Abstract
RNA silencing is as an adaptive immune response in plants that limits the accumulation or spread of invading viruses. Successful virus infection entails countering the RNA silencing machinery for efficient replication and systemic spread in the host. The viruses encode proteins with the ability to suppress or block the host silencing mechanism, resulting in severe pathogenic symptoms and diseases. Tungro is a viral disease caused by a complex of two viruses and it provides an excellent system to understand the host and virus interactions during infection. It is known that Rice tungro bacilliform virus (RTBV) is the major determinant of the disease while Rice tungro spherical virus (RTSV) accentuates the symptoms. This study brings to focus the important role of RTBV ORF-IV in disease manifestation, by acting as both the victim and silencer of the RNA silencing pathway. The ORF-IV is a weak suppressor of the S-PTGS or stable silencing, but its suppression activity is augmented in the presence of specific RTSV proteins. Among these, RTBV ORF-IV and RTSV CP3 proteins interact with each other. This interaction may lead to the suppression of localized silencing as well as the spread of silencing in the host plants. The findings present a probable mechanistic glimpse of the requirement of the two viruses in enhancing tungro disease.
Highlights
Academic Editor: Elvira Fiallo-OlivéViruses represent the most invasive group of pathogens that are harmful for any host system they infect
This study brings to focus the important role of Rice tungro bacilliform virus (RTBV) open reading frames (ORFs)-IV in disease manifestation
This locus acts as both the victim and silencer of the RNA silencing pathway in host plants, representing a key target that can be exploited for boosting host plant resistance against tungro virus infection
Summary
Academic Editor: Elvira Fiallo-OlivéViruses represent the most invasive group of pathogens that are harmful for any host system they infect. Resistance against viruses was observed as early as 1929 followed by observations of the phenomenon popularly known as “cross protection”. It was shown that the plants experiencing disease symptoms on virus infection quickly recovered and the new tissues emerged without any symptoms [2]. These observations served as the early basis for engineering plants for viral resistance by integrating the viral genetic material into the plant genome and was termed as “pathogen derived resistance” (PDR) [2,3,4]. It could be later explained that cross protection and the recovery by PDR were associated with small
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