Map of herpes virus protein suggests new target for antiviral drugs
July 7th, 2010 - 5:28 pm ICT by ANILondon, July 7 (ANI): Researchers have uncovered the unusual structure of the protein complex that allows a herpes virus to invade cells.
This detailed map of a key piece of the herpes virus “cell-entry machinery” gives scientists a new target for antiviral drugs.
The study appears online in Nature Structural & Molecular Biology.
Senior author Ekaterina Heldwein, assistant professor in the molecular biology and microbiology department at Tufts University School of Medicine, said: “Most viruses need cell-entry proteins called fusogens in order to invade cells. We have known that the herpes virus fusogen does not act alone and that a complex of two other viral cell-entry proteins is always required. We expected that this complex was also a fusogen, but after determining the structure of this key protein complex, we found that it does not resemble other known fusogens,”
“This unexpected result leads us to believe that this protein complex is not a fusogen itself but that it regulates the fusogen. We also found that certain antibodies interfere with the ability of this protein complex to bind to the fusogen, evidence that antiviral drugs that target this interaction could prevent viral infection,”
Jeremy M. Berg, director of the US National Institute of General Medical Sciences (NIGMS) at the National Institutes of Health, said: “Katya Heldwein’s work has resulted in a map of the protein complex needed to trigger herpes virus infection. The NIH Director’s New Innovator Awards are designed to support such breakthroughs. This research not only adds to what we know about how herpes viruses infect mammalian cells, but also sets the stage for new therapeutics that restrict herpes virus’s access to the cell,”
“We hope that determining the structure of this essential piece of the herpes virus cell-entry machinery will help us answer some of the many questions about how herpes virus initiates infection. Knowing the structures of cell-entry proteins will help us find the best strategy for interfering with this pervasive family of viruses,” said first author Tirumala K. Chowdary, PhD, a postdoctoral associate in the department of molecular biology and microbiology at TUSM and member of Heldwein’s lab. (ANI)
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