Journal
VIRUSES-BASEL
Volume 1, Issue 3, Pages 1240-1264Publisher
MDPI
DOI: 10.3390/v1031240
Keywords
herpesvirus; nuclear domain 10; PML nuclear bodies; PML; Sp100; hDaxx; antiviral defense; intrinsic immunity; interferon
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Funding
- Deutsche Forschungsgemeinschaft [SFB 473, SFB 796]
- IZKF Erlangen
- elite graduate school BIGSS
- GRK1071
- Wilhelm Sander Stiftung
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In recent studies we and others have identified the cellular proteins PML, hDaxx, and Sp100, which form a subnuclear structure known as nuclear domain 10 (ND10) or PML nuclear bodies (PML-NBs), as host restriction factors that counteract herpesviral infections by inhibiting viral replication at different stages. The antiviral function of ND10, however, is antagonized by viral regulatory proteins (e.g., ICP0 of herpes simplex virus; IE1 of human cytomegalovirus) which induce either a modification or disruption of ND10. This review will summarize the current knowledge on how viral replication is inhibited by ND10 proteins. Furthermore, herpesviral strategies to defeat this host defense mechanism are discussed.
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