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Trends Mol Med. 2018 Oct;24(10):904-915. doi: 10.1016/j.molmed.2018.07.009. Epub 2018 Aug 13.

RNA Polymerase III as a Gatekeeper to Prevent Severe VZV Infections.

Author information

1
Department of Infectious Diseases, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200 Aarhus N, Denmark; Department of Biomedicine, Aarhus University, Wilhelm Meyers Alle 4, 8000 Aarhus C, Denmark.
2
Department of Biomedicine, Aarhus University, Wilhelm Meyers Alle 4, 8000 Aarhus C, Denmark; Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
3
Department of Infectious Diseases, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200 Aarhus N, Denmark; Department of Biomedicine, Aarhus University, Wilhelm Meyers Alle 4, 8000 Aarhus C, Denmark; Department of Clinical Medicine, Aarhus University, Palle Juul Jensens Boulevard 82, 8200 Aarhus N, Denmark. Electronic address: trine.mogensen@biomed.au.dk.

Abstract

In most individuals, varicella zoster virus (VZV) causes varicella upon primary infection and zoster during reactivation. However, in a subset of individuals, VZV may cause severe disease, including encephalitis. Host genetics is believed to be the main determinant of exacerbated disease manifestations. Recent studies have demonstrated that defects in the DNA sensor RNA polymerase III (POL III) confer selective increased susceptibility to VZV infection, thus providing fundamental new insight into VZV immunity. Here we describe the roles of POL III in housekeeping and immune surveillance during VZV infection. We present the latest knowledge on the role of POL III in VZV infection and discuss outstanding questions related to the role of POL III in VZV immunity, and how this insight can be translated into clinical medicine.

KEYWORDS:

DNA sensing; RNA polymerase III; interferon; varicella zoster virus

PMID:
30115567
DOI:
10.1016/j.molmed.2018.07.009
[Indexed for MEDLINE]

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