Rockefeller Scientists Illuminate Role of miR-122 in Hepatitis C Infections

In the battle between a cell and a virus, either side may resort to subterfuge. Molecular messages, which control the cellular machinery both sides need, are vulnerable to interception or forgery. New research at Rockefeller University has revealed the unique twist on just such a strategy deployed by the liver-infecting hepatitis C virus - one that may help explain the progression of liver disease and that the researchers suspect may be found more widely in the world of disease-causing viruses. Led jointly by Dr. Charles Rice, the Maurice R. and Corinne P. Greenberg Professor in Virology and Head of the Laboratory of Virology and Infectious Disease and Dr. Robert Darnell, Senior Attending Physician, Robert and Harriet Heilbrunn Professor, and Head of the Laboratory of Molecular Neuro-Oncology, the research was published online on March 12, 2015 in Cell. It employed a powerful combination of techniques to map the interactions between the hepatitis C virus and a small piece of genetic material - known as miRNA-122 - that is produced almost exclusively by liver cells, which normally use it to regulate expression of their own genes. "It is well known that once inside a liver cell, the hepatitis C virus must bind to miRNA-122 in order to establish a persistent infection. We found an unanticipated consequence of this interaction: By binding to miRNA-122, the virus acts like a sponge, soaking up these gene-regulating molecules," says first author Joseph Luna, a graduate student with a joint appointment in the labs. "Our experiments showed this has the effect of skewing gene activity in infected liver cells." The fight between an infecting virus and its host is often viewed as proteins fighting like soldiers.
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