Innate immunity represents the capacity of any cell types to mount a reaction against any potential danger and is conserved in all domains of life. The recent discovery of a virus able to infect C. elegans in the wild offers the opportunity for characterization of its antiviral immunity mechanisms. We previously showed that the RNAi pathway is a major component of antiviral innate immunity, and is initiated by DRH-1 (1), a member of the family of RIG-I like receptors conserved in mammals (2). Surprisingly, despite the absence of interferon in C. elegans, DRH-1 also acts upstream of a transcriptional response to viral infection (3). Through further analysis of the antiviral transcriptional response, we identified the STAT family transcription factor STA-1 as a main effector of innate immunity. Intriguingly, just as in mammals, STA-1 acts downstream of viral sensing by DRH-1. However, unlike in mammals, STA-1 acts as a constitutive repressor of viral response genes, with DRH-1 acting to release repression as a result of viral infection.
Altogether, we propose that DRH-1 has a conserved role in a STAT signaling pathway during viral infection in addition to its initiator of the RNAi response. The respective contribution of RNA interference and interferon pathways across species or even within an organism is a current challenge of antiviral research. In this study, we take advantage of Orsay virus infection in C. elegans and the dual role of its RIG-I like receptor to better understand how organism can shape an efficient response to pathogen.
1. Ashe A et al. Elife. 2(0):e00994. (2013)
2. Yoneyama M et al. Curr. Opin. Immunol. 32C:48. (2015)
3. Sarkies P et al. Genome Res. 23(8):1258. (2013).
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