Polyomavirus T antigens activate an antiviral state
| Autor: | James M. Pipas, Andrew T. Coxon, Tushar Gupta, Nicholas S. Giacobbi |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Large T antigen
viruses Amino Acid Motifs JC virus Simian virus 40 Biology medicine.disease_cause Article Virus Mice SV40 03 medical and health sciences 0302 clinical medicine Antigen Interferon Virology medicine Animals Humans STAT1 Antigens Viral Tumor 030304 developmental biology BKV Polyomavirus Infections 0303 health sciences Innate immune system virus diseases Fibroblasts JC Virus Immunity Innate Up-Regulation 3. Good health BK virus JCV STAT1 Transcription Factor BK Virus 030220 oncology & carcinogenesis biology.protein Ectopic expression Polyomavirus medicine.drug |
| Zdroj: | Virology. 476:377-385 |
| ISSN: | 0042-6822 |
| DOI: | 10.1016/j.virol.2014.12.032 |
| Popis: | Ectopic expression of Simian Virus 40 (SV40) large T antigen (LT) in mouse embryonic fibroblasts (MEFs) increased levels of mRNAs encoding interferon stimulated genes (ISGs). The mechanism by which T antigen increases levels of ISGs in MEFs remains unclear. We present evidence that expression of T antigen from SV40, Human Polyomaviruses BK (BKV) or JC (JCV) upregulate production of ISGs in MEFs, and subsequently result in an antiviral state, as determined by inhibition of VSV or EMCV growth. The first 136 amino acids of LT are sufficient for these activities. Furthermore, increased ISG expression and induction of the antiviral state requires STAT1. Finally, the RB binding motif of LT is necessary for activation of STAT1. We conclude that the induction of the STAT1 mediated innate immune response in MEFs is a common feature shared by SV40, BKV and JCV. |
| Databáze: | OpenAIRE |
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