Viral modulation of type II interferon increases T cell adhesion and virus spread

Carina Jacobsen, Nina Plückebaum, George Ssebyatika, Sarah Beyer, Lucas Mendes-Monteiro, Jiayi Wang, Kai A. Kropp, Víctor González-Motos, Lars Steinbrück, Birgit Ritter, Claudio Rodríguez-González, Heike Böning, Eirini Nikolouli, Paul R. Kinchington, Nico Lachmann, Daniel P. Depledge, Thomas Krey and Abel Viejo-Borbolla ()
Additional contact information
Carina Jacobsen: Hannover Medical School
Nina Plückebaum: Hannover Medical School
George Ssebyatika: Hannover Medical School
Sarah Beyer: Hannover Medical School
Lucas Mendes-Monteiro: Hannover Medical School
Jiayi Wang: Hannover Medical School
Kai A. Kropp: Hannover Medical School
Víctor González-Motos: Hannover Medical School
Lars Steinbrück: Hannover Medical School
Birgit Ritter: Hannover Medical School
Claudio Rodríguez-González: Hannover Medical School
Heike Böning: Hannover Medical School
Eirini Nikolouli: Hannover Medical School
Paul R. Kinchington: University of Pittsburgh
Nico Lachmann: Hannover Medical School
Daniel P. Depledge: Hannover Medical School
Thomas Krey: Hannover Medical School
Abel Viejo-Borbolla: Hannover Medical School

Nature Communications, 2024, vol. 15, issue 1, 1-18

Abstract: Abstract During primary varicella zoster virus (VZV) infection, infected lymphocytes drive primary viremia, causing systemic dissemination throughout the host, including the skin. This results in cytokine expression, including interferons (IFNs), which partly limit infection. VZV also spreads from skin keratinocytes to lymphocytes prior to secondary viremia. It is not clear how VZV achieves this while evading the cytokine response. Here, we show that VZV glycoprotein C (gC) binds IFN-γ and modifies its activity, increasing the expression of a subset of IFN-stimulated genes (ISGs), including intercellular adhesion molecule 1 (ICAM1), chemokines and immunomodulatory genes. The higher ICAM1 protein level at the plasma membrane of keratinocytes facilitates lymphocyte function-associated antigen 1-dependent T cell adhesion and expression of gC during infection increases VZV spread to peripheral blood mononuclear cells. This constitutes the discovery of a strategy to modulate IFN-γ activity, upregulating a subset of ISGs, promoting enhanced lymphocyte adhesion and virus spread.

Date: 2024
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DOI: 10.1038/s41467-024-49657-4

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