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B protected: from vertical HCV transmission?
  1. Katharina Zoldan,
  2. Maike Hofmann
  1. Department of Medicine II, University Hospital Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany
  1. Correspondence to Dr Maike Hofmann, Department of Medicine II, University Hospital Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany; Maike.Hofmann{at}uniklinik-freiburg.de

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HCV infection is a global health burden with about 71 million chronically infected people worldwide, putting them at risk of progressive liver disease, including liver cirrhosis and hepatocellular carcinoma. HCV is transmitted via parenteral routes. The most frequent transmission nowadays is by contaminated instruments used for injections. Only few HCV infections occur through vertical mother-to-child transmission (MTCT). Still, the major cause of paediatric hepatitis is vertical transmission of HCV affecting roughly 3.5 million children and adolescents worldwide. The risk of MTCT in viraemic pregnant women is about 5%.1 This vertical transmission rate is rather low compared with other chronic viral infections, for example, HIV and HBV infection. The mechanisms underlying the low vertical transmission of HCV are still elusive and include possible successful immune protection and/or an effective barrier function by the placenta.

In this issue, Lutckii et al2 investigate vertical HCV exposure from an immunological perspective. The study was conducted in a unique cohort of children who were unexposed, HCV-exposed but uninfected or HCV-infected compared with healthy newborns and HCV-infected adults. Here, the comparison of HCV-exposed but uninfected children to unexposed children was of special interest in order to address the question of immune alterations on vertical HCV exposure. HIV coinfection was an exclusion criterion in this study to further pinpoint HCV-specific effects. The analyses were focused on B cells, innate immune cells (myeloid cells and natural killer (NK) cells) and soluble factors (eg, …

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Footnotes

  • Contributors ZK and MH wrote the manuscript.

  • Funding MH acknowledges support by the German Research Foundation (grant TRR179 project 01).

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; externally peer reviewed.

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