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

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-

• Jacobsen, C.
• Plückebaum, N.
• Ssebyatika, G.
• Beyer, S.
• Mendes-Monteiro, L.
• Wang, J.
• Kropp, K. A.
• González-Motos, V.
• Steinbrück, L.
• Ritter, B.
• Rodríguez-González, C.
• Böning, H.
• Nikolouli, E.
• Kinchington, P. R.
• Lachmann, N.
• Depledge, D. P.
• Krey, T.
• Viejo-Borbolla, A.