Marie B. Iversen

TL;DR: Type III IFN to target a specific subset of cells and to contribute to the antiviral response evoked by TLRs, and it is shown that TLR-activated antiviral defense requires expression of IL-28Rα only on nonhemopoietic cells.

TL;DR: NRF2 agonists 4-OI and DMF induce a distinct IFN-independent antiviral program that is broadly effective in limiting virus replication and in suppressing the pro-inflammatory responses of human pathogenic viruses, including SARS-CoV2.

TL;DR: It is demonstrated that the HSV-1 capsid was ubiquitinated in the cytosol and degraded by the proteasome, hence releasing genomic DNA into the cytoplasm for detection by DNA sensors, which is important for induction of IFN-β in human macrophages postinfection with HSv-1 and CMV.

TL;DR: It is shown that in mice TLR3 provides early control of HSV-2 infection immediately after entry into the CNS by mediating type I IFN responses in astrocytes, possibly preventing HSV from spreading beyond the neurons mediating entry intoThe CNS.

TL;DR: Nrf2 activation decreases STING expression and responsiveness to STING agonists while increasing susceptibility to infection with DNA viruses, and a link between metabolic reprogramming and antiviral cytosolic DNA sensing in human cells is suggested.