Abstract Cucumber mosaic virus （CMV）， a positivesense singlestranded RNA virus， has a very wide host range and a worldwide distribution， and is considered as one of the most virulent plant viruses in the world. The CMV gene sequences， gene products， and their interaction with hosts have been extensively reported since it was discovered in 1916. With the development of highthroughput sequencing and proteomics， great progress has been made in the molecular mechanism of CMV pathogenesis in recent years. In this review， we introduce CMVencoded proteins， CMVrelated satellite RNAs and the roles of host factors in the pathogenesis of CMV， to provide a theoretical basis for future study of CMV.
　　Key words Cucumber mosaic virus （CMV）； Pathogenic mechanism； Small interfering RNA； Proteinprotein interaction
　　Received： November 20， 2017 Accepted： January 18， 2018
　　Supported by the Special Fund for Basic Scientific Research of Chinese Academy of Inspection and Quarantine （2017JK035）.
　　Yanhong QIU （1986-）， female， P. R. China， assistant professor， devoted to the research about plant virology， Email： qiuyh@caiq.gov.cn.
　　*Corresponding author. Email： zhusf@caiq.gov.cn
　　Cucumber mosaic virus （CMV）， a typical member in the family Bromoviridae， was first reported in 1916， when Doolittle and Jagger[1-2]found that it caused diseases in cucumber and other cucurbits. At present， it is widely distributed all over the world， especially in temperate and tropical regions. CMV has a variety of strains and can infect more than 1 200 species of plants， which makes it the most widely occurring and damaging virus to cereals， grasses， woody and herbal ornamental plants， vegetables and fruit trees[3].
　　CMV genome contains three positivesense singlestranded RNAs （RNA1， RNA2 and RNA3）， encoding a total of five proteins （1a， 2a， 2b， MP and CP）. Some CMV strains carry noncoding satellite RNAs （satRNAs） in addition to genomic RNAs[4-5]. CMV infection can cause stunt， leaf malformation， mosaic and other symptoms in plants. It has been proven that the occurrence of these symptoms is associated with CMV genes and the products encoded by these genes[4]. Therefore， this paper reviewed CMVrelated pathogenic factors， and the host proteins involved in the pathogenesis of the virus， to provide a theoretical basis for the study of CMV in the future.
　　The proteins encoded by CMV genes
　　1a protein
　　The 1a protein， encoded by RNA1， is an important component of replicase. It has the activity of RNAdependent RNA polymerase （RdRp） and is an important factor affecting host symptoms[5]. By comparing the pathogenicity of the Fny strain （CMVFny） and Sny strain （CMVSny） of CMV in zucchini， it was found that RNA1 affects not only the replication， but also the movement of the virus between cells and over long distances[6]. The CMVNs strain causes a systemic necrotic response in a wide range of tobacco species， which is found to be associated to the cysteine at position 461 of la protein[7]. There are two amphipathic αhelixes between the amino acids at positions 443 and 472 of 1a protein， and the mutation of the cysteine at position 461 to arginine or lysine affects the helical structures integrity and amphipathic nature， leading to the disappearance of necrotic reactions. However， mutation of the cysteine at position 461 to alanine or serine does not change the higher structure of 1a protein and thus does not affect the necrosis symptoms of CMVinfected hosts[8]. In addition， the amino acids at positions 865， 866， 957 and 980 of 1a protein together affect the replication and movement of the virus between cells， resulting in the systemic infection of CMVP1 in pepper plants carrying Cmr1 gene[9-10 ]. 　　2a protein
　　The 2a protein， encoded by RNA2， is involved in viral replication together with 1a protein， and also affects the development of host symptoms. Du et al.[11]found that deleting the Cterminal of 2a protein reduces the content of the virus in hosts and the pathogenic symptoms in tobacco. Choi et al.[12]proved that 2a protein and MP together affected the rate of celltocell movement in spinach leaves， thereby affecting the development of systemic symptoms. In addition， 2a protein is also an important factor that causes cell necrosis. The mutation of amino acid at position 631 of the protein results in a change of symptoms in cowpea[13-14].
