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Positive-sense single-stranded RNA (+ssRNA) viruses, the most abundant viruses of eukaryotes in nature, require the synthesis of negative-sense RNA (-RNA) using their genomic (positive-sense) RNA (+RNA) as a template for replication. Based on current evidence, viral proteins are translated via viral +RNAs, whereas -RNA is considered to be a viral replication intermediate without coding capacity. Here, we report that plant and animal +ssRNA viruses contain small open reading frames (ORFs) in their -RNA (reverse ORFs [rORFs]). Using turnip mosaic virus (TuMV) as a model for plant +ssRNA viruses, we demonstrate that small proteins encoded by rORFs display specific subcellular localizations, and confirm the presence of rORF2 in infected cells through mass spectrometry analysis. The protein encoded by TuMV rORF2 forms punctuate granules that are localized in the perinuclear region and co-localized with viral replication complexes. The rORF2 protein can directly interact with the viral RNA-dependent RNA polymerase, and mutation of rORF2 completely abolishes virus infection, whereas ectopic expression of rORF2 rescues the mutant virus. Furthermore, we show that several rORFs in the -RNA of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have the ability to suppress type I interferon production and facilitate the infection of vesicular stomatitis virus. In addition, we provide evidence that TuMV might utilize internal ribosome entry sites to translate these small rORFs. Taken together, these findings indicate that the -RNA of +ssRNA viruses can also have the coding capacity and that small proteins encoded therein play critical roles in viral infection, revealing a viral proteome larger than previously thought., (Copyright © 2023 The Author. Published by Elsevier Inc. All rights reserved.)

Viruses infect all cellular life forms and cause various diseases and significant economic losses worldwide. The majority of viruses are positive-sense RNA viruses. A common feature of infection by diverse RNA viruses is to induce the formation of altered membrane structures in infected host cells. Indeed, upon entry into host cells, plant-infecting RNA viruses target preferred organelles of the cellular endomembrane system and remodel organellar membranes to form organelle-like structures for virus genome replication, termed as the viral replication organelle (VRO) or the viral replication complex (VRC). Different viruses may recruit different host factors for membrane modifications. These membrane-enclosed virus-induced replication factories provide an optimum, protective microenvironment to concentrate viral and host components for robust viral replication. Although different viruses prefer specific organelles to build VROs, at least some of them have the ability to exploit alternative organellar membranes for replication. Besides being responsible for viral replication, VROs of some viruses can be mobile to reach plasmodesmata (PD) via the endomembrane system, as well as the cytoskeleton machinery. Viral movement protein (MP) and/or MP-associated viral movement complexes also exploit the endomembrane-cytoskeleton network for trafficking to PD where progeny viruses pass through the cell-wall barrier to enter neighboring cells.

Tomato brown rugose fruit virus (ToBRFV) is an emerging and rapidly spreading RNA virus that infects tomato and pepper, with tomato as the primary host. The virus causes severe crop losses and threatens tomato production worldwide. ToBRFV was discovered in greenhouse tomato plants grown in Jordan in spring 2015 and its first outbreak was traced back to 2014 in Israel. To date, the virus has been reported in at least 35 countries across four continents in the world. ToBRFV is transmitted mainly via contaminated seeds and mechanical contact (such as through standard horticultural practices). Given the global nature of the seed production and distribution chain, and ToBRFV's seed transmissibility, the extent of its spread is probably more severe than has been disclosed. ToBRFV can break down genetic resistance to tobamoviruses conferred by R genes Tm-1, Tm-2, and Tm-2 2 in tomato and L 1 and L 2 alleles in pepper. Currently, no commercial ToBRFV-resistant tomato cultivars are available. Integrated pest management-based measures such as rotation, eradication of infected plants, disinfection of seeds, and chemical treatment of contaminated greenhouses have achieved very limited success. The generation and application of attenuated variants may be a fast and effective approach to protect greenhouse tomato against ToBRFV. Long-term sustainable control will rely on the development of novel genetic resistance and resistant cultivars, which represents the most effective and environment-friendly strategy for pathogen control., Taxonomy: Tomato brown rugose fruit virus belongs to the genus Tobamovirus, in the family Virgaviridae. The genus also includes several economically important viruses such as Tobacco mosaic virus and Tomato mosaic virus., Genome and Virion: The ToBRFV genome is a single-stranded, positive-sense RNA of approximately 6.4 kb, encoding four open reading frames. The viral genomic RNA is encapsidated into virions that are rod-shaped and about 300 nm long and 18 nm in diameter. Tobamovirus virions are considered extremely stable and can survive in plant debris or on seed surfaces for long periods of time., Disease Symptoms: Leaves, particularly young leaves, of tomato plants infected by ToBRFV exhibit mild to severe mosaic symptoms with dark green bulges, narrowness, and deformation. The peduncles and calyces often become necrotic and fail to produce fruit. Yellow blotches, brown or black spots, and rugose wrinkles appear on tomato fruits. In pepper plants, ToBRFV infection results in puckering and yellow mottling on leaves with stunted growth of young seedlings and small yellow to brown rugose dots and necrotic blotches on fruits., (© 2022 Her Majesty the Queen in Right of Canada. Molecular Plant Pathology published by British Society for Plant Pathology and John Wiley & Sons Ltd. Reproduced with the permission of the Minister of Agriculture and Agri-Food Canada.)

