The Ubiquitin-Specific Protease Usp7, a Novel Merkel Cell Polyomavirus Large T-Antigen Interaction Partner, Modulates Viral DNA Replication

Author:

Czech-Sioli Manja1,Siebels Svenja1,Radau Sonja2,Zahedi René P.2,Schmidt Claudia1,Dobner Thomas3,Grundhoff Adam3,Fischer Nicole1

Affiliation:

1. Institute for Medical Microbiology, Virology and Hygiene, University Medical Center Hamburg-Eppendorf, Hamburg, Germany

2. Leibniz-Institut für Analytische Wissenschaften–ISAS–e.V., Dortmund, Germany

3. Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany

Abstract

MCPyV is the only human polyomavirus that is associated with cancer; the majority of Merkel cell cancers have a viral etiology. While much emphasis was placed on investigations to understand the transformation process by MCPyV oncoproteins and cellular factors, we have only limited knowledge of cellular factors participating in the MCPyV life cycle. Here, we describe Usp7, a cellular deubiquitination enzyme, as a new factor involved in MCPyV replication. Usp7 is known in the context of large DNA tumor viruses, Epstein-Barr virus (EBV) and Kaposi’s sarcoma herpesvirus, to restrict viral replication. Similar to EBV, where Usp7 binding to EBNA1 increases EBNA1 binding affinity to viral DNA, we find MCPyV LT binding to the origin of replication to be increased in the presence of Usp7, resulting in restriction of viral DNA replication. However, Usp7-induced restriction of MCPyV replication is independent of its enzymatic activity, thereby constituting a novel mechanism of Usp7-induced restriction of viral replication.

Funder

Landesforschungsförderung Hamburg

Publisher

American Society for Microbiology

Subject

Virology,Insect Science,Immunology,Microbiology

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