Plant viruses are obligate parasites that highjack the resources of the host to facilitate their infection cycle. Plants defend themselves using a variety of mechanisms, including antiviral RNA silencing. Viruses counteract these defense responses, by encoding specialized proteins such as suppressors of silencing. In some plant-virus interactions, notably in plants infected with nepoviruses, symptom recovery is observed. In this complex phenotype, plants are initially diseased but later recover from infection and become asymptomatic. Symptom recovery can be considered as a form of inducible tolerance in which the virus persists but does not cause significant disease. Using Nicotiana benthamiana plants infected with tomato ringspot virus (ToRSV) as a model system, we have shown that symptom recovery is dependent on environmental conditions and on the specific ToRSV strain. In this pathosystem, the plant antiviral RNA silencing is activated to reduce but not eliminate virus infection. Temperature-dependent symptom recovery against a severe strain of ToRSV was shown to be associated with specific repression of the translation of viral RNAs, preventing the formation of viral proteins. This process was dependent on the plant ARGONAUTE 1 (AGO1), a key enzyme of the antiviral RNA silencing mechanism. A suppressor of silencing encoded by ToRSV was shown to counteract the AGO1-dependent translation repression mechanism although inefficiently. In contrast, symptom recovery against a mild strain of ToRSV at a lower temperature did not depend on AGO1. AGO2 restricted virus accumulation under these conditions but was not absolutely required for symptom recovering, suggesting that other AGOs are also likely to be involved. The results highlight the complexity and diversity of molecular mechanisms associated with symptom recovery and illustrate how the delicate balance between plant defense responses and virus counter-defenses determines the outcome from infection.
1. Understand the diversity and complexity of plant antiviral defense mechanisms, in particular antiviral RNA silencing
2. Understand how the balance between plant defense responses and viral counter-defenses determine the outcome from infection from susceptibility to tolerance to resistance
3. Understand that redundant and overlapping defense mechanisms can simultaneously operate in virus-infected plants
4. Understand the impact of environmental factors on plant virus-induced disease