Fast type I interferon response protects astrocytes from flavivirus infection and virus-induced cytopathic effects

Lindqvist, Richard; Mundt, Filip; Gilthorpe, Jonathan D.; Wölfel, Silke; Gekara, Nelson O.; Kröger, Andrea; Överby, Anna K.

Astrocytes resistance to viral infection might be due to high basal expression of antiviral genes, fast response via IFNAR signaling, or both. In order to distinguish between these possibilities, monoclonal antibodies were used to block IFNAR signaling in WT astrocytes [63] ( Fig. 8a-c) . Interestingly, the numbers of TBEV-infected cells and TBEV replication were increased to levels similar to those measured in IFNAR −/− cells. This indicated that response to type I IFN is more important for restricting viral growth than the basal expression level of antiviral ISGs. Previous studies have shown that astrocytes are resistant to TBEV-induced cytopathic effects [34, 35] . We can now show that the viability of WT Asterisk indicates the significance level between WT astrocytes and MEF. *p < 0.05, **p < 0.01, ***p < 0.001. Protein levels of viperin, TBEV, and actin was detected in TBEV-infected WT and IFNAR −/− astrocytes over time (c) astrocytes after TBEV infection is dependent on the type 1 IFN response, since IFNAR −/− , as well as WT astrocytes treated with an IFNAR-specific antibody, rendered them susceptible to TBEV-induced cytopathic effect 48 hpi (Fig. 8d) .