When incubated with replication-deficient and UV-irradiated EV71, XBP1-overexpressing RD cells exhibited reduced viral RNA levels, suggesting that the inhibition of XBP1s by viral infection may underlie viral entry, which is required for viral replication.
In this review, we will summarize the current findings on the involvement of XBP-1 in viral infection/ replication and discuss the potential anti-viral strategies by targeting XBP-1.
Because the XBP1 transcription factor is involved in stress and immunological responses, our results suggest an alternative way to activate XBP1 upon viral infection or nuclear localization of PABP.<b>IMPORTANCE</b> Rotavirus is one of the most important pathogens causing severe gastroenteritis in young children worldwide.
Here, we demonstrate that the endoplasmic reticulum stress sensor inositol-requiring enzyme 1 (IRE1α) and its substrate transcription factor X-box-binding protein 1 (XBP1) drive NK cell responses against viral infection and tumors in vivo.