The natural outcome of some plant–virus interactions is symptom recovery, which is characterized by the emergence of asymptomatic leaves following a systemic symptomatic infection. Symptom recovery is generally accompanied with reduced virus titers and sequence-specific resistance to secondary infection and has been linked with the induction of antiviral RNA silencing. Recent studies have revealed an unsuspected diversity of silencing mechanisms associated with symptom recovery in various host virus
interactions, including degradation or translation repression of viral RNAs and in the case of DNA viruses, transcriptional arrest of viral minichromosomes. RNA silencing may also contribute to symptom alleviation by regulating plant gene expression. In this review, we discuss the evidence supporting the role of various RNA silencing mechanisms in symptom recovery. We also discuss how a delicate equilibrium between RNA silencing and virus counter-defense responses in recovered leaves may help maintain virus titers at levels below the threshold required for symptom induction.