　　2b protein
　　The 2b protein is encoded by RNA4A， a subgenomic RNA of RNA2 of CMV. On the one hand， it acts as a viral suppressor of RNA silencing （VSR）， which protects the genome of the virus from degradation， thereby affecting the accumulation and pathogenicity of the virus[15]. On the other hand， 2b protein inhibits gene silencingmediated antiviral pathways and affects the metabolic pathways of hosts microRNAs （miRNAs）， resulting in symptoms of CMVinfected plants[16-17]. Arabidopsis thaliana expressing the 2b protein of CMVFny strain has obviously dwarf plants and other symptoms. Further studies showed that 2b protein could interfere with the metabolic pathway of miR159 in host A. thaliana and affect the transcription of miR159 target gene， resulting in the generation of host symptoms[17-18].
　　In addition， mutation of 2b protein of CMVQ results in delayed and diminished virus infection on tobacco and even leads to its inability to systematically infect cucumber， suggesting that 2b protein indirectly affects the development of symptoms by influencing the systemic movement of the virus[19]. DiazPendon et al.[20]also found that the 2b protein of CMVQ， although affecting the systemic infection of the virus in A. thaliana， is not required for the development of symptoms.
　　MP protein
　　The MP protein is encoded by the RNA3 of CMV and is responsible for the movement of the virus between cells and over long distances[5]. Tobacco plants infected by CMVFny strain showed chronic symptoms rather than cycles of acute disease followed by no symptoms， and the chronic infection and high MP accumulation in tobacco plants were associated with the mutations of Asn to Lys at position 51 and Ile to Phe at position 240 of MP protein[21]. However， the same two amino acid mutations affected systematic movement of CMV in spinach[22]. The results showed that the effect of MP amino acid mutation on symptom development is host specific. 　　CP protein
　　CP protein is encoded by the subgenomic RNA4 derived from RNA3 of CMV and plays a crucial role in the packaging， replication， intercellular transport and longdistance transport of the virus， and is also the most important symptom determinant[23-24].
　　Plants infected with CMV usually show mosaic symptoms. For example， tobacco plants infected with CMVM show severe yellow/white mosaic symptoms， and those infected with CMVFny show chlorotic symptoms. Studies have proven that the occurrence of mosaic symptoms has a direct correlation with CP protein of CMV. Using some CMV pseudorecombinants， Rao and Francki[25]found that the symptom expression in host plants is determined by RNA3. In the study of Shintaku et al.[26]， recombination between cDNA clones of RNA 3 from FnyCMV and MCMV revealed that the mosaic symptoms in host plants are determined by the amino acid at position 129 of coat protein （CP129）. However， no significant correlation was observed between amino acid polarity and host symptoms by using the coat protein mutants of pepo strain， in which CP129 was substituted with acidic amino acids， basic amino acids and nonpolar amino acids[27]， suggesting that CP129 does not play a decisive role in CP structure. In addition， it can also be seen from the tertiary structure of CP that CP129 is not exposed on the surface of CP， but only the first amino acid of the βEαEF loop. Therefore， the mutations in CP129 are likely to affect only the flexibility of the βEαEF loop[28].
　　The production of mosaic symptoms is often accompanied by impaired chloroplast metabolism[29]. By analyzing the gene expression profiles of CMVM infected tobacco plants at different stages via highthroughput sequencing， we found that the expression of a large number of chloroplastrelated genes was suppressed[30]. Mutations of CP129 of CMVpepo strain into different amino acids produced different mosaic symptoms， and further studies showed that the chloroplastrelated genes were expressed at different levels in leaves with different mosaic symptoms[31]. The amounts of six proteins differentially decreased in CMVinfected tobacco leaves， and the decrease in oxygenevolving complex in photosystem II was the most significant[32]. Using twodimensional difference gel electrophoresis （DIGE） and mass spectrometry， Di Carli et al.[33]found that the protein expression pattern of CMVinfected wildtype tomato was different from that of CMVresistant transgenic tomato， and many of the differentially expressed proteins were involved in photosynthesis. The influence of virus infection on chloroplastrelated genes and proteins further disrupts the structure of chloroplasts. By observing the subcellular structures of leaves under a scanning electron microscope， we found that both the number of chloroplasts in chlorotic leaves and the number of thylakoid membranes in chloroplasts were reduced due to CMV infection[34]. In addition， the content of hydrogen peroxide in CMVinfected tobacco leaves was significantly increased[35]. Song et al.