Case report of intravenous milkthistle as antiviral

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Aquar1us

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Found this paper when searching for milkthistle's effects at reducing immune activation (through its NF-kB inhibition) - Although as it turns out it works via affecting glucose metabolism as well:

Successful HCV eradication and inhibition of HIV replication by intravenous silibinin in an HIV–HCV coinfected patient
www.ncbi.nlm.nih.gov/pubmed/20709593
Abstract
Introduction: The efficacy of antiviral therapy with pegylated interferon (PEGIFN) plus ribavirin (RBV) in patients with HIV and hepatitis C virus (HCV) coinfection is limited. Intravenous silibinin (ivSIL), a milk thistle extract with proven antiviral effects represents a novel therapeutic strategy for virological nonresponders.
Methods: We report a case of an HIV–HCV coinfected patient, who has not responded to a prior course of PEGIFN-α2a (180 μg/week/s.c.) and RBV (1000 mg/day/p.o.). Testing for IL-28β small nucleotid polymorphism revealed the nonfavourable genotype T/T. Antiretroviral therapy was not prescribed because the patients presented with well-preserved CD4+ cell counts and low HIV-RNA levels. She received retreatment with ivSIL for two weeks followed by PEGIFN/RBV combination therapy starting at week 1.
Results: After 2 weeks of ivSIL therapy both HCV-RNA and HIV-RNA become undetectable. On ivSIL monotherapy we noticed a trend towards an increase of CD4+ cell counts and a decrease of HIV-RNA. After 16 weeks PEGIFN + RBV was discontinued due to patients wish because of adverse events. HCV-RNA was still negative 24 weeks after cessation of therapy, while HIV-RNA returned to baseline levels.
Conclusion: ivSIL may represent a potential treatment option for retreatment of HIV–HCV coinfected patients nonresponding to PEGIFN + RBV combination therapy. Further investigations on the possible beneficial effects of ivSIL on CD4+ cell counts and HIV-RNA levels are necessary.

Received: May 12, 2010; Received in revised form: July 1, 2010; Accepted: July 6, 2010; Published Online: August 16, 2010
DOI: http://dx.doi.org/10.1016/j.jcv.2010.07.006 B.A. Payer, T. Reiberger, K. Rutter, S. Beinhardt, A.F. Staettermayer, M. Peck-Radosavljevic, P. Ferenci Medical University of Vienna, Department of Internal Medicine III, Division of Gastroenterology & Hepatology, Waehringer Guertel 18-20, A1090 Vienna, Austria
 
Silibinin resistance is possible though... albeit, I can't find a clinical case for it.
http://www.ncbi.nlm.nih.gov/pubmed/23322644

Got to love/hate viruses yeh?
truth! I am so into viruses atm... I just love the way they play fast and loose with all the ways and tricks having and transforming and dealing with the genetic information in DNA and RNA... taking the 'central dogma' of molecular biology and BANISHING IT LIKE A BOSS 😎:astronaut:
although clinical HCV subtype 1 (the one that's more vulnerable to silibinin) is the harder to deal with to begin with, so there is that kind of value
they mention a silibinin resistance case in the paper you gave, only in passing though
for HCV/HIV coinfection you have that recovery of CD4 numbers to factor in also... this will increase the immune response and cooperate with the antiviral effect
'Previous studies suggested multiple antiviral mechanisms of SIL; however, the dominant mode of action has not been determined.'
gotta love (non-nuke) antivirals too
(well I just think they're more interesting)

what interested me most is the effect on HIV... there are several mechanisms for silibinin's anti-HIV action, and I think entry inhibition is one of them... theoretically HIV could resist this; but silibinin also decreases glucose metabolism in T-cells, and decreases proliferation by antagonizing NF-kB - and this simply reduces the number of cells HIV can infect. no resistance, because you're not attacking HIV directly. such anti-hiv therapies fascinate me most
 
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There are so many new drugs in the treatment of HCV, I don't see this catching on at all, especially since they have something like 90+% cure rates even for the incredibly resistant HCV genotype 1. Since 2012 alone, I think 3-4 drugs have come to market, including ones that rid of using pegylated interferon altogether, usually the biggest culprit in side effects/non-compliance/cessation of treatment.

Oral silibinin has also been found to be completely ineffective at treating HCV.
 
Oral silibinin has also been found to be completely ineffective at treating HCV.
because it has low oral avilability and so only cultivates resistant virus... you need to eliminate the virus in one go, with a strong bioavailable formulation. There are some better ones using lecithin for better mobilisation of the lipophilic silimarin. or possibly liposomes

the main use for silimarin I see however is as an immune deactivator, potentialy useful against HIV.

Silibinin inhibits HIV-1 infection by reducing cellular activation and proliferation.

Abstract
Purified silymarin-derived natural products from the milk thistle plant (Silybum marianum) block hepatitis C virus (HCV) infection and inhibit T cell proliferation in vitro. An intravenous formulation of silibinin (SIL), a major component of silymarin, displays anti-HCV effects in humans and also inhibits T-cell proliferation in vitro. We show that SIL inhibited replication of HIV-1 in TZM-bl cells, PBMCs, and CEM cells in vitro. SIL suppression of HIV-1 coincided with dose-dependent reductions in actively proliferating CD19+, CD4+, and CD8+ cells, resulting in fewer CD4+ T cells expressing the HIV-1 co-receptors CXCR4 and CCR5. SIL inhibition of T-cell growth was not due to cytotoxicity measured by cell cycle arrest, apoptosis, or necrosis. SIL also blocked induction of the activation markers CD38, HLA-DR, Ki67, and CCR5 on CD4+ T cells. The data suggest that SIL attenuated cellular functions involved in T-cell activation, proliferation, and HIV-1 infection. Silymarin-derived compounds provide cytoprotection by suppressing virus infection, immune activation, and inflammation, and as such may be relevant for both HIV mono-infected and HIV/HCV co-infected subjects.
 
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