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Viral modulation of type II interferon increases T cell adhesion and virus spread
Carina Jacobsen1, Nina Plückebaum1, George Ssebyatika1,2
1Institute of Virology, Hannover Medical School, Hannover, 30625, Germany.
Nature Communications
|June 22, 2024
Summary
Varicella zoster virus (VZV) glycoprotein C binds and modifies the activity of interferon-gamma (IFN-γ). This enhances VZV spread by promoting T cell adhesion and increasing specific immune-stimulated genes.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Primary varicella zoster virus (VZV) infection disseminates systemically, with infected lymphocytes driving viremia.
- Interferons (IFNs) are cytokines that partially limit VZV infection, but the virus spreads from skin keratinocytes to lymphocytes before secondary viremia, evading this response.
Purpose of the Study:
- To elucidate the mechanism by which VZV evades the host's cytokine response during its spread.
- To investigate the role of VZV glycoprotein C (gC) in modulating interferon-gamma (IFN-γ) activity and facilitating viral dissemination.
Main Methods:
- Analysis of VZV glycoprotein C's interaction with IFN-γ.
- Assessment of IFN-γ activity modulation and its effect on IFN-stimulated genes (ISGs) expression.
- Evaluation of intercellular adhesion molecule 1 (ICAM1) expression and its role in T cell adhesion and VZV spread to peripheral blood mononuclear cells.
Main Results:
- VZV glycoprotein C (gC) binds to IFN-γ, altering its activity.
- This interaction leads to increased expression of a subset of IFN-stimulated genes (ISGs), including ICAM1, chemokines, and immunomodulatory genes.
- Elevated ICAM1 on keratinocytes enhances T cell adhesion, promoting VZV spread to lymphocytes.
Conclusions:
- VZV employs a strategy involving glycoprotein C to modulate IFN-γ activity.
- This modulation upregulates specific ISGs, enhances lymphocyte adhesion via ICAM1, and facilitates VZV's spread to peripheral blood mononuclear cells.
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