[36]also found that CMV infection interferes with the electron transport of chloroplasts and mitochondria and affects the antioxidant systems of cucumber and tomato leaves， and the accumulation of hydrogen peroxide resulted in oxidative stress in organelles. In plants， cytosomes， mitochondria and chloroplasts can all produce hydrogen peroxide， among which chloroplasts is the major site of hydrogen peroxide generation. A high concentration of hydrogen peroxide is toxic to plant cells. Whether the production of hydrogen peroxide is related to the disturbance of electron transfer of chloroplasts， the changes in chloroplast structure and the development of viral symptoms in infected plants is still unknown. 　　The Satellite RNAs （sat RNAs） Related to CMV Pathogenesis
　　The satRNAs are a class of noncoding RNA molecules， whose replication， packaging， movement and transport are thought to be completely dependent on their helper viruses[5]. The satRNAs can enhance， attenuate or unchanged the pathogenicity of helper viruses. Because satRNA competes with the genomic RNAs of helper viruses during replication， resulting in reduced accumulation of the genomic RNAs of helper viruses in hosts， thereby reducing viral symptoms； a minority of satRNAs can still cause necrosis[37]， mosaic symptoms in tobacco and tomato[38-39]. However， in host plants inoculated with CMVsatRNA and tomato aspermy virus （TAV）， the symptoms of TAV were relieved， but the genomic content of TAV was not decreased[40-41]. Furthermore， in host plants coinfected with CMVsatRNA and zucchini yellow mosaic virus （ZYMV）， the level of ZYMV was increased[42]. These studies revealed that the pathogenicity of satRNA is due to the interaction between satRNA， helper viruses and hosts[43].
　　In 1982， Gonsalves et al.[38]found that WL2 satRNA could cause white leaf disease in tomato， accompanied by significant decrease in chlorophyll content and carotene content in the leaves. The reduction in chlorophyll content was also found in B5 satRNAinfected tomato leaves[39]. Until 2011， it was found that the small interfering RNA （siRNA） produced by satRNA during CMV infection is the key factor that induces leaf yellowing. Viral siRNAs are a class of about 21-24 nt RNAs produced from viral doublestranded RNA under the cleavage of plant DCL protein， are important intermediates during antiviral immune responses of plants[44]. However， due to the presence of a 22 nt complementary region between the viral siRNA and the chlorophyll biosynthetic gene （CHLI）， the mRNA of CHLI is degraded with the production of siRNA of satRNA， affecting chlorophyll synthesis and leading to yellowing of tobacco leaves[45-46]. A large number of CMV siRNA data were obtained in tobacco， and sequence alignment showed that the CMV siRNAs target abundant host genes[47]. The specific function of the siRNA in CMVM pathogenesis needs to be studied in depth.
　　Table 1 The main host proteins that have been proven to interact with CMVencoded proteins
　　Host proteinHostCMVencoded proteinRole of host protein in viral infectionLiterature
　　Tcoi1Tobacco1aTo methylate 1a protein， and assist in the replication and transport of CMV[48] 　　Tcoi2Tobacco1aTo phosphorylate the methyl transferase domain of 1a protein[49]
　　BRP1Tobacco1aRelated to viral replication[50]
　　FDH/CRT3Pepper1aRelated to viral replication[51]
　　Tsip1Tobacco1aRelated to viral replication[52]
　　Tsip1Tobacco2aRelated to viral replication[52]
　　NtCIPK12Tobacco2aInvolved in the phosphorylation of 2a protein[53]
　　AGO1Arabidopsis2bInvolved in gene silencingmediated antiviral pathways and miRNA mentalism[57]
　　AGO4Arabidopsis2bInvolved in gene silencingmediated antiviral pathways and miRNA mentalism[55]
　　JAZArabidopsis/tobacco2bRelated to aphidmediated spread of CMV[58]
　　CATArabidopsis2bRelated to the development of necrosis symptom in hosts[59]
　　CsAO4CucumberMPTo assist in viral movement at early stage of infection[60]
　　Yanhong QIU et al. A Review on the Pathogenicity of Cucumber Mosaic Virus
　　The Host Proteins Related to CMV Pathogenesis
