Thank you for your efforts and tolerance. I didn't mean to overlook your post!
Best wishes and Happy Holidays.
Susan
Thanks for your comments, Mike.
My main question that I hoped you could answer was whether there's anything conclusive in peer-reviewed studies about high viral load being associated with greater risk of transmission.
If there are such studies, that seems to broaden the importance of viral load and the value of having a low one. I had tended to think of its significance only in terms of beginning SOC but do recollect someone here mentioning this second aspect.
Any thoughts on this specifically?
Our liver experts are physicians who run major liver transplant programs at leading hospitals - not pharmaceutical companies!
Cindy
That is why I posted the title so no one would have to look it up to see that it was about a pediatric population (though the population did extend to 18 or 19 years of age). I found it counter-intuitive that, while Viral load is not associated with histology, here, in a pediatric cohort, it seemed to be associated with symptoms (whatever "symptoms" means).
Regardless, it is crystal clear that VL is not associated with liver histology.
Now, could it possibly be associated with something else? Well, I suppose that's possible. Maybe we could sit around and imagine some intriguing scenarios. That would be fun. My guess is that, in light of the fact that this disease has been studied intensely for a while, some studies might make mention of an association with VL. I think something would have surfaced by now if it was consistently seen in high or low viral loads. That's just my opinion but it seems reasonable.
My opinion is that it is our immune response to the virus which damages the liver - for the most part. Recently there has been evidence that the virus is, in and of itself, cytopathic so apparently some damage is due directly to the virus. The studies still acknowledge that damage is done indirectly though immune mediated response. So, that's how I see the virus - it's either there or it isn't and, if it is, then regardless of VL you are at risk for liver damage as well as the diseases associated with HCV.
Mike
To Mike...I vaguely recall that there's a direct association between levels of viral load and transmission rates of the virus, that it's not exclusively about viral load significance for starting SOC...can't check that right now but could you? That's kind of important, I think.
Accepting that the liver itself isn't histologically affected by high viral load, which is what seems to be conclusive out there in studyland, I still wonder if something else isn't affected adversely by high serum titers, something not understood or studied to date, maybe fatigue levels or something. Do millions of virons just pedal around and have zero impact on absolutely nothing else just because it has no impact on liver histology?
That second study you cited concerns pediatric patients, so don't know if it applies to members here.
Stay well.
"God, I wish I had a 7 million viral count again!
300 thousand is so un-"ample evidence"!
A low viral load is more likely to respond to SOC treatment so, in that respect, a low VL is a good thing - if you're going to treat with SOC, that is.
However VL doesn't appear to be indicative of liver damage.
From: Clinical Care Options
"In contrast to the correlations between the magnitude of HIV or hepatitis B virus replication and risk of clinical disease, the level of HCV replication has never correlated with fibrosis progression or ALT levels. The important parameter in hepatitis C is the presence or absence of viral replication—not the magnitude."
See; http://tinyurl.com/ya5b6ju
From: Symptomatic and pathophysiologic predictors of hepatitis C virus progression in pediatric patients.
"There was a significant inverse relationship between viral load and symptoms (chi = 4.75, P = 0.03). Patients with low viral load (<2 million copies) were 5 times more likely to have symptoms than those with high viral loads (P = 0.03)."
See; http://tinyurl.com/y86knrt
From: Clinical Care Options:
"Management of HCV-Associated Fibrosis"
"While viral factors such as HCV genotype and viral load influence the likelihood of response to interferon therapy, viral factors do not correlate with fibrosis progression. A person with a high viral load and HCV genotype 1 may have very rapid or very slow
fibrosis progression."
See: http://tinyurl.com/ycxswlk
We've been over this issue before. These are article I saved but I know there are a lot more out there which state the same thing. VL does not correlate with progression.
What is your ALT, AST and platelet count, by the way?
Mike