My watch list
my.bionity.com  
Login  

Hepatitis C virus hijacks liver microRNA

Mechanism explains how virus survives in the liver and how a new antiviral works

04-Jan-2012

Viral diseases are still one of the biggest challenges to medical science. Thanks to thousands of years of co-evolution with humans, their ability to harness the biology of their human hosts to survive and thrive makes them very difficult to target with medical treatment.

Scientists at the University of North Carolina at Chapel Hill, working with colleagues from the University of Colorado, have shown for the first time how a small RNA molecule that regulates gene expression in human liver cells has been hijacked by the hepatitis C virus to ensure its own survival – helping medical scientists understand why a new antiviral drug appears to be effective against the virus.

MicroRNAs are involved in regulating the expression of genes in cells, usually by blocking the production of key proteins or by destabilizing the messenger RNAs that encode the cell's proteins as it grows and divides. Normally they act by downregulating gene expression. The research team found that the binding of a prominent microRNA in liver cells, called miR-122, to the viral RNA results in its stabilization, promoting efficient replication of the virus genome in the liver and supporting the virus' lifecycle.

"The hepatitis C virus has done two very interesting things with miR-122," says Stanley M. Lemon, MD, professor of medicine and microbiology and immunology and a member of UNC Lineberger Comprehensive Cancer Center and the Center for Translational Immunology.

"First, it has evolved a unique relationship with a key regulator, since miR-122 represents about half of all microRNAs present in the liver. Second, the virus has usurped a process that usually downregulates gene expression to upregulate the stability of its RNA and expression of viral proteins needed for its lifecycle. It's a classic example of how viruses subvert normally beneficial functions of the cell to their own nefarious purposes."

Work by Dr. Lemon and his colleagues in 2005 helped to demonstrate that miR-122 was required for hepatitis C to replicate itself, but the mechanism was not understood. Now the UNC research team has shown how it works, which helps to explain how a new experimental antiviral drug target the virus. The drug, called an "antagomer", binds to miR-122 and sequesters it in the liver and thus destabilizes the viral genome, accelerating its degradation in the liver. Results of the most recent study are published in Proceedings of the National Academy of Sciences.

Facts, background information, dossiers
More about University of North Carolina at Chapel Hill
  • News

    The science of fluoride flipping

    So much of what happens inside cells to preserve health or cause disease is so small or time-sensitive that researchers are just now getting glimpses of the complexities unfolding in us every minute of the day. UNC School of Medicine researchers have discovered one such complexity -- a prev ... more

    How a cancer gene protects genome organization

    UNC School of Medicine researchers have cracked a long-standing mystery about an important enzyme found in virtually all organisms other than bacteria. The basic science finding may have implications for understanding cancer development and how to halt it. Researchers have known that the en ... more

    A gene's journey from covert to celebrated

    Like a bank robber on the lam, Gpr182 had assumed a variety of identities over several decades: G10D, HrhAMR, Gamrh, 7TMR, ADMR. Unable to put a finger on what exactly the gene does, scientists largely left it alone. The protein it codes for was designated an "orphan" receptor -- a lock on ... more

  • Videos

    Multiplexed optogenetic control, using PA- Vav2 and PI-Rac1 in the same cell

    Multiplexed optogenetic control, using Photo-inhibitable Vav2 (PA-Vav2) and Photo-inhibitable Rac1 (PI-Rac1) in the same cell.Upon irradiation, area and roundness changed as they did in response to PA-Vav2 alone, but edge dynamics were clearly reduced, unlike response to either PA-Vav2 alon ... more

  • Universities

    University of North Carolina at Chapel Hill

    Carolina’s vibrant people and programs attest to the University’s long-standing place among leaders in higher education since it was chartered in 1789 and opened its doors for students in 1795 as the nation’s first public university. Situated in the beautiful college town of Chapel Hill, N. ... more

More about University of Colorado
  • News

    Association between gene mutation and rare heart disease found

    A strong association between a genetic mutation and a rare kind of heart muscle disease has been discovered by researchers at the University of Colorado Anschutz Medical Campus. The finding could improve understanding of the disease and lead to new treatments. "There are many kinds of cardi ... more

    A new window on mitochondria division

    A new University of Colorado Boulder study shows for the first time the final stages of how mitochondria, the sausage-shaped, power-generating organelles found in nearly all living cells, regularly divide and propagate. In 2011, CU Boulder Associate Professor Gia Voeltz and her colleagues s ... more

    Engineers transform brewery wastewater into energy storage

    University of Colorado Boulder engineers have developed an innovative bio-manufacturing process that uses a biological organism cultivated in brewery wastewater to create the carbon-based materials needed to make energy storage cells. This unique pairing of breweries and batteries could set ... more

  • Universities

    University of Colorado

    As the flagship university of the state of Colorado, CU-Boulder is a dynamic community of scholars and learners situated on one of the most spectacular college campuses in the country. more

Your browser is not current. Microsoft Internet Explorer 6.0 does not support some functions on Chemie.DE