The plant phloem vasculature is crucial for plant growth and development, and is essential for the systemic movement (SM) of plant viruses. Recent transcriptomic studies of the phloem during virus infection have shown the importance of this tissue, yet transcript levels do not provide definitive answers how virus-host interactions favour successful viral SM. Proteomic analyses have been used to identify host-virus protein interactions, uncovering a variety of ways by which viruses utilize host cellular machinery for completion of the viral infection cycle. Despite this new evidence through proteomics, very few phloem centric studies during viral infection have been performed. Here, we describe a protocol for the isolation of phloem tissues and proteins and the subsequent label-free quantitation (LFQ), for identification of proteomic alterations caused by viral infection., (© 2022. Springer Science+Business Media, LLC, part of Springer Nature.)

Protein-protein interactions play a crucial role in diverse biological processes. As obligate intracellular parasites, plant viruses live and reproduce in living cells and recruit host proteins through protein-protein interactions to complete their infection process. Elucidation of the protein-protein interaction network between viruses and hosts can advance knowledge in the viral infection process at the molecule level and facilitate the development of novel antiviral technologies. One of the most classic and widely used methods to discover or confirm novel protein interactions in plant cells is the pull-down assay. For plant virology research, this method begins with the expression of a tagged viral protein (such as GST- or His-tagged) as "bait" in model plant species such as Nicotiana benthamiana. The expressed "bait" protein is purified by affinity agarose resin (e.g., glutathione or cobalt chelate) followed by a series of washes. Finally, the "bait"-"prey" protein complexes are subjected to mass spectrometry or immunoblotting analysis. In this chapter, we describe a practical protocol of the tag-based pull-down assay and discuss solutions to some common problems associated with this assay., (© 2022. Springer Science+Business Media, LLC, part of Springer Nature.)

Plant viruses have evolved efficient mechanisms to move cell-to-cell through plasmodesmata (PD) for systemic infection. Potyviruses including many economically important viruses constitute the largest group of known plant-infecting RNA viruses. Potyviral intercellular movement is accomplished by the coordinated action of at least three viral proteins and diverse host components. It requires the viral coat protein and is interlinked with active virus replication that generates, through RNA-polymerase slippage, a small percentage of frameshift viral RNA for the production of another essential movement protein named P3N-PIPO. This PD-located protein targets the virus-encoded cylindrical inclusion protein to PD to form special conical structures for potyviral passage, possibly in the form of virion. Here, I highlight and discuss major advances of potyviral intercellular trafficking., (Crown Copyright © 2021. Published by Elsevier B.V. All rights reserved.)

Endocytosis and endosomal trafficking play essential roles in diverse biological processes including responses to pathogen attack. It is well established that animal viruses enter host cells through receptor-mediated endocytosis for infection. However, the role of endocytosis in plant virus infection still largely remains unknown. Plant dynamin-related proteins 1 (DRP1) and 2 (DRP2) are the large, multidomain GTPases that participate together in endocytosis. Recently, we have discovered that DRP2 is co-opted by Turnip mosaic virus (TuMV) for infection in plants. We report here that DRP1 is also required for TuMV infection. We show that overexpression of DRP1 from Arabidopsis thaliana (AtDRP1A) promotes TuMV infection, and AtDRP1A interacts with several viral proteins including VPg and cylindrical inclusion (CI), which are the essential components of the virus replication complex (VRC). AtDRP1A colocalizes with the VRC in TuMV-infected cells. Transient expression of a dominant negative (DN) mutant of DRP1A disrupts DRP1-dependent endocytosis and supresses TuMV replication. As adaptor protein (AP) complexes mediate cargo selection for endocytosis, we further investigated the requirement of AP in TuMV infection. Our data suggest that the medium unit of the AP2 complex (AP2β) is responsible for recognizing the viral proteins as cargoes for endocytosis, and knockout of AP2β impairs intracellular endosomal trafficking of VPg and CI and inhibits TuMV replication. Collectively, our results demonstrate that DRP1 and AP2β are two proviral host factors of TuMV and shed light into the involvement of endocytosis and endosomal trafficking in plant virus infection., (© 2019 Her Majesty the Queen in Right of Canada The Plant Journal © 2019 John Wiley & Sons Ltd and Society for Experimental Biology.)

