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Citrus tristeza virus (CTV), belonging to the family Closteroviridae, is one of the most biologically complex viruses, with extremely complex biological properties, and is considered to be the most damaging pathogen of citrus from an economic point of view. Today the virus continues to threaten the citrus industry around the world, and CTV is one of the most challenging viruses from a research perspective due to the large size of its RNA genome, the fragile shape of the virus which resembles curved filaments, and its narrow host range, which predominantly infects phloem-associated cells in slow-growing citrus varieties.
CTV is a single-stranded positive-sense RNA genome containing 19.3 kb, the largest non-fragmented RNA genome in the field of plant viruses. The RNA genome of CTV contains 12 open reading frames (ORFs) encoding polyproteins required for viral replication (ORF 1a and 1b); major (CP) and minor capsid proteins, p65 (an HSP70 homologue) and p61, which are involved in viral assembly; the hydrophobic p6 protein, which is thought to play a role in viral motility; and p20 and p23, which together with CP inhibit RNA silencing. The CTV genome also includes a number of unique genes that can be used to sensitize host viral infections, such as genes for the p33, p13, and p18 proteins. ORF1a produces a 349 kDa protein that contains two leading protease domains as well as methyltransferase-like and helicase-like domains. Translation of ORF1a is occasionally carried over to ORF1b, which encodes the polymerase-like domain, by a frameshift in the unusual +1 conformation. The L1 protease is essential for virus accumulation and establishment of initial infection. L2 is indispensable for systemic infection of the virus in the natural citrus host. The 3'-coterminal subgenomic RNAs (sgRNAs) express 10 ORFs encoding proteins involved in different stages of the viral infection cycle. p33 is a membrane-associated protein whose binding to the membrane confers the ability of the virus to extend its host range, and p33 has been found to be a viral effector that influences the pathogenicity of CTV. In addition, the p33 protein is required for efficient virus transmission by aphid vectors, but how it functions in the transmission process is unclear.
Figure 1. Schematic diagram of the CTV genome organization
(Source: Folimonova SY, et al. 2020)
Viruses rely on many co-opted host factors to complete their infection cycle, so certain host factors limit virus infection by inhibiting different steps of the viral cycle or mediating recognition of the virus by the host immune system, thereby triggering a defense response. Identifying these factors is critical for developing durable antiviral strategies, such as methods to generate virus-resistant cultivars through molecular breeding. In natural infection, CTV enters the citrus host through aphid vectors. After the virus is decomposed, the genomic RNA is translated to produce proteins involved in virus replication. Replication of the CTV genome takes place in a virus-induced vesicular complex and produces a large number of different RNA species. These include the progeny genome; negative stranded copies; a set of 3'-coterminal sgRNAs that act as messenger RMAs to translate internal and 3' end genes, as well as their respective negative-sense complementary RNAs; two relatively short positive stranded non-coding sgRNAs at the 5' end, namely, LMT1 and LMT2 (low-molecular-weight tristeza RNA 1 and 2); a number of additional sgRNAs; and various defective RNAs. The next step is the production of viral proteins that mediate further steps in the viral infection cycle, such as virion assembly, movement of the virus between cells and throughout the body, and suppression of the host's immune response.
The p23 protein interacts with glyceraldehyde 3-phosphate dehydrogenase (GAPDH) from N. benthamiana in the cytoplasm and plasma membrane. p23 of CTV was found to play a role in controlling the replication ratios of viral positive- and negative-sense RNA molecules, as well as intercellular movement of the virus, and the interaction of p23 with GAPDH may support some of these processes. Inhibition of GAPDH expression reduced CTV titers in herbaceous hosts, suggesting that hijacking of GAPDH by the p23 protein facilitates the CTV infection cycle. Both p23 and CP interact with FK506-binding protein (FKBP 17-2), a member of a family of proteins with prolyl isomerase activity. These proteins are chaperone proteins for proline residue-containing proteins and are involved in different cellular processes such as stress response, cell signaling, protein transport, and photosynthesis. Knockdown of FKBP 17-2 expression in N. benthamiana reduced CTV accumulation, suggesting a proviral role for this protein in viral infections.
As viral silencing repressors, p20 and CP interact with argonaute 1 (AGO1) and argonaute 4 (AGO4), key components of the host RNA silencing mechanism; AGO1 associates with small interfering RNAs derived from viruses and targets the viral genome for degradation, while AGO4 is involved in the methylation of host DNA and thus plays a role in the regulation of host gene expression.
Invasion of CTV triggers accumulation of ROS and salicylic acid (SA), expression of plant immune-related genes, and programmed cell death (PCD), with p20, p23, and p33 being responsible for inducing such responses. Deletion of the p33 gene in the CTV genome reduces ROS production in herbaceous and citrus hosts and weakens the plant response to CTV, which allows the virus to spread beyond the phloem and invade the xylem. Further studies found that p33 can be recognized by host immune-related miraculin-like protein 2 (MLP2), which has been shown to be involved in the defense of bacteria, fungi and insects. On the one hand, MLP2 induced by p33 expression during virus infection hijacks p33 and changes its location in cells, thus hindering the function of p33 in virus movement. On the other hand, the induction of MLP2 induces cellular stress, ROS accumulation and even PCD through the combination of endoplasmic reticulum and Golgi, thus inhibiting the reproduction of CTV.
Figure 2. CTV-host interactions
(Source: Folimonova SY, et al. 2022)
Plants lack a humoral immune system, and the main reason for their success against a wide range of pathogens is using many different structural and acquired resistance strategies. These strategies are based on single or multiple genetic components that interact and evade lethal interactions between the pathogen and the host plant. In addition, the outcome of pathogen infection usually depends on pre-existing microbial communities in the same host, which may participate in synergism or antagonism to enhance or mitigate the effects of pathogen-induced diseases. Virus cross-protection is that the host plant is infected with asymptomatic or mild varieties of a virus, and then infected with closely related serious variants of the virus to protect against diseases. Cross protection is the result of the interaction between the genetic characteristics of protective viruses and challenging viruses.
One of the classic examples of the control of severe plant virus diseases through cross-protection is the large-scale use of mild CTV virus isolates to control the manifestations of the devastating stem pitting disease caused by a number of invasive virus isolates. Grafted on C. aurantium L. Citrus trees showed typical symptoms of rapid decline, which can be effectively controlled by using citrus rootstocks or citrus related rootstocks that are tolerant or resistant to CTV. Cross-protection does not depend on the symptoms of the CTV isolates, but on genetic similarity. When repeated attempts to control with completely mild isolates are unsuccessful, the reason is that the isolates belong to different CTV strains.
Figure 3. CTV-based cross protection for disease control
(Source: Folimonova SY, et al. 2022)
References
| Target | Cat. No. | Product Name | Size | Species Reactivity | Application | Detection Sample | |
| CTV | DEIABL-PV5 | Citrus Tristeza Virus ELISA Development Kit | 500T | Citrus petiole, ovary | Inquiry | ||
| CTV | DEIAPV128 | Citrus tristeza virus (CTV) ELISA Kit | 500T/1000T/5000T | Qualitative | Host plants | Inquiry |
| Target | Cat. No. | Product Name | Host | Isotype | Application | |
| CTV | CABT-B1003 | Anti-CTV polyclonal antibody | Rabbit | IgG | ELISA | Inquiry |
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