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Viral diseases are still one of the biggest challenges to medicalscience. Thanks to thousands of years of co-evolution with humans,their ability to harness the biology of their human hosts tosurvive and thrive makes them very difficult to target with medicaltreatment. Scientists at the University of North Carolina at Chapel Hill,working with colleagues from the University of Colorado, have shownfor the first time how a small RNA molecule that regulates geneexpression in human liver cells has been hijacked by the hepatitis C virus to ensure its own survival - helping medical scientistsunderstand why a new antiviral drug appears to be effective againstthe virus. MicroRNAs are involved in regulating the expression of genes incells, usually by blocking the production of key proteins or bydestabilizing the messenger RNAs that encode the cell's proteins asit grows and divides. Normally they act by downregulating geneexpression. The research team found that the binding of a prominentmicroRNA in liver cells, called miR-122, to the viral RNA resultsin its stabilization, promoting efficient replication of the virusgenome in the liver and supporting the virus' lifecycle. "The hepatitis C virus has done two very interesting things withmiR-122," says Stanley M. Lemon, MD, professor of medicine andmicrobiology and immunology and a member of UNC LinebergerComprehensive Cancer Center and the Center for TranslationalImmunology. "First, it has evolved a unique relationship with a key regulator,since miR-122 represents about half of all microRNAs present in theliver. Second, the virus has usurped a process that usuallydownregulates gene expression to upregulate the stability of itsRNA and expression of viral proteins needed for its lifecycle. It'sa classic example of how viruses subvert normally beneficialfunctions of the cell to their own nefarious purposes." Work by Dr. Lemon and his colleagues in 2005 helped to demonstratethat miR-122 was required for hepatitis C to replicate itself, butthe mechanism was not understood. Now the UNC research team hasshown how it works, which helps to explain how a new experimentalantiviral drug target the virus. The drug, called an "antagomer",binds to miR-122 and sequesters it in the liver and thusdestabilizes the viral genome, accelerating its degradation in theliver. Results of the most recent study are published online thisweek in the journal Proceedings of the National Academy of Sciences. Hepatitis C is a continuing public health problem, which isdifficult to measure because symptoms occur months to years afterinfection. The Centers for Disease Control and Prevention estimatesas many as 4 million people in the United States may bepersistently infected with hepatitis C virus, and most do not knowthey are infected. More than a third of those who are long-termcarriers may develop chronic liver disease or liver cancer , a deadly form of cancer that is becoming increasingly common due to the spread of thisvirus. Additional References Citations. I am an expert from agmatine-sulfate.com, while we provides the quality product, such as Bodybuilding Nutritional Supplements , Medicinal Plant Extracts, Topical Local Anesthetic,and more.
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