Research demonstrates selective autophagy's dual role during viral infections, indicating complex interactions in plants.
Selective autophagy has emerged as a central interface in plant–virus interactions, acting at once as an antiviral defense, a proviral vulnerability, and a regulator of host immune homeostasis. In plants, autophagy can directly target viral proteins, replication complexes, and even entire virions for degradation, while viruses have evolved diverse strategies to exploit, evade, or repurpose the autophagy machinery. Recent work has revealed an expanding repertoire of plant- and virus-encoded selective autophagy receptors, as well as unexpected roles for autophagy in restraining excessive immune activation and tissue damage during infection. These findings challenge a binary classification of autophagy as either antiviral or proviral. Here, we synthesize recent advances in the field and propose a conceptual framework in which multiple selective autophagy pathways operate in parallel during viral infection, each targeting distinct viral or host components and collectively shaping infection outcomes.
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Mülders et al. (2026) studied this question.
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