Author
Listed:
- Michel Crameri
(University of Zurich
Life Science Zurich Graduate School)
- Michael Bauer
(Life Science Zurich Graduate School
University of Zurich)
- Nicole Caduff
(Life Science Zurich Graduate School
University of Zurich)
- Raphael Walker
(University of Zurich)
- Fiona Steiner
(University of Zurich
Life Science Zurich Graduate School)
- Francesca D. Franzoso
(University of Zurich
University Hospital Zurich)
- Cornelia Gujer
(University of Zurich)
- Karin Boucke
(University of Zurich)
- Talissa Kucera
(University of Zurich)
- Andrea Zbinden
(University of Zurich)
- Christian Münz
(University of Zurich)
- Cornel Fraefel
(University of Zurich)
- Urs F. Greber
(University of Zurich)
- Jovan Pavlovic
(University of Zurich)
Abstract
The type I interferon (IFN) system plays an important role in controlling herpesvirus infections, but it is unclear which IFN-mediated effectors interfere with herpesvirus replication. Here we report that human myxovirus resistance protein B (MxB, also designated Mx2) is a potent human herpesvirus restriction factor in the context of IFN. We demonstrate that ectopic MxB expression restricts a range of herpesviruses from the Alphaherpesvirinae and Gammaherpesvirinae, including herpes simplex virus 1 and 2 (HSV-1 and HSV-2), and Kaposi’s sarcoma-associated herpesvirus (KSHV). MxB restriction of HSV-1 and HSV-2 requires GTPase function, in contrast to restriction of lentiviruses. MxB inhibits the delivery of incoming HSV-1 DNA to the nucleus and the appearance of empty capsids, but not the capsid delivery to the cytoplasm or tegument dissociation from the capsid. Our study identifies MxB as a potent pan-herpesvirus restriction factor which blocks the uncoating of viral DNA from the incoming viral capsid.
Suggested Citation
Michel Crameri & Michael Bauer & Nicole Caduff & Raphael Walker & Fiona Steiner & Francesca D. Franzoso & Cornelia Gujer & Karin Boucke & Talissa Kucera & Andrea Zbinden & Christian Münz & Cornel Frae, 2018.
"MxB is an interferon-induced restriction factor of human herpesviruses,"
Nature Communications, Nature, vol. 9(1), pages 1-16, December.
Handle:
RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-04379-2
DOI: 10.1038/s41467-018-04379-2
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