Thanks Will
Just trying to get all my ducks in order before starting tx!
The way your liver is damaged when HCV infected is a very complex process dependant on many factors.
Studies have been done and for the most part show no direct correlation between VL and amount of fibrosis progression (however like everything else with HCV there is some controversy on this subject also)
Basically it is the complex interrelation between the virus and your own immune response rather than the direct effect of the virus itself.
That is the very simplified version ,however there are articles and studies that have been done if you are interested in the medical jargon (linked one below)
desrt makes a good point about the actual numbers.
If you think about your VL in log form and that is how we keep score when treating yours was log 5.9.(869,000) and now is log 5.2 (159,000 ) so if you were treating and had that response it is basically very little or poor response
Can you cure yourself with Vit. D alone?.....there is no documented case of Vit. D alone curing HCV...however studies show as you have seen here it can be a good adjunct to tx.
Good luck..
Will.
http://www.turkgastro.org/text.php?id=2
Such findings supporting the hypothesis that chronic HCV infection is not directly related to the levels of viral replication and may be mediated by the host immune response against HCV-infected hepatocytes.
In some studies, although no relationship was found between the serum HCV-RNA levels and HAI, a relationship was determined between HCV-RNA and fibrosis level. It was thus shown that as fibrosis progresses, the viral load decreases [29]. In this study, viral load was lower in the high fibrosis stage group (Group B) although this finding was not significant (p>0.05). This may be due to the small number of cases in these groups.
In conclusion, this study found no direct correlation between either serum AST, ALT and viral load (HCVR-RNA b-DNA) levels and HAI or fibrosis scores. These findings suggest that liver injury in chronic HCV infection is related to immune mediated mechanisms rather than the direct cytopathic effect of the virus. Therefore, laboratory findings can not take the place of histopathological examination as a predictive indicator of liver injury.
Discussion
References
Thanks guys, I guess wishful thing on my part!
So far as I know, VL is only important in providing a baseline and understanding response to therapy. My husband's VL was 552,588 when he was diagnosed in 2007 prior to1st treatment (SOC): failed. His VL was 800,000 in 2010 prior to 2nd treatment (daily infergen injections/1400 mg Riba): failed. His VL was 290,000 in 2011 prior to current treatment (triple tx/Inc., which he began on 9/30/11. The VL will go up and down at any given time in between treatments and in response to treatment. The change from VL 869,000 to 159,000 that you described would not be considered significant.
Advocate1955
869,000 to 159,000 only seems like a nosedive because of the large numbers involved. A doctor would probably only sit up and take notice if it changed to 8,690 or 86,9000,000 - a 2 log change.
Ones viral load can and will change, the reason one does not realize it is because its only tested at certain times. And no viral load plays no part in the amount of damage one might have. I was dx in 2005 with cirrhosis, at that time my viral load was almost 10 millon. When i began tx some 8 months later it was 2 millon, afte relapsed it rose back to 10 millon. When i treated again 18 months later it was only around 800,000.
The reason your VL plays an important part during tx is to see how well the drugs are working and the length of time tx should be, or when to halt tx. As for vitaim D, really doubt its playing a role in your viral load, and for sure it won't cure hep-c.......... Good luck
I forgot to mention that my last biopsy was in November and I am stage 2/2
So this minimal viral load has no correlation to having less of a healthy liver or cirrhosis
I directly think the dramatic drop in my VL has been the vitamin d supplementation's , as I was extremely low with osteoporosis at age 58