Ribavirin mechanism
Common Questions and Answers about Ribavirin mechanism
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When ribavirin is used in conjunction with IFN-α, induction of specific ISGs is synergistic when compared with either drug applied separately. Direct up-regulation of these antiviral genes by ribavirin is mediated by a novel mechanism different from those associated with IFN signaling and intracellular double-stranded RNA sensing pathways such as RIG-I and MDA5. RNA interference studies excluded the activation of the Toll-like receptor and nuclear factor κB pathways in the action of ribavirin.
The interferon (IFN)-free regimen of sofosbuvir and ribavirin for 24 weeks was recently approved to treat chronic hepatitis C virus (HCV) genotype 1 (GT-1) infection for patients ineligible for IFN. However, sofosbuvir plus ribavirin therapy is associated with relapse in 15% to 30% of patients with HCV GT-1. Neither the mechanism of relapse nor the optimal re-treatment strategy for these patients is defined.
It's an approximate computation based on the half life of ribavirin which is quite long. My guess it's probably a bit on the conservative side but why take a risk when potential birth defects are involved.
Despite the presence of conflicting results, accumulating data from several in vivo studies support the concept of ribavirin-induced HCV mutagenesis as a possible mechanism of action in patients with chronic hepatitis C. However, several precautions should be taken. Firstly, the fact that ribavirin leads to a significant decline of ALT levels when administered as monotherapy is not sufficiently explained by the lethal mutagenesis hypothesis.
Ribavirin is an antiviral drug. It is used in combination with interferon for the treatment of chronic hepatitis C. Although the exact mechanism of its action is unknown, it is thought to interfere with the production and/or action of viral DNA and RNA which are critical to the survival and multiplication of the virus.
GENERIC: no
PRESCRIPTION: yes
PREPARATIONS: Capsule: 200 mg.
STORAGE: Ribavirin should be refrigerated at 2-8 C (36-46 F).
Not a question but a comment about hep C. Am at 24 weeks and just got results back...virus undetectable. I'm genotype 1, over 60, and long term. Dr. has me on peginterferon + ribavirin. At 12 weeks, just barely 2 log drop. Then started daily Vitamin D supplements (5000mg) after reading latest studies. Doc was hesitant but agreed. Now says was good idea. I hope this helps someone out their. Just hoping no relapse for next 24 weeks.
s decision of approval status is expected by May 23, 2011. I hear that this med in combination with the pegylated interferon and ribavirin could boost the sustained response rate above 70%..
This is a rather detailed and complicated article about ribavirin and its role in HCV treatment. It's a Medscape article so you must be registered to view. Registration is easy and free and worth the effort.
I will paste the beginning paragraph of the article so you'll have an idea of what you're getting into.
The mechanism by which the IL28B genotype mediates pegylated interferon/ribavirin treatment response in HCV genotype 1 is not yet understood and is the subject of intense research. The impact of the IL28B polymorphism on response rates in HCV genotypes other than genotype 1 is still being investigated.
It is approved for treatment of cryptosporidiosis and lambliasis in the United States. In vitro nitazoxanide was shown to inhibit HCV replication and the mechanism of action was proposed to be induction of double-strand RNA activated protein kinase.118 In a placebo-controlled study monotherapy with nitazoxanide for 24 weeks led to a mean reduction of HCV-RNA viral load in genotype 4-infected patients by 1.55 log10 IU/mL with 30% of patients having undetectable HCV RNA at the end of treatment.
WEEK 28 INTERIM ANALYSIS
M. Shiffman1, A. Ahmed2, I. Jacobson3, R. Pruitt4, E.
“The current standard anti-HCV treatment, which combines pegylated interferon-alpha with ribavirin, is effective in only about 50% of patients and is often associated with severe side effects. Because of the unique mechanism of action of SPC3649 and its tolerability profile, this new therapy could have the potential to replace interferon to treat disease progression or be combined with current treatments.
I don't think that the mechanism of ribavirin induced anemia is known. We do know it accumulates in red cells. But when does that happen? is it in the bone marrow where the cells originate or does it happen later on? I am not saavy enough to understand much about this.
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