Hepatitis C and Viral Load
October 18, 2004
Are you confused about what viral load actually indicates regarding Hepatitis C? One of the most common misconceptions among Hepatitis C patients I speak with is that a higher viral load indicates a greater severity of the disease. This leads many to conclude that if their viral load is high they are in much more serious trouble than if it was low.
The study referenced at the bottom of this post finds that there is absolutely no correlation between viral load and the severity or progression of Hepatitis C.
It has previously been shown, in numerous studies, that lower viral load responds better to current interferon therapies. Doctors, therefore, often believe that people with higher viral load have a more serious condition—just because they are not good candidates for interferon.
High viral load does not, however, indicate that these patients have any more to worry about than anyone else with Hepatitis c.
In fact, I have spoken with people who have a viral load below 200,000 who could not get out of bed because of their physical reaction to the disease, as well as people in the tens of millions who feel just fine.
It seems, then, that viral load levels are only relevant as an indicator of possible interferon treatment success or when used to track treatment progress while trying to achieve a sustained virilogic response with interferon—NOT as an indicator of disease severity.
Incidentally, regardless of your viral load, Maximum Milk Thistle helps protect your liver 8 to 10x more effectively than any standardized milk thistle product. If you are taking any other milk thistle, you are not getting near the protection and support you should be. Go to MaximumMilkThistle.com for more info.
Is There a Correlation Between HCV Viral Load and Severity of Liver Disease?
The significance of hepatitis C virus (HCV) serum titers (HCV viral load) has been examined in several clinical situations. There is much evidence that patients with a lower viral load have better response rates to anti-viral therapy compared to those with higher levels.
Moreover, a direct association has been observed between serum titers of HCV and transmission rates of the virus.
The aim of the present study was to determine if there was any correlation between HCV viral load and the severity of liver disease.
Fifty patients with HCV infection were included in the study. These comprised of 34 subjects with a history of alcohol use and 16 non-alcoholics.
Quantitative serum HCV RNA assay was carried out using the branched DNA (bDNA) technique. Linear regression analysis was performed between serum viral titers and liver tests.
In addition, for the purpose of comparison, the subjects were divided into two groups: those with low viral titers (<=50 genome mEq/mL) and high titers (>50 mEq/mL).
All subjects were men, with a mean+/-SD age of 47+/-7.8 years. The mean HCV RNA level in the blood was 76.3X10(5)+/-109.1 genome equivalents/mL.
There was no correlation between HCV RNA levels and age of the patients (r = 0.181), and the history or amount (g/d) of alcohol consumption (r = 0.07).
Furthermore, no correlation was observed between serum HCV RNA levels and the severity of liver disease as judged by the values of serum albumin (r = 0.175), bilirubin (r = 0.217), ALT (r = 0.06) and AST (r = 0.004) levels.
Similarly, no significant difference was observed between patients with low viral titers and high titers with respect to any of the parameters.
The authors conclude, “Our results indicate that the severity of liver disease is independent of serum levels of hepatitis C virus. These findings are important since they have a direct impact on the current debate regarding the role of direct cytopathic effect of hepatitis C virus versus immune-mediated injury in the pathogenesis of HCV-related liver damage.”
Digestive Diseases Section (111D), VA Medical Center, 2002 Holcombe Blvd. Houston, Texas.
B S Anand and M Velez. Assessment of correlation between serum titers of hepatitis c virus and severity of liver disease. World Journal of Gastroenterology 10(16):2409-12411. August 15, 2004.