ATG-3 limits Orsay virus infection in through regulation of collagen pathways.

Autophagy is an essential cellular process which functions to maintain homeostasis in response to stressors such as starvation or infection. Here, we report that a subset of autophagy factors including ATG-3 play an antiviral role in Orsay virus infection of . Orsay virus infection does not modulate autophagic flux, and re-feeding after starvation limits Orsay virus infection and blocks autophagic flux, suggesting that the role of ATG-3 in Orsay virus susceptibility is independent of its role in maintaining autophagic flux. mutants phenocopy mutants, which have a defect in RNA interference (RNAi), in susceptibility to Orsay virus infection and transcriptional response to infection. However, mutants do not exhibit defects in RNAi. Additionally, limits viral infection at a post-entry step, similar to mutants. Differential expression analysis using RNA sequencing revealed that antiviral , which encodes a collagen trimer protein, is depleted in naïve and infected mutants, as well as in infected WT animals, as are numerous other collagen genes. These data suggest that ATG-3 has a role in collagen organization pathways that function in antiviral defense in .