Viperin has species-specific roles in response to herpes simplex virus infection
| Autor: | Stewart A Smith, Si Ming Man, Karla J. Helbig, Sarah N Croft, David C. Tscharke, Anjali Gowripalan, Yeu-Yang Tseng |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Herpes simplex virus infection
Cell type Oxidoreductases Acting on CH-CH Group Donors viruses Herpesvirus 1 Human Biology medicine.disease_cause Antiviral Agents Cell Line 03 medical and health sciences Mice Viral Proteins Ribonucleases Downregulation and upregulation Transcription (biology) Virology Chlorocebus aethiops medicine Animals Humans Gene innate immunity Uncategorized 030304 developmental biology 0303 health sciences Innate immune system Animal 030302 biochemistry & molecular biology HSV species-specificity DNA Viruses Proteins Herpes Simplex Fibroblasts herpes simplex virus 3. Good health Mice Inbred C57BL Herpes simplex virus Viperin viperin |
| Zdroj: | The Journal of General Virology |
| ISSN: | 1465-2099 0022-1317 |
| Popis: | Viperin is a gene with a broad spectrum of antiviral functions and various mechanisms of action. The role of viperin in herpes simplex virus type 1 (HSV-1) infection is unclear, with conflicting data in the literature that is derived from a single human cell type. We have addressed this gap by investigating viperin during HSV-1 infection in several cell types, spanning species and including immortalized, non-immortalized and primary cells. We demonstrate that viperin upregulation by HSV-1 infection is cell-type-specific, with mouse cells typically showing greater increases compared with those of human origin. Further, overexpression and knockout of mouse, but not human viperin significantly impedes and increases HSV-1 replication, respectively. In primary mouse fibroblasts, viperin upregulation by infection requires viral gene transcription and occurs in a predominantly IFN-independent manner. Further we identify the N-terminal domain of viperin as being required for the anti-HSV-1 activity. Interestingly, this is the region of viperin that differs most between mouse and human, which may explain the apparent species-specific activity against HSV-1. Finally, we show that HSV-1 virion host shutoff (vhs) protein is a key viral factor that antagonises viperin in mouse cells. We conclude that viperin can be upregulated by HSV-1 in mouse and human cells, and that mouse viperin has anti-HSV-1 activity. |
| Databáze: | OpenAIRE |
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