"In other words, in patients that respond to treatment, they usually expect to see large viral drops initially, followed by progressively smaller and smaller drops until UND."
I would have been a skeptic too if it hadn't been for the fact that my husband's response to treatment matches that explanation all too well:
wk 0: 17.9 million
wk 4: 9,170
wk 8: 71
wk 12: <50 but detected
Would definitely be an interesting graphic to see the means and averages of response.
I suppose the only real way to learn the how and why would be to consistently test for quasispecies and/or mutants along with VL, but with the current cost of sequencing, no chance of that happening anytime soon...
~eureka
Bill ,I believe it was you who asked if I would be
able to have info on possible mutation from my 28 week boceprevir treatment. I,m happy to report that after I complete the study that info will be given to me.
Yeah, I know Charley....we never quite saw eye to eye on the Methylene Blue thing either. :)
Trinity
"Although the genetic basis for this resistance is unknown, accumulated evidence SUGGESTS that changes in the heterogeneous viral population (quasispecies) may be an important determinant of viral persistence and response to therapy. "
So, maybe . . . . . . maybe not.
Not conclusive but suggestive that the resistant species were present in the initial population.
,
Early changes in hepatitis C viral quasispecies during interferon therapy predict the therapeutic outcome.
P Farci, R Strazzera, HJ Alter, S Farci, D Degioannis, A Coiana, G Peddis, F Usai, G Serra, L Chessa, G Diaz, A Balestrieri, RH Purcell
Despite recent treatment advances, the majority of patients with chronic hepatitis C fail to respond to antiviral therapy. Although the genetic basis for this resistance is unknown, accumulated evidence suggests that changes in the heterogeneous viral population (quasispecies) may be an important determinant of viral persistence and response to therapy. Sequences within hepatitis C virus (HCV) envelope 1 and envelope 2 genes, inclusive of the hypervariable region 1, were analyzed in parallel with the level of viral replication in serial serum samples obtained from 23 patients who exhibited different patterns of response to therapy and from untreated controls. Our study provides evidence that although the viral diversity before treatment does not predict the response to treatment, the early emergence and dominance of a single viral variant distinguishes patients who will have a sustained therapeutic response from those who subsequently will experience a breakthrough or relapse. A dramatic reduction in genetic diversity leading to an increasingly homogeneous viral population was a consistent feature associated with viral clearance in sustained responders and was independent of HCV genotype. The persistence of variants present before treatment in patients who fail to respond or who experience a breakthrough during therapy strongly suggests the preexistence of viral strains with inherent resistance to IFN. Thus, the study of the evolution of the HCV quasispecies provides prognostic information as early as the first 2 weeks after starting therapy and opens perspectives for elucidating the mechanisms of treatment failure in chronic hepatitis C.
Considering over 50% geno 1s fail treatment.........