I will be adding 20 mg of Fluvastatin (leschol) to my therapy (alinia, infergen, riba) and from reading the studies I was under the impression that statins reduce viral load by interfering with how the virus can utilize cholesterol from the host. But I recently came across this little scientific nugget http://tinyurl.com/23hgdg which says that statins actually act as immunomodulators of the immune system. What are your thoughts? Is it cholesterol synthesis or immunemodulation that statins perform in the war on hep c?
You might be interested in the link below. I believe that the reseaon given for statins working
"cell membrane protein composition conducive to HCV replication" is the same reason as to why it took so long to grow HCV in the Lab. Add the proteins and bingo.
You would basically be conducting your own trial, with all the risks that entails and without any of the backup. So laying your hands on the full studies would be a good idea.
The quatities require might be higher than what you could rerasonably be expected to take though.
In 2003, researchers reported that lovastatin administered to human hepatoma cells significantly
reduced the normal hepatitis C virus (HCV) RNA replication rate by 70% after 24 hours and by 95% after 72 hours regardless of viral genome variation.
Statins regulate cholesterol by blocking the mevalonate pathway, which is also responsible for maintaining a cell membrane protein composition conducive to HCV replication. However, the authors noted that lovastatin would have to be delivered to the liver in doses much higher than are currently used in order to achieve a reduction in HCV replication, which raises concerns about toxicity.
As CS pointed out correctly, statins might require higher doses than you could tolerate to exert their anti HCV effect in vivo.
Hepatology. 2007 Apr;45(4):895-8.
Atorvastatin does not exhibit antiviral activity against HCV at conventional
doses: a pilot clinical trial.
O'Leary JG, Chan JL, McMahon CM, Chung RT.
Gastrointestinal Unit, Department of Medicine, Harvard Medical School,
Massachusetts General Hospital, Boston, MA, USA.
Cholesterol biosynthesis is an integral part of HCV RNA replication. Not only
does HCV RNA replicate on lipid rafts, but it also requires cholesterol
intermediates to replicate. In addition, it has been shown in vitro that several
HMG-CoA reductase inhibitors can decrease HCV RNA replication by > or = 1 log.
Therefore, we designed a clinical trial to evaluate the effect of atorvastatin on
HCV RNA levels. In this prospective clinical trial, where patients served as
their own control, 10 HCV-infected patients who required treatment for high
cholesterol were given 20 mg atorvastatin per day. Although serum cholesterol and
LDL predictably decreased significantly, there was no statistically significant
change in week 4 and week 12 HCV RNA levels compared to pretreatment HCV RNA
levels by the paired Student t test. It is unclear whether the addition of an
HMG-CoA reductase inhibitor to interferon or a more potent inhibitor of
cholesterol biosynthesis may be required to inhibit HCV RNA replication in vivo.
In conclusion, atorvastatin, and likely all HMG-CoA reductase inhibitors, does
not inhibit HCV RNA replication in vivo at conventional doses.
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