As described previously, RNA silencing is a nucleotide sequence-specific process that induces mRNA degradation or translation inhibition at the post-transcriptional levels. It is also involved in epigenetic modification at the transcriptional level, and is dependent on RNA-directed DNA methylation (RdDM) [93]. Besides the involvement in diverse biological processes, RNA silencing also functions as a natural anti-viral defense mechanism, via a process termed virus-induced gene silencing (VIGS) [94] and [95]. When the host anti-viral surveillance system recognizes a foreign viral RNA, the RNA silencing machinery is activated to target and process the virus-derived dsRNA, which is either derived from pathogen replication or amplified by the host in a RdRp-dependent manner, into vsiRNA (virus-derived siRNAs). These vsiRNAs are then recruited to the host RISC to target and destroy viral RNAs. This in turn, hinders the accumulation of viral RNA and affects the infection process [96]. In cases where plant mRNA has sequence homology with the viral genome, both the viral and plant transcripts will be targeted for destruction [97] and [98]. Similarly, when plants are transformed to express transgene-induced PTGS, the exogenous foreign transgenic sequence is recognized and amplified by the plant-encoding RdRp, into dsRNA, which serves as the downstream substrate to trigger RNA silencing [99] and [100]. The resulting PTGS can target against transcripts of the transgenes and any homologous pathogen endogenous genes for degradation, such that the corresponding gene products are greatly reduced [101]. In addition, PTGS may confer cross-protection against infection with a second virus in a nucleotide sequence-specific manner [96]. Besides protecting infected cells against viral infection, PTGS are capable of moving in-between cells via plasmodesmata, and migrate systemically over long distance through the vascular system to direct sequence-specific degradation of target RNAs at a distal site [102] and [103]. This movement of VIGS signal in advance of the infection front may potentiate systemic RNA sequence-specific virus resistance in the non-infected tissues and consequently, delay the spread of virus. Therefore, the abundant expression of dsRNAs to trigger efficient RNA silencing becomes crucial for effective resistance.