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Published on: March 22, 2011
Hepatitis C virus genotype 3a infection and hepatocellular carcinoma: Pakistan experience
Muhammad Idrees1, Shazia Rafique, Irshadur Rehman
1Division of Molecular Virology & Molecular Diagnostics, National Centre of Excellence in Molecular Biology, University of the Punjab Lahore, 87-West Canal Bank Road Thokar Niaz Baig, Lahore-53700, Pakistan. idreeskhan@cemb.edu.pk
Insights
Chronic hepatitis C virus (HCV) infection is a major risk factor for hepatocellular carcinoma (HCC) in Pakistan. HCV genotype 3a is strongly associated with HCC development in this population.
Area of Science:
- Hepatology
- Virology
- Oncology
Background:
- Hepatocellular carcinoma (HCC) is a significant global health concern.
- Chronic hepatitis C virus (HCV) infection is a known risk factor for HCC.
- Understanding the epidemiological link and genotypic distribution of HCV in HCC patients in Pakistan is crucial.
Purpose of the Study:
- To investigate the association between chronic HCV infection and HCC in Pakistan.
- To determine the distribution of HCV genotypes among HCC patients in Pakistan.
Main Methods:
- Study included 161 HCC patients; 145 underwent liver biopsy.
- Hepatitis B virus and HCV were detected using qualitative polymerase chain reaction (PCR).
- HCV RNA-positive samples were genotyped using genotype-specific PCR and sequencing.
Main Results:
- Chronic HCV infection was identified in 63.44% of tested HCC patients.
- HCV genotype 3a was the predominant genotype (40.96%), followed by 3b (15.66%), 1a (9.63%), and 1b (2.40%).
- Approximately 28% of cases had mixed HCV genotypes; HCC developed a median of 3.8 years after treatment discontinuation in cirrhotic patients.
Conclusions:
- A strong association exists between chronic HCV infection and HCC in Pakistan.
- HCV genotype 3a is significantly linked to the development of HCC in the Pakistani population.
Aim:
To assess the association between chronic hepatitis C virus (HCV) infection and hepatocellular carcinoma (HCC) in Pakistan, and the genotype distribution among these HCC patients.
Methods:
One hundred and sixty-one subjects with HCC were included in this study. Liver biopsy was performed on 145 of the patients; sixteen were excluded because they failed to fulfill the inclusion criteria. Qualitative polymerase chain reaction (PCR) was performed for hepatitis B virus and HCV. Samples positive for HCV RNA were genotyped using genotype-specific PCR and confirmed by HCV 5' noncoding region sequencing analysis.
Results:
Chronic HCV infection was identified a major risk factor (63.44% of tested HCC patients) for the development of HCC. The time from HCV infection to appearance of cancer was 10-50 years. In the HCC patient population, broader distributions of genotypes were present with genotype 3a as the predominant genotype. Using the type-specific genotyping method, we found HCV genotype 3a in 40.96%, 3b in 15.66%, 1a in 9.63%, and 1b in 2.40% of HCC tissue samples. About 28% of cases were found with mixed genotypes. Two cases were unable to be genotyped because of low viral load. Sixty-six percent of treated patients with cirrhosis had an end of treatment response, but unfortunately they relapsed quickly when the treatment was discontinued, and HCC developed during a median 3.8 years.
Conclusion:
There was a strong association between chronic HCV infection and HCC in Pakistan, and between HCV genotype 3a and HCC.
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