　　Viruses can encode very limited number of proteins， so they rely on hostencoded proteins for replication. Table 1 shows the host proteins that have been proven to interact with CMVencoded proteins. During the replication of CMV， 1a protein is anchored first on the tonoplast or tonoplast proteins. Then 2a protein is also anchored on the tonoplast by interacting with 1a protein through the amino acid at position 126 at the Nterminal， to enable viral replication with the assistance of other proteins. After the replication is completed， 2a protein is phosphorylated， and dissociates in the cytoplasm， participating in the infection of other viruses[5]. Tcoi1 protein of tobacco was screened via yeast twohybrid system， and proven to be able to interact with the methyltransferase domain of 1a protein. High level of Tcoi1 expression is beneficial to CMV infection， whereas reducing Tcoi1 expression inhibits CMV infection， indicating that Tcoi1 protein is able to methylate 1a protein， assisting the replication and transport of the virus[48]. Tobacco Tcoi2 protein can also interact with and phosphorylate the methyltransferase domain of 1a protein， and it is assumed that the phosphorylation of 1a protein may affect the interaction between 1a protein and 2a protein or other host factors[49]. In addition， there is an interaction between tobacco Bromodomain containing RNA binding protein （BRP1） and 1a protein. However， silencing BRP1 does not completely inhibit the replication of the virus， suggesting that the protein probably influences indirectly viral replication by affecting directly the stability of the virus replication complex[50]. Formate dehydrogenase （FDH） and calreticulin3 precursor （CRT3） which interact with 1a protein helicase were also isolated and identified from Capsicum annuum ‘Bukang’ by Choi et al.[51]， and they found that FDHsilenced plants showed local infection in inoculated leaves， but not in upper （systemic） leaves， and in CRT3silenced plants， infection was not observed in either the inoculated or the upper leaves. Tobacco Tsip1 protein can interact with both 1a and 2a proteins. The level of viral RNA decreases in Tsip1overexpressing transgenic tobacco plants， and continues to increase in Tsip1silenced plants， suggesting that Tsip1 directly affects viral replication by complexing with 1a and 2a proteins[52]. Tobacco calcineurin Blike interacting protein kinase （NtCIPK12） that interacts with and phosphorylates 2a protein[53]， affecting the interaction of 2a with 1a[54]. 　　Argonaute （AGO） protein is an important factor in small RNA metabolic pathways of plants. The 2b protein can interact with AGO1 and AGO4， and inhibits AGO1 cleavage activity to inhibit miRNA pathways， attenuate RNA silencing， and counter host defense[55-57]. In addition to a wellcharacterized viral suppressor of host RNA interference （VSR）， 2b protein also acts as a viral inducer of host attractiveness to insect vectors （VIA）. JAZ （Jasmonate ZIMdomain protein） is an important inhibitor of jasmonic acid signaling pathway. 2b protein interacts with JAZ protein to inhibit jasmonic acid signal pathway and enhance the host plants attraction to aphids[58]. In addition， 2b protein can interact with catalase 3 （CAT3） in Arabidopsis and inhibit its enzymatic activity. As an important hydrolase of hydrogen peroxide， the inhibition of CAT activity will lead to hydrogen peroxide accumulation and cell necrosis[59].
　　CsAO4 is a cell wall localized ascorbate oxidase in cucumber. Viral infection induces CsAO4 expression in tobacco plants. Virus infection can induce the expression of the protein in tobacco. The accumulation of CMV in systemic leaves was reduced by knocking down CsAO4encoding gene， while overexpression of this protein did not significantly increase the accumulation of CMV in systemic leaves， indicating that CsAO4 together with MP protein helps virus move to neighboring cells[60].
　　Conclusions
　　The molecular pathogenesis of plant viruses has been a hot topic in recent years. A number of host proteins involved in CMV infection have been identified using molecular techniques such as yeast twohybrid screening， bimolecular fluorescence complement （BiFC） and coimmunoprecipitation （COIP）. In addition， a large number of host genes and proteins involved in the pathogenesis of plant viruses have been determined using transcriptome sequencing and proteomics techniques. All of these studies provide a theoretical basis for revealing the molecular pathogenesis of CMV.
　　The indepth studies of gene silencingmediated antiviral defense in plants， and especially the discovery that the siRNA produced by satRNA during CMV infection is the key factor that induces yellow/white mosaic symptoms in plants， open new paths for the research of plant virus pathogenicity.
　　Although great progresses have been made in the study of the pathogenesis of CMV， how CP and the amino acid at position 129 affect host symptoms， chloroplast structure and function is still unclear. Moreover， how the siRNAs produced by the viral genome target the host genes and their role in viral pathogenesis remain to be explored. 　　References
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