Oxidative stress and antioxidative responses in plant–virus interactions

• We review the role of ROS and the antioxidative metabolism in incompatible and compatible plant–virus interactions.
• An early and efficient ROS accumulation and signalling could result in at least a partial suppression of the invading virus even during compatible infections.
• During early, short-term responses to compatible virus infections the induction of antioxidant defences seems to interfere with ROS signalling needed to initiate resistance responses.
• Finally, during advanced stages of pathogenesis an imbalance in the antioxidative metabolism contributes to senescence-like symptoms in virus susceptible plant tissues.

During plant–virus interactions, defence responses are linked to the accumulation of reactive oxygen species (ROS). Importantly, ROS play a dual role by (1) eliciting pathogen restriction and often localized death of host plant cells at infection sites and (2) as a diffusible signal that induces antioxidant and pathogenesis-related defence responses in adjacent plant cells. The outcome of these defences largely depends on the speed of host responses including early ROS accumulation at virus infection sites. Rapid host reactions may result in early virus elimination without any oxidative stress (i.e. a symptomless, extreme resistance). A slower host response allows a certain degree of virus replication and movement resulting in oxidative stress and programmed death of affected plant cells before conferring pathogen arrest (hypersensitive response, HR). On the other hand, delayed host attempts to elicit virus resistance result in an imbalance of antioxidative metabolism and massively stressed systemic plant tissues (e.g. systemic chlorotic or necrotic symptoms). The final consequence of these processes is a partial or almost complete loss of control over virus invasion (compatible infections).