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New strategy for inhibiting virus replication
Date:8/14/2009

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A cell contains numerous variants of cyclophilins that are inhibited by cyclosporin and cyclosporin derivatives. The research team from Heidelberg analyzed liver cells to determine which cyclophilin is critical for hepatitis C virus replication. They found that only blocking cyclophilin A leads complete inhibition of virus replication and this cyclophilin is also the target of DEBIO-025.

Two complementary effects are responsible for the inhibition of hepatitis C virus replication: cyclophilin A is required both for the formation of the viral replication machinery and for the activity of a viral enzyme that is essential for the assembly of infectious virus particles. Inhibiting cyclophilin A with DEBIO-025 thus blocks hepatitis C virus replication from two different sides. By contrast, blocking cyclophilin B had no effect.

"The therapeutic potential of inhibiting cellular factors essential for virus replication has thus far hardly been tapped," explains Professor Bartenschlager. "But this approach has the major advantage that resistance arises less frequently and to a lesser extent in comparison to therapies directly targeting viral factors."


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Contact: Dr. Ralf Bartenschlager
Ralf_Bartenschlager@med.uni-heidelberg.de
062-215-64569
University Hospital Heidelberg
Source:Eurekalert

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