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Hepatitis C virus mixed genotype infection in patients on haemodialysis
K P Qian1, S N Natov, B J Pereira
1Section of Hepatobiliary Diseases, Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, University of Florida, Gainesville, FL 32610, USA.
Insights
Hepatitis C virus (HCV) mixed infections in dialysis patients show genotype 1 may prevail over genotypes 2 and 3 over time. Molecular methods reliably detect these complex HCV infections.
Area of Science:
- Virology
- Hepatology
- Infectious Diseases
Background:
- Hepatitis C virus (HCV) exhibits diverse genotypes with clinical significance.
- Biological differences between HCV genotypes remain largely unknown.
- Patients with end-stage renal disease (ESRD) on hemodialysis are a vulnerable population for viral infections.
Purpose of the Study:
- To determine HCV genotypes in patients with ESRD on hemodialysis.
- To investigate the prevalence and dynamics of mixed HCV genotype infections.
- To explore potential biological differences or dominance patterns among HCV genotypes in this cohort.
Main Methods:
- Serological assays for anti-HCV antibodies.
- Molecular assays including restriction fragment length polymorphism (RFLP) and line-probe reverse hybridization (LiPA) for HCV genotyping.
- Reverse transcription-polymerase chain reaction (RT-PCR) for HCV RNA detection.
- Analysis of longitudinal samples to track genotype changes.
Main Results:
- HCV RNA was detected in 88% of 120 patients.
- Mixed genotype infections were identified in 14 patients using molecular methods.
- In follow-up samples from patients with mixed infections, genotype 1 showed a tendency to prevail over genotypes 2 and 3.
Conclusions:
- Molecular methods reliably detect mixed HCV infections.
- In hemodialysis patients with mixed HCV genotypes, genotype 1 may dominate over time.
- Further research is needed to understand the clinical implications of genotype dominance in mixed HCV infections.
Abstract:
Hepatitis C virus (HCV) has been classified into different genotypes/subtypes with demonstrated clinical implications. Whether there is biological difference between genotypes is unknown. We determined HCV genotype in 120 anti-HCV-positive patients with end-stage renal disease and on haemodialysis, by both serological assay (which showed evidence of previous exposure) and by two molecular assays: restriction fragment length polymorphism (RFLP) and line-probe reverse hybridization (LiPA). In mixing experiments, RFLP and LiPA was able to detect the minor HCV genotypes (if present) in 5-30% and 1-2% of the viral population, respectively. Of the 120 patients studied, genotype-specific antibodies were detected in 50 (42%), and eight patients had reactivities to peptides derived from multiple genotypes (genotypes 1 and 2 and/or 3). Only genotype 1 infection was found by RFLP/LiPA in these eight patients with reactivities to multiple HCV genotypes. One-hundred and five of the 120 (88%) patients were positive for HCV RNA by reverse transcription-polymerase chain reaction (RT-PCR) analysis and 14 were found to have mixed genotype infection. Follow-up serum samples (4-21 months later) were available in five patients (genotype 1a with another genotype/subtype). All five patients had a reduced number of HCV genotypes detected during follow-up; four of the five patients still had detectable genotype 1a, and one patient lost genotype 1a and was positive for genotype 2b only. These data showed that HCV mixed infection can be reliably detected by molecular methods and, in patients with end-stage renal disease and mixed genotype infection, there is a trend that during follow-up, HCV genotype 1 may prevail, or 'take over' the genotype 2 and 3 infection.