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Post Info TOPIC: GT3's - (and more so, maybe "certain" GT3 sub-types) - perhaps why we have most often been considered "hard to treat"
Tig


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RE: GT3's - (and more so, maybe "certain" GT3 sub-types) - perhaps why we have most often been considered "hard to treat
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I honestly don't know how anyone or anything could resist you, Chuck! That virus couldn't keep you down for long, just a few decades and it got wise to your plan and hauled butt!

It continues to amaze me why it took so long for them to realize that GT 1 wasn't the worst of the bunch. Maybe it was the prevalence of it, or lack thereof that kept them thinking GT3 was rare and therefore not as concerning. I don't know honestly. I've seen so much over the years, I'm not sure where their head was at during those darkest days. Whatever the case, I'm happy they figured it out and have placed their boot on the throat of the Dragon with 3 heads before more suffered the complexity it delivered.

Cheers to all that have thus far vanquished the Beast...



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Tig

63 yo GT1A - 5 Mil - A2/F3 - (1996) Intron A - Non Responder, (2013) Peg/Riba/Vic SOT:05/23/13 EOT:12/04/13 SVR 5+ years!

Hep C FAQ Lab Ref. Ranges HCV Resistance

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Another study regarding rare resistance effects for certain GT3's.

Helio - HCV Next

IN THE JOURNALS

Common polymorphism responsible for HCV genotype 3 resistance to Sovaldi

Researchers identified a common polymorphism and a rare variant combination in hepatitis C genotype 3 that are responsible for a reduced response to Sovaldi, according to a study published inGastroenterology.

Studies on [Sovaldi] resistance have been hampered by theextraordinary efficacy of the drug,which has led to very few treatment failures,Peter A.C. Wing, PhD,from the Queen Mary University of London in the United Kingdom, and colleagues wrote. Our analysis shows that reduced response to [Sovaldi] may occur if multiple viral polymorphisms are combined.

To evaluate resistance to Sovaldi (sofosbuvir, Gilead Sciences) as well as ribavirin, Wing and colleagues used capture-fusion assays to assess 14 samples of HCV genotype 3. Ten of the samples were from treatment-naive patients with advanced liver disease, while the other four were from patients who had shown response in early access programs or in vitro testing.

They found that alanine at position 150 was particularly common (40.55%) along with the valine variant (36.66%). At position 206, lysine demonstrated a frequency of 76.31% and glutamic acid presented at a frequency of 12.74%. However, an analysis of the combination of polymorphisms (A150V and K206E) showed both were present in less than 4% of the population.

Using transient replicon assay, the researchers found that each common polymorphism correlated with an eightfold reduction in sensitivity to sofosbuvir and the combination correlated with a reduced sensitivity of more than 35-fold.

The effect of these polymorphisms on ribavirin sensitivity ranged from 10-fold for K206E to more than 40-fold for A150V, but in combination, the effect was enhanced to approximately 70-fold.

For treatment naive patients, responses to [sofosbuvir] based treatments are so effective that any impact of these viral variants is likely to be minimal and we would not recommend that such patients undergo pre-treatment resistance testing, Wing and colleagues concluded. For patients who have been exposed to multiple drug regimens (including interferon and NS5a inhibitors that can lead to resistance associated polymorphisms) we speculate that the polymorphisms identified here might be of significance and wesuggest that pre-treatment viral sequencingmay be useful in selecting the optimal regimen for such patients. by Talitha Bennett

Disclosure:Wing reports no relevant financial disclosures. Please see the full study for all other authors relevant financial disclosures.



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HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 64 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

(SEE UPDATES IN BIO)



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GT3's - (and more so, maybe "certain" GT3 sub-types) - perhaps why we have most often been considered "hard to treat"
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Published inGastroenterology

Journal Scan/ResearchMay 20, 2019

Resistance Analysis of Genotype 3 HCV Indicates Subtypes Inherently Resistant to Nonstructural Protein 5A Inhibitors

Hepatology (Baltimore, Md.)

TAKE-HOME MESSAGE



__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 64 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

(SEE UPDATES IN BIO)

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