Findings reveal a difference between strains of HCV
- Date:
- June 8, 2017
- Source:
- University of North Carolina Health Care
- Summary:
- For the first time, researchers show how the antiviral class of drugs called NS5A inhibitors interacts with the hepatitis C virus, and these findings show a difference between strains of HCV.
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FULL STORY
Globally, an estimated 71 million
people are living with chronic hepatitis C virus (HCV). Over decades of
infection, chronic HCV infection results in progressive damage to the
liver and an increased risk for end stage liver disease and liver
cancer, making the virus the leading cause of liver-related deaths in
the United States today.
While effective combination therapies have recently been developed,
HCV can evolve to become resistant to these antiviral drugs, potentially
resulting in treatment failures. Resistance is particularly important
for one class of medications used in treatment, for which the mechanism
by which it stops growth of the virus is poorly understood. For the
first time, researchers at the University of North Carolina at Chapel
Hill have identified how the class of antiviral drugs known as NS5A
inhibitors interacts with the virus, and their findings show a
difference between strains of HCV. These results were published in PLOS Pathogens.
"When HCV infects a liver cell, it establishes replication complexes (RCs) within the cell," said David McGivern, Ph.D., lead-author and an associate professor in the UNC Division of Infectious Diseases. "These may be thought of as factories that replicate the virus genetic material. We wanted to understand how long these factories persist in an infected cell after treatment with an NS5A inhibitor."
The research team has shown previously NS5A inhibitors block the formation of new RCs, but do not affect existing RCs, which are ultimately lost from the cell during treatment. The team used NS5A inhibitors to estimate the half-life of the existing RCs and found a difference in the speed of decline depending upon the strain of HCV.
"The majority of people who undergo antiviral treatment clear their HCV infection," said McGivern. "But about 5 percent of people experience treatment failure, often associated with drug resistance. Our findings have potentially important implications for this group of people. Did the treatment fail because replication complexes turned over more slowly? Do some strains of HCV need longer treatment? A better understanding of these issues may lead to more effective therapies active against a broader range of viruses."
"When HCV infects a liver cell, it establishes replication complexes (RCs) within the cell," said David McGivern, Ph.D., lead-author and an associate professor in the UNC Division of Infectious Diseases. "These may be thought of as factories that replicate the virus genetic material. We wanted to understand how long these factories persist in an infected cell after treatment with an NS5A inhibitor."
The research team has shown previously NS5A inhibitors block the formation of new RCs, but do not affect existing RCs, which are ultimately lost from the cell during treatment. The team used NS5A inhibitors to estimate the half-life of the existing RCs and found a difference in the speed of decline depending upon the strain of HCV.
"The majority of people who undergo antiviral treatment clear their HCV infection," said McGivern. "But about 5 percent of people experience treatment failure, often associated with drug resistance. Our findings have potentially important implications for this group of people. Did the treatment fail because replication complexes turned over more slowly? Do some strains of HCV need longer treatment? A better understanding of these issues may lead to more effective therapies active against a broader range of viruses."
Story Source:
Materials provided by University of North Carolina Health Care.
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