tetano
Editor, Senior Moderator
J Virol
. 2023 Dec 15:e0123923.
doi: 10.1128/jvi.01239-23. Online ahead of print. DYRK1A is a multifunctional host factor that regulates coronavirus replication in a kinase-independent manner
Zhen Fu[SUP] 1 2 [/SUP], Yixin Xiang[SUP] 1 2 [/SUP], Yanan Fu[SUP] 1 2 [/SUP], Zhelin Su[SUP] 1 2 [/SUP], Yubei Tan[SUP] 1 2 [/SUP], Mengfang Yang[SUP] 1 2 [/SUP], Yuanyuan Yan[SUP] 1 2 [/SUP], Hakimeh Baghaei Daemi[SUP] 1 2 [/SUP], Yuejun Shi[SUP] 1 2 [/SUP], Shengsong Xie[SUP] 3 [/SUP], Limeng Sun[SUP] 1 2 [/SUP], Guiqing Peng[SUP] 1 2 4 5 [/SUP]
Affiliations
Coronaviruses, like other positive-sense RNA viruses, can remodel the host membrane to form double-membrane vesicles (DMVs) as their replication organelles. Currently, host factors involved in DMV formation are not well defined. In this study, we used transmissible gastroenteritis virus (TGEV) as a virus model to investigate the regulatory mechanism of dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) on coronavirus. Results showed that DYRK1A significantly inhibited TGEV replication in a kinase-independent manner. DYRK1A knockout (KO) can regulate the expression of receptor aminopeptidase N (ANPEP) and endocytic-related genes to inhibit virus entry. More importantly, our results revealed that DYRK1A KO notably inhibited the formation of DMV to regulate the virus replication. Further data proved that DYRK1A is also essential in the replication of mouse hepatitis virus, porcine deltacoronavirus, and porcine sapelovirus. Taken together, our findings demonstrated that DYRK1A is a conserved factor for positive-sense RNA viruses and provided new insights into its transcriptional regulation activity, revealing its potential as a candidate target for therapeutic design.
Keywords: DYRK1A; coronavirus; double-membrane vesicle; replication; virus entry.
. 2023 Dec 15:e0123923.
doi: 10.1128/jvi.01239-23. Online ahead of print. DYRK1A is a multifunctional host factor that regulates coronavirus replication in a kinase-independent manner
Zhen Fu[SUP] 1 2 [/SUP], Yixin Xiang[SUP] 1 2 [/SUP], Yanan Fu[SUP] 1 2 [/SUP], Zhelin Su[SUP] 1 2 [/SUP], Yubei Tan[SUP] 1 2 [/SUP], Mengfang Yang[SUP] 1 2 [/SUP], Yuanyuan Yan[SUP] 1 2 [/SUP], Hakimeh Baghaei Daemi[SUP] 1 2 [/SUP], Yuejun Shi[SUP] 1 2 [/SUP], Shengsong Xie[SUP] 3 [/SUP], Limeng Sun[SUP] 1 2 [/SUP], Guiqing Peng[SUP] 1 2 4 5 [/SUP]
Affiliations
- PMID: 38099687
- DOI: 10.1128/jvi.01239-23
Coronaviruses, like other positive-sense RNA viruses, can remodel the host membrane to form double-membrane vesicles (DMVs) as their replication organelles. Currently, host factors involved in DMV formation are not well defined. In this study, we used transmissible gastroenteritis virus (TGEV) as a virus model to investigate the regulatory mechanism of dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) on coronavirus. Results showed that DYRK1A significantly inhibited TGEV replication in a kinase-independent manner. DYRK1A knockout (KO) can regulate the expression of receptor aminopeptidase N (ANPEP) and endocytic-related genes to inhibit virus entry. More importantly, our results revealed that DYRK1A KO notably inhibited the formation of DMV to regulate the virus replication. Further data proved that DYRK1A is also essential in the replication of mouse hepatitis virus, porcine deltacoronavirus, and porcine sapelovirus. Taken together, our findings demonstrated that DYRK1A is a conserved factor for positive-sense RNA viruses and provided new insights into its transcriptional regulation activity, revealing its potential as a candidate target for therapeutic design.
Keywords: DYRK1A; coronavirus; double-membrane vesicle; replication; virus entry.