Autophagy gene atg-3 limits Orsay virus infection in C. elegans through regulation of collagen pathways. null

Autophagy is an essential process which functions to maintain cellular homeostasis in response to stressors such as starvation or infection. Here, we report that a subset of autophagy genes including atg-3 played an antiviral role in Orsay virus infection of Caenorhabditis elegans although infection itself did not modulate autophagic flux. Re-feeding after starvation limited Orsay virus infection and blocked autophagic flux, which suggested that the role of atg-3 in Orsay virus susceptibility was independent of its role in maintaining autophagic flux. Interestingly, atg-3 mutants phenocopied rde-1 mutants, which have a defect in RNA interference (RNAi), in transcriptional response to infection though atg-3 mutants did not exhibit defects in RNAi. Additionally, atg-3 limited viral infection at a post-entry step similar to rde-1 mutants. Differential expression analysis using RNA sequencing revealed that sqt-2, which encodes a collagen trimer protein, was depleted in infected WT animals and in naïve and infected atg-3 mutants, suggesting that atg-3 has a role in collagen organization pathways that play a role in antiviral defense in C. elegans.