A successful viral infection requires complex, compatible molecular interactions between the invading virus and the host. A better understanding of such interactions may assist in the development of novel approaches to control viral diseases for sustainable crop production. In the past decade, the cell biology of virus-host and virus-vector interactions has been one of the most exciting areas of research in the molecular plant-microbe field. This is partially attributed to the availability of powerful cell biology techniques, including imaging tools like confocal microscopy and electron microscopy and tomography. As a result, there has been an unprecedented increase in knowledge in the areas of the bi- and tripartite interactions of virus, host, and vector. We now have a much clearer picture of viral virulence mechanisms, virus-induced host defenses, viral counteracting strategies, and viral circulations in the insect vectors. This Focus Issue highlights molecular virus-plant and virus-vector interactions in the areas of cell biology and closely related disciplines and explores biotechnology-based antiviral strategies using knowledge generated from these research areas.

The Potyviridae is the largest family of RNA plant viruses, members of which have single-stranded, positive-sense RNA genomes and flexuous filamentous particles 680-900 nm long and 11-20 nm wide. There are eight genera, distinguished by the host range, genomic features and phylogeny of the member viruses. Genomes range from 8.2 to 11.3 kb, with an average size of 9.7 kb. Most genomes are monopartite but those of members of the genus Bymovirus are bipartite. Some members cause serious disease epidemics in cultivated plants. This is a summary of the International Committee on Taxonomy of Viruses (ICTV) Report on the taxonomy of the Potyviridae, which is available at www.ictv.global/report/potyviridae.

In this study, we report the genome sequence of five isolates of strawberry mottle virus (family Secoviridae, order Picornavirales) from strawberry field samples with decline symptoms collected in Eastern Canada. The Canadian isolates differed from the previously characterized European isolate 1134 in that they had a longer RNA2, resulting in a 239-amino-acid extension of the C-terminal region of the polyprotein. Sequence analysis suggests that reassortment and recombination occurred among the isolates. Phylogenetic analysis revealed that the Canadian isolates are diverse, grouping in two separate branches along with isolates from Europe and the Americas.

As an organelle only found in plant cells and some protists, the chloroplast is not only the main metabolic energy originator, but also the abiotic/biotic stress sensor and defense signal generator. For a long time, chloroplasts have been recognized as a common target by many plant viruses. Viruses may directly modify chloroplast membranes to assemble their replication complex for viral genome replication. Viruses may downregulate chloroplast-related and photosynthesis-related genes via an as yet unknown mechanism to support their infection. Viruses may also interrupt functionality of the photosynthetic machinery through protein-protein interactions. This review briefly summarizes current knowledge about modifications of the photosynthetic machinery by plant viruses, highlights the important role of chloroplasts in the infection process and discusses chloroplast-associated pathogenesis., (Crown Copyright © 2015. Published by Elsevier B.V. All rights reserved.)

A successful infection by a plant virus results from the complex molecular interplay between the host plant and the invading virus. Thus, dissecting the molecular network of virus-host interactions advances the understanding of the viral infection process and may assist in the development of novel antiviral strategies. In the past decade, molecular identification and functional characterization of host factors in the virus life cycle, particularly single-stranded, positive-sense RNA viruses, have been a research focus in plant virology. As a result, a number of host factors have been identified. These host factors are implicated in all the major steps of the infection process. Some host factors are diverted for the viral genome translation, some are recruited to improvise the viral replicase complexes for genome multiplication, and others are components of transport complexes for cell-to-cell spread via plasmodesmata and systemic movement through the phloem. This review summarizes current knowledge about host factors and discusses future research directions.

The use of genetic resistance is considered to be the most effective and sustainable approach to the control of plant pathogens. Although most of the known natural resistance genes are monogenic dominant R genes that are predominant against fungi and bacteria, more and more recessive resistance genes against viruses have been cloned in the last decade. Interestingly, of the 14 natural recessive resistance genes against plant viruses that have been cloned from diverse plant species thus far, 12 encode the eukaryotic translation initiation factor 4E (eIF4E) or its isoform eIF(iso)4E. This review is intended to summarize the current state of knowledge about eIF4E and the possible mechanisms underlying its essential role in virus infection, and to discuss recent progress and the potential of eIF4E as a target gene in the development of genetic resistance to viruses for crop improvement., (© HER MAJESTY THE QUEEN IN RIGHT OF CANADA 2012. MOLECULAR PLANT PATHOLOGY © 2012 BSPP AND BLACKWELL PUBLISHING LTD.)

The replication of positive-strand RNA viruses occurs in cytoplasmic membrane-bound virus replication complexes (VRCs). Depending on the virus, distinct cellular organelles such as the endoplasmic reticulum (