Plant viruses, which can cause devastating plant diseases, are obligate intracellular pathogens that replicate their genomes inside cells and spread infection by cell-to-cell movement through cell wall nanochannels called plasmodesmata (PD). Double-stranded RNA, which occurs as a replication intermediate of RNA viruses, triggers adaptive and innate host defense responses that are controlled by virus-encoded effector proteins. These defenses include RNA silencing and RNA decay, which target viral RNA and inhibit virus accumulation, and pattern-triggered immunity (PTI), which targets PD and inhibits virus movement. A new review article published by Manfred Heinlein (IBMP) in Annual Review of Virology provides a holistic discussion about the role of RNA silencing, RNA decay, PTI, and effector-triggered immunity (ETI) as antiviral defense mechanisms, how they are interrelated, and how viruses interact with these mechanisms to ensure their successful replication and spread throughout the plant organism.
Antiviral Double-Stranded RNA Sensing Immunity in Plants
