Viruses need living cells for replication and production of virus progeny. Thus far, antiviral therapy primarily targets viral factors but often induces therapy resistance. New improved therapies attempt to targets cellular factors that are essential for viral replication.
The team led by Professor Dr. Ralf Bartenschlager, Director of the Department of Molecular Virology at the Hygiene Institute of Heidelberg University Hospital, has identified a protein in infected liver cells that is essential for hepatitis C virus replication. Inhibiting this protein is highly efficient in blocking virus replication. The study is to be published in the prestigious journal Public Library of Science Pathogens.
Viruses need cellular proteins for replication
More than 170 million people worldwide are affected by chronic hepatitis C. In up to 80 percent of infections, the virus can not be eliminated but persists in the infected individual. These chronically infected persons have a high risk of developing serious liver inflammation, liver cirrhosis and even a liver cell tumor.
Viruses contain only a minimum of genetic material and therefore need a host cell for replication. An essential cell factor required for hepatitis C virus replication is cyclophilin, which promotes the proper folding of proteins and the formation of large protein assemblies. Cyclophilin can be inhibited very efficiently by a drug used primarily in the context of organ transplantation the immunosuppressant cyclosporin. In search for better tolerated drugs to trea chronic hepatitis C, derivatives of cyclosporin were developed that no longer suppress the immune system, but still effectively inhibit cyclophilin. One of these derivatives is DEBIO-025. Although the exact antiviral mechanism by which DEBIO-025 inhibits hepatitis C virus replication is not yet known, clinical studies are already being conducted.
The critical protein is cyclophilin A
|Contact: Dr. Ralf Bartenschlager|
University Hospital Heidelberg