Lack of correlation between hepatitis C virus genotypes and clinical course of hepatitis C virus-related cirrhosis |
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| Affiliation: | 1. Department of Biotechnology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi 110062, India;2. Department of Life Sciences, School of Sciences, IGNOU, New Delhi 110068, India;3. Kusuma School of Biological Sciences, Indian Institute of Technology, New Delhi 110016, India;4. HAH Centenary Hospital, Jamia Hamdard, New Delhi 110062, India;5. ICGEB-Emory Vaccine Center, ICGEB, New Delhi 110067, India;6. Department of Pediatrics, Emory University School of Medicine, 30322 Atlanta, GA, USA;1. Department of Medical Parasitology, Pham Ngoc Thach University of Medicine, Ho Chi Minh City 700000, Vietnam;2. Department of Fundamental Chemistry-Biochemistry, Pham Ngoc Thach University of Medicine, Ho Chi Minh City 700000, Vietnam;3. Clinical Epidemiology Research Unit, Institute of Malariology, Parasitology, and Entomology Quy Nhon, Binh Dinh 55000, Vietnam;4. Department of Infectious Disease, Military Hospital 103, Hanoi 100000, Vietnam;5. Department of Epidemiology, Hanoi University of Public Health, Hanoi 100000, Vietnam;6. Department of Microbiology – Parasitology, Hanoi University of Public Health, Hanoi 100000, Vietnam;7. Department of Medicine, University of Medicine and Pharmacy, Vietnam National University, Hanoi, 100000 Vietnam;1. Department of Infectious Diseases and Tropical Medicine, North Manchester General Hospital, M8 5RB Manchester, UK;2. Department of Virology, Manchester University NHS Foundation Trust, M13 9WL Manchester, UK;3. Faculty of Biology, Medicine and Health, University of Manchester, M13 9PL Manchester, UK |
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| Abstract: | The influence of the hepatitis C virus (HCV)-genotype on liver disease severity was evaluated in 429 consecutive patients with chronic hepatitis C, including 109 with cirrhosis who were followed up prospectively, allowing for the assessment of the role of the HCV-genotype on disease outcome and on the development of hepatocellular carcinoma (HCC). HCV-1 was detected in 147 (46%) patients without cirrhosis and in 47 (43%) with cirrhosis (P: not significant), being mainly HCV-1b. HCV-2 was found in 103 (32%) cases without cirrhosis and in 30 (27.5) with cirrhosis (P: not significant), being mainly HCV-2a. HCV-3 was detected in 32 (10%) patients without cirrhosis and in 2 (2%) with cirrhosis (P < 0.005). Infection with more than one genotype (HCV-1/HCV-2 and HCV-1/HCV-3) was observed only in cirrhotic patients (6 of 109; 5.5%). During a mean follow-up of 67 +/- 22 months, 21 (19%) patients with cirrhosis showed worsening in Child's stage, 5 (4.5%) underwent liver transplantation, 23 (21%) developed HCC, and 24 (22%) died of complication of liver disease; the overall incidence of at least one of these events was 38.5%. By the Kaplan-Meier method and log-rank test, the cumulative probability of developing each or at least one of the above events did not differ in relation to the genotype of infecting HCV, apart from patients with mixed genotype infection who showed a significantly higher incidence of death (P < .05). These data indicate that HCV-genotypes do not have a significant effect on the severity and outcome of liver disease in patients with chronic HCV-infection. Patients with cirrhosis who are also infected by HCV-1 and HCV-2 had a similar prognosis and progression to HCC, while patients infected by more than one genotype showed the most unfavorable course of disease.(Hepatology 1997 Jan;25(1):211-5) |
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