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Updated: Jun 20, 2026

A Protocol for Analyzing Hepatitis C Virus Replication
Published on: June 26, 2014
Clinicopathological features and genotype distribution in patients with hepatitis C virus chronic liver disease
Rachel Abraham1, Banumathi Ramakrishna, Avinash Balekuduru
1Department of Pathology, Christian Medical College, Vellore, India.
Background And Objective:
Hepatitis C virus (HCV) genotype influences the severity of disease and response to therapy. This retrospective study examined the clinical and histological features and the genotype distribution in biopsied patients with HCV related chronic liver disease.
Methods:
Of 105 biopsies from patients with HCV infection, 96 from patients with chronic liver disease were reviewed. The Ishak scoring system was used for histological analysis.
Results:
Genotype 3 was most common accounting for 77.1%, and genotype 1 for 9.4% of cases. There was no significant association of transaminase levels, viral load or necro-inflammatory activity score with genotype. A severe degree of fibrosis was seen in 77.8% cases of genotype 1 and in 63.5% of genotype 3 (p=0.76). Variable degrees of steatosis were noted in 68.8% of cases. However, severe steatosis was noted only in genotype 3 (7 cases). Serum transaminase levels did not correlate with either histological activity (p=0.43) or degree of fibrosis (p=0.72). Severe fibrosis / cirrhosis was seen in 74.24% of patients above 40 years of age as compared to 33.3% of patients below 40 years (p=0.001). The frequency of Mallory hyaline was significantly different between genotypes 1 and 3 infection (P<0.001).
Conclusions:
This study confirms the preponderance of genotype 3 in Indian patients with HCV related chronic liver disease. Severe steatosis was seen only in genotype 3 and Mallory hyaline was very common in genotype 1. The small numbers of patients in non genotype 3 could be a reason for the apparent lack of histological differences between different HCV genotypes. Severe fibrosis seen in older age groups confirms that HCV infection is progressive and major acceleration of the disease process occurs after 40 years of age.
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