Are opiates bad for hep c?

Answer 1

This is from a study which seems to be saying 'withdrawal' of pain medication, whether a drug addiction, or just a chronic pain patient will escalate the virus.

Similar to what they found in their previous study,3 Ho and his colleagues learned that removing morphine boosted levels of HCV RNA (the genetic material used by the virus) and hepatitis C viral protein in the cells. This, in essence, indicates that the viral infeWithdrawing the morphine also blocked interferon-alfa production in the liver cells compared to cells in which morphine was not withdrawn. Since interferon-alfa is a critical self-defense mechanism used by liver cells to fight off attacks by the hepatitis C virus or HIV, the findings suggest that drug abusers who quit using morphine can weaken their immune system's ability to defend the body against an HCV infection, and provides a favorable environment for hepatitis C viral growth in the liver action is spreading.

Next, Ho's group wanted to understand why removing morphine created such a beneficial environment for the hepatitis C virus. They learned that removing morphine from liver cells blocked the production of interferon-alfa by, in turn, suppressing its activator, interferon regulatory factor-7 (IRF-7). The team also found that the ability of interferon-alfa to block HCV replication (or the model of HCV in this case) fell by nearly two-thirds.

The same detrimental effect of morphine removal also occurred in relation to manmade interferon alfa. This manmade, or recombinant, form is similar to the interferon medication used for people with hepatitis C today. When synthetic interferon was added to the cell lines, they demonstrated a strong ability to fight off the hepatitis virus. However, when morphine was withdrawn from the cells, the anti-HCV ability of interferon-alfa "was significantly diminished," Ho and his colleagues wrote.

These results were observed when morphine was directly withdrawn or indirectly removed by using naloxone, they reported, and even to a greater extent in the latter case.

"Collectively, these new observations in conjunction with our earlier findings support the notion that opioid abuse is a co-factor that promotes HCV replication," wrote Ho and his colleagues.

They recommend both clinical and epidemiological studies be launched to better define the rule of drug abuse in the context of HCV infection. In the meantime, they say drug abusers who use such opioids as morphine, followed by periods of withdrawal due to lack of supplies, may be doing much more harm to their livers.

"Our findings provide a plausible interpretation of the high failure rate of interferon-alfa therapy in intravenous drug users," the investigators concluded. "The identification of mechanism(s) involved in morphine's action on the anti-HCV effect of interferon-alfa has the potential to improve interferon-alfa-based treatment for HCV-infected IV drug users."

Until recently, there were no data on the effects of opiates on HCV replication or the development of liver injury and fibrosis, one of the earliest features of progression to cirrhosis," wrote Moore and Dusheiko.

"The growing implication from these and other studies is that continued opiate abuse leads to enhanced viral replication, liver injury, and … fibrosis. Further studies are required to determine whether these effects occur in humans, as well," they wrote.