Hi thank you for your replay and congratulations for the successful tx
can you please tel me what treatment you had
Im a genotype 3a as well and my VL went from 1 million to 12 million in one month so it can happen. Like the above poster mentioned, if you have Hepatic Steotosis then your VL can be relevant since you are a G3 but other than that it will just be used as an indicator whether or not you are responding to treatment when you are treating.
My VL was 12 million when I started TX but am SVR now.
Hi Yannis,
The viral load goes up and down on its own. The viral load is of no significance till the time you start treatment.
Viral load is important when you are being treated for the virus. If the viral load reduces during treatment, it shows that, most probably, the treatment is working.
Liver damage also does not have a co-relation with viral load. A person with a low viral load can have more damage than one with high viral load.
Fibroscan of 12.5 kpa shows considerable liver damage.
You should consider starting treatment.
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It has been shown that HCV genotype 3 is independently associated with hepatocellular steatosis in patients with chronic hepatitis C. [23] Furthermore, the severity of steatosis in these patients is directly related to the burden of the HCV RNA load. This relationship between the HCV viral load and the magnitude of steatosis was not observed in other HCV genotypes. [24] It has also been noticed that the steatosis which was initially present in patients with genotype 3 infection resolves after a sustained virologic response is achieved through treatment with pegylated interferon-α and ribavirin. [25] Not only does the steatosis resolve with eradication of the virus but it also recurs if relapse transpires. All of these findings were only observed with the HCV genotype 3 virus and was not reproducible with other HCV genotypes. These findings all point to the ability of the HCV genotype 3 virus to directly induce steatosis, although the mechanism still remains elusive.
Thus, there seems to be two distinct forms of steatosis in patients with chronic hepatitis C. Metabolic steatosis generally occurs in all genotypes of HCV infections and likely worsens the progression of HCV induced fibrosis. Then there are those patients with genotype 3 infections who have a form of steatosis that is directly induced by the hepatitis C virus and which also resolves with successful treatment. These two forms of steatosis can certainly coexist in patients with genotype 3 infections with other underlying metabolic diseases. In these patients, we would expect that the steatosis would only partially resolve with successful eradication of the virus and that the remaining fatty infiltration is a result of NAFLD.
http://www.medsci.org/v03p0053.htm
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