Oxidative stress and antioxidative responses in plant-virus interactions

Abstract

[eng] During plantevirus 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).