LEEDS (UK)—Common drugs used to treat conditions such as diabetes and obesity appear to also successfully treat hepatitis C.
New research finds the anti-diabetic drug Metformin, and AICAR, used to combat obesity, can prevent the hepatitis C virus from replicating in the body.
Recovery rates for hepatitis C, which affects the liver, are low—only around 40 percent of sufferers fully recover, with others developing cirrhosis and in many cases, liver cancer.
An estimated three percent of the world’s population are affected. There are four million carriers of the virus in Europe alone.
“We’re very excited about these findings,” says Mark Harris, professor of biological sciences at the University of Leeds.
“These drugs are already on the market, and whilst substantial clinical trials still need to take place before they can be used to treat hepatitis C infection, we think it could be an enormous step forward in the battle against the virus.”
Drugs such as Metformin and AICAR work by stimulating an enzyme called AMP kinase (AMPK) which regulates energy within cells—the very enzyme that hepatitis C virus represses to enable it to replicate.
AMPK’s usual function is to conserve the energy balance in cells, which it does by temporarily shutting down the production of lipids (fats) and membranes when it senses an increase in energy requirements.
In his research, Harris has shown that the hepatitis C virus switches off AMPK so that the cell continues production of lipids and membranes, both of which are vital to its survival.
“You’d expect AMPK to be activated when a cell becomes infected by a virus, because it would sense the increase in energy required to enable the virus to replicate,” he says.
“In such cases, AMPK would shut down certain functions of the cell temporarily until the cell’s energy is rebalanced. We found that hepatitis C virus, because it needs lipids and membranes, causes the opposite to happen.”
Building on this finding, researchers were able to examine how cells would react when treated with common drugs that stimulate AMPK. They found that in infected cells, the drugs were able to halt virus replication, enabling cells to clear the infection.
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