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Not AvailableVirus-derived siRNAs (vsiRNAs) generated by the host RNA silencing mechanism are
effectors of plant’s defense response and act by targeting the viral RNA and DNA in posttranscriptional
gene silencing (PTGS) and transcriptional gene silencing (TGS) pathways,
respectively. Contrarily, viral suppressors of RNA silencing (VSRs) compromise the
host RNA silencing pathways and also cause disease-associated symptoms. In this
backdrop, reports describing the modulation of plant gene(s) expression by vsiRNAs via
sequence complementarity between viral small RNAs (sRNAs) and host mRNAs have
emerged. In some cases, silencing of host mRNAs by vsiRNAs has been implicated
to cause characteristic symptoms of the viral diseases. Similarly, viroid infection results
in generation of sRNAs, originating from viroid genomic RNAs, that potentially target
host mRNAs causing typical disease-associated symptoms. Pathogen-derived sRNAs
have been demonstrated to have the propensity to target wide range of genes including
host defense-related genes, genes involved in flowering and reproductive pathways.
Recent evidence indicates that vsiRNAs inhibit host RNA silencing to promote viral
infection by acting as decoy sRNAs. Nevertheless, it remains unclear if the silencing
of host transcripts by viral genome-derived sRNAs are inadvertent effects due to
fortuitous pairing between vsiRNA and host mRNA or the result of genuine counterdefense
strategy employed by viruses to enhance its survival inside the plant cell. In
this review, we analyze the instances of such cross reaction between pathogen-derived
vsiRNAs and host mRNAs and discuss the molecular insights regarding the process
of pathogenesis.Not Availabl