中文摘要：

南方水稻黑条矮缩病毒（SRBSDV）由介体白背飞虱以持久增殖型方式传播,但有关病毒在介体内高效增殖的机制仍不明确.RNA干扰（RNAi）是昆虫保守的抗病毒免疫途径.为了探索SRBSDV在介体白背飞虱体内的持久增殖是否受到RNAi抗病毒免疫途径的调控,本研究采用小分子RNA深度测序发现SRBSDV侵染白背飞虱培养细胞后诱导产生病毒来源的主要长度为21和22 nt的小分子RNA,暗示病毒侵染可激活RNAi反应.在白背飞虱及其培养细胞中通过dsR NA处理干扰RNAi途径中的关键组分Dicer2和Argonaute2基因表达后,SRBSDV的侵染率和积累量显著提高,带毒昆虫的存活率下降、寿命减短.因此,RNAi途径具有调控SRBSDV在介体白背飞虱体内的持久侵染、控制植物病毒在介体昆虫内过度积累从而避免病毒对昆虫造成不利影响的作用.

英文摘要：

Southern rice black-streaked dwarf virus （SRBSDV） is transmitted by the white-backed planthopper （WBPH; Sogatella furcifera Horvth） in a persistent-propagative manner. The mechanism for the highly efficient propagation of SRBSDV in the WBPH vector is unknown. RNA interference （RNAi） is generally thought to be an evolutionarily conserved antiviral immunity pathway in insects. To determine whether the persistent propagation of SRBSDV in the WBPH vector is modulated by an RNAi antiviral immunity pathway, we used small-RNA deep sequencing to detect 21- and 22-nt virus-derived small RNAs in cultured cells derived from WBPH infected with SRBSDV; the presence of these small RNAs implied that an RNAi response was trigged by viral infection. In addition, knockdown of the expressions of key RNAi pathway factors Dicer2 and Argonaute2 by treatment with dsRNA synthesized from Dicer2 and Argonaute2 genes strongly increased viral infection and accumulation in the WBPH vector and its cultured cells. Furthermore, the knockdown of Dicer2 and Argonaute2 expression reduced the survival rate and lifespan of the viruliferous insects. Taken together, these results indicate that the RNAi pathway effectively modulates the persistent infection of SRBSDV in the WBPH vector. This pathway thus plays a crucial role by preventing excessive plant virus accumulation in insect vectors, thereby protecting them from the negative impact of these viruses.