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Morphine Withdrawal Complicates Hepatitis C Infection in Drug Abusers

Hepatitis C, a condition that leads to inflammation of the liver is common among intravenous drug users. There are nearly 70-80 % of abusers are suffering from // the disease in the United States.

This high association has generated interest in determining the effects of drug abuse, specifically opiates, on progression of the disease. The discovery of such an association would impact treatment of both HCV infection and drug abuse. It has now been established from a recent study that morphine withdrawal complicates the Hepatitis C infection by suppressing IFN-alpha-mediated immunity and enhancing virus replication.

It has previously been shown using cell culture techniques that morphine enhances virus replication and inhibits IFN-alpha (a natural anti-viral factor produced by immune, as well as host cells, and the only one approved in recombinant form for treating HCV infection).

The researchers examined the effects of morphine withdrawal (MW) on HCV-infected cultured liver cells by exposing cells to the drug for four days followed by its removal. They also assessed the effects of using naloxone.

To measure HCV replication, they used a virus-like “replicon” that mimics the events that occur in liver cells. Although the replicon does not produce the infectious virus, the HCV replicon system represents the best available system for examining the impact of opiates on HCV at the time of the study.

It was found that there was an increase in the number of HCV replicon in both the withdrawal scenario. Furthermore, there was an inhibition of the IFN-alpha expression in liver cells in the presence or absence of HCV replicon in both the cases.

Since IFN-alpha is a critical self-defense mechanism utilized by liver cells to fight off viral infection, including HIV, this study suggests that morphine withdrawal weakens host cell immunity and provides a favorable environment for HCV growth in the liver. The s
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