Yes, thanx for that link. I've bookmarked it, so I'll read it when I want to feel happy.
C
DWBH Thank you for the question, I have had the same question and was thinking of asking. Over the years I have heard so many different opinions, this is great.
Mike - Thank you
Cando - Thank you
I thins the following sums it up pretty well.
"...(4) residual HCV was not detected in plasma or PBMCs of any spontaneous or treatment-recovered subjects or in chimpanzee liver, suggesting that the classic pattern of recovery from HCV infection is generally equivalent to viral eradication...."
http://www.ncbi.nlm.nih.gov/pubmed/22729600.1
So you have a type of hepatitis C (occult) that can't replicate but is detected in some after hepatitis C treatment. Nobody knows if it will do anything but who knows because nobody really knows what it is.
I will spend no time worrying about what if or might happen.
DWBH
sounds like double-speak:
"Recent studies have found hepatitis C virus (HCV) RNA in peripheral blood mononuclear cells (PBMCs) of the majority of presumed recovered subjects."
"residual HCV was not detected in plasma or PBMCs of any spontaneous or treatment-recovered subjects"
So did they detect it? Or didn't they detect it? Is this a problem? Or isn't this a problem?
It's my understanding that SVR means that treatment has worked and you no longer have the hepatitis C virus in your body.
Hepatology. 2013 Feb;57(2):483-91. doi: 10.1002/hep.25921. Epub 2012 Dec 6.
Investigation of residual hepatitis C virus in presumed recovered subjects.
Fujiwara K, Allison RD, Wang RY, Bare P, Matsuura K, Schechterly C, Murthy K, Marincola FM, Alter HJ.
Source
Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892, USA.
Abstract
Recent studies have found hepatitis C virus (HCV) RNA in peripheral blood mononuclear cells (PBMCs) of the majority of presumed recovered subjects. We investigated this unexpected finding using samples from patients whose HCV RNA and anti-HCV status had been serially confirmed. HCV RNA was detected in PBMCs from 66 of 67 chronic HCV carriers. Subpopulation analysis revealed that the viral load (log copies/10(6) cells) in B cells (4.14 ± 0.71) was higher than in total PBMCs (3.62 ± 0.71; P < 0.05), T cells (1.67 ± 0.88; P < 0.05), and non-B/T cells (2.48 ± 1.15; P < 0.05). HCV negative-strand RNA was not detected in PBMCs from any of 25 chronically infected patients. No residual viral RNA was detected in total PBMCs or plasma of 59 presumed recovered subjects (11 spontaneous and 48 treatment induced) using nested real-time polymerase chain reaction with a detection limit of 2 copies/μg RNA (from ≈ 1 × 10(6) cells). PBMCs from 2 healthy HCV-negative blood donors became HCV RNA positive, with B-cell predominance, when mixed in vitro with HCV RNA-positive plasma, thus passively mimicking cells from chronic HCV carriers. No residual HCV was detected in liver or other tissues from 2 spontaneously recovered chimpanzees.
CONCLUSION:
(1) HCV RNA was detected in PBMCs of most chronic HCV carriers and was predominant in the B-cell subpopulation; (2) HCV detected in PBMCs was in a nonreplicative form; (3) HCV passively adsorbed to PBMCs of healthy controls in vitro, becoming indistinguishable from PBMCs of chronic HCV carriers; and (4) residual HCV was not detected in plasma or PBMCs of any spontaneous or treatment-recovered subjects or in chimpanzee liver, suggesting that the classic pattern of recovery from HCV infection is generally equivalent to viral eradication.
http://www.ncbi.nlm.nih.gov/pubmed/22729600.1