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Vertical transmission of hepatitis C virus: a tale of multiple outcomes
Alejandro Escobar-Gutiérrez1, Hugo Soudeyns, Ariane Larouche
1Instituto de Diagnóstico y Referencia Epidemiológicos, Mexico City, Mexico.
Insights
Hepatitis C virus (HCV) molecular evolution varied in children, with HIV coinfection or weak immune responses potentially limiting viral adaptation. Treatment did not significantly alter viral diversity in these cases.
Area of Science:
- Virology
- Immunology
- Genetics
Background:
- Hepatitis C virus (HCV) infection impacts 130 million globally, causing chronic liver disease, especially in children.
- HCV's error-prone RNA polymerase drives rapid evolution, enabling immune evasion and disease progression.
- Mother-to-child transmission is a significant route for pediatric HCV infection.
Purpose of the Study:
- To investigate the molecular evolution of HCV in three children with vertically acquired chronic infection.
- To assess the impact of HIV-1 coinfection and treatment on HCV genetic diversity.
- To explore factors influencing HCV variant persistence and population structure.
Main Methods:
- Analysis of HCV molecular evolution in three pediatric cases using median joining network and Bayesian approaches.
- Assessment of viral variants and population structure in relation to HIV-1 coinfection and HCV serostatus.
- Evaluation of treatment effects (PegIFN) on HCV variant spectrum complexity.
Main Results:
- Distinct patterns of viral evolution were observed among the three subjects.
- Lack of significant molecular evolution in some cases was associated with HIV-1 coinfection or persistent HCV seronegativity.
- PegIFN treatment did not correlate with increased complexity in the HCV variant spectrum.
Conclusions:
- Immune system dysfunction, particularly from HIV-1 coinfection, may inhibit HCV molecular evolution.
- Persistent HCV seronegativity could also contribute to limited viral adaptation.
- Viral evolution appears independent of transmission mode, with host factors playing a more significant role.
Abstract:
Globally, hepatitis C virus (HCV) infection affects approximately 130 million people and 3 million new infections occur annually. HCV is also recognized as an important cause of chronic liver disease in children. The absence of proofreading properties of the HCV RNA polymerase leads to a highly error prone replication process, allowing HCV to escape host immune response. The adaptive nature of HCV evolution dictates the outcome of the disease in many ways. Here, we investigated the molecular evolution of HCV in three unrelated children who acquired chronic HCV infection as a result of mother-to-child transmission, two of whom were also coinfected with HIV-1. The persistence of discrete HCV variants and their population structure were assessed using median joining network and Bayesian approaches. While patterns of viral evolution clearly differed between subjects, immune system dysfunction related to HIV coinfection or persistent HCV seronegativity stand as potential mechanisms to explain the lack of molecular evolution observed in these three cases. In contrast, treatment of HCV infection with PegIFN, which did not lead to sustained virologic responses in all 3 cases, was not associated with commensurate variations in the complexity of the variant spectrum. Finally, the differences in the degree of divergence suggest that the mode of transmission of the virus was not the main factor driving viral evolution.
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