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Multitasking May Be Achilles Heel for Hepatitis C

Despite its tiny genome, the hepatitis C virus packs a mean punch. The virus is a microcosm of efficiency, and each of its amino acids plays multiple roles in its survival and ability to sidestep attack. But new research from Rockefeller University suggests that this fancy footwork and multitasking could be the key to bringing down the virus. The work, which focuses on a once-ignored protein, provides insights on how drug therapy for sufferers of the disease might be improved.

The protein, NS2, which is one of the 10 proteins that make up the hepatitis C virus, gained momentum as a plausible drug target in 2006, when Charles M. Rice, head of the Laboratory of Virology and Infectious Disease, and his team solved the structure of its protease domain. The domain spans the second half of NS2 and acts like a molecular scissor, cleaving itself from its neighbor, NS3. (At first, the 10 proteins that make up the virus are strung together in a continuous chain, which is later cleaved by various enzymes.) By that time, it's also known to aid in the production of infectious virus particles.
 
 

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