Prof Daniel Pinschewer; University of Basel
09/2013 – present Full professor of virology, University of Basel, CH 2007 – 2013 Associate professor, University of Geneva, CH 2004 – 2007 Independent group leader University Hospital of Zurich, CH 2002– 2004 Postdoctoral fellow, University of Zurich, CH (R. Zinkernagel, H. Hengartner) 2001 – 2002 Postdoctoral fellow, The Scripps Research Institute, La Jolla, CA, USA 1998 – 2000 Medical doctorate, University of Zurich (R. Zinkernagel, H. Hengartner)
Perinatal infection often results in viral persistence as observed for hepatitis B virus in humans. Commonly held concepts suggest persistence is associated with immunotolerance, but this fails to predict the emergence of antiviral antibodies and eventual viral load control. Studying congenital lymphocytic choriomeningitis virus infection, the prototypic mouse model of neonatal antiviral immunotolerance, we observe antibody-mediated viral load suppression, which is driven by canonical antiviral CD4 Tfh responses independently of CD8 T cells. Viral epitope-specific CD4 T cells in congenitally infected animals are less abundant than in adult infection. They exhibit reduced clonal diversity and subtly different gene expression patterns. Importantly, CD4 T cell supplementation of congenitally infected mice augments germinal center responses of transferred antiviral B cells. Hence, humoral immune defense is partially exempt from neonatal tolerance and remains effective against congenital infection. Numerically and clonally restricted CD4 Tfh responses lend themselves as immunotherapeutic target for a functional cure.
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