期刊
TRENDS IN MOLECULAR MEDICINE
卷 24, 期 10, 页码 904-915出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2018.07.009
关键词
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资金
- European Union under the Horizon 2020 Research and Innovation Program (H2020)
- Marie Sklodowska-Curie Actions-Innovative Training Networks Programme [MSCA-ITN GA 675278 EDGE]
- Independent Research Fund Denmark [12-124330, 4004-00047B]
- Lundbeck Foundation [R198-2015-171, R268-2016-3927]
- Novo Nordisk Foundation [NNF15OC0017462, NNF18OC0030274]
- Aarhus University Research Foundation [AUFF-E-2015-FLS-66]
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.
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