Abstract
Numerous plant viruses that cause significant agricultural problems are persistently transmitted by insect vectors. We wanted to see if apoptosis was involved in viral infection process in the vector. We found that a plant reovirus (rice gall dwarf virus, RGDV) induced typical apoptotic response during viral replication in the leafhopper vector and cultured vector cells, as demonstrated by mitochondrial degeneration and membrane potential decrease. Fibrillar structures formed by nonstructural protein Pns11 of RGDV targeted the outer membrane of mitochondria, likely by interaction with an apoptosis-related mitochondrial protein in virus-infected leafhopper cells or nonvector insect cells. Such association of virus-induced fibrillar structures with mitochondria clearly led to mitochondrial degeneration and membrane potential decrease, suggesting that RGDV Pns11 was the inducer of apoptotic response in insect vectors. A caspase inhibitor treatment and knockdown of caspase gene expression using RNA interference each reduced apoptosis and viral accumulation, while the knockdown of gene expression for the inhibitor of apoptosis protein improved apoptosis and viral accumulation. Thus, RGDV exploited caspase-dependent apoptotic response to promote viral infection in insect vectors. For the first time, we directly confirmed that a nonstructural protein encoded by a persistent plant virus can induce the typical apoptotic response to benefit viral transmission by insect vectors.
Highlights
In mammals, viral infection can induce or activate apoptosis, a process of programmed cell death, which generally is important in the regulation of viral pathogenesis [1]
By applying a system that combines insect vector cell cultures, immunofluorescence and electron microscopy, we revealed that the fibrillar structures that are composed of nonstructural protein Pns11 of rice gall dwarf virus (RGDV), targeted mitochondria and activated typical apoptotic response to promote viral infection and transmission by insect vectors
To explore how the virus causes these adverse effects, we first investigated whether RGDV infection caused apoptotic changes in continuous cultured cells of R. dorsalis, which were originally established from embryonic fragments dissected from eggs [17]
Summary
Viral infection can induce or activate apoptosis, a process of programmed cell death, which generally is important in the regulation of viral pathogenesis [1]. Apoptosis is a normal process during development and aging to regulate cell populations in multicellular organisms [2,3]. The chromatin is cleaved into nucleosomal fragments, and apoptotic bodies are generated [11]. These fundamental stages are first elucidated for mammalian systems, due to the important function of apoptosis in development and diseases [2]. Apoptosis is commonly involved in viral pathogenesis, some viruses appear to have evolved to exploit this mechanism to promote their survival and replication in different ways [12,13,14]. The role of apoptosis in host–virus interactions is diverse among different viruses
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