusogen. The team noted that certain antibodies appear
to interfere with the activity of this complex, and this is
"evidence that antiviral drugs that target this interaction could
prevent viral infection," Heldwein explained.
The U.S. National Institute of Allergy and Infectious Diseases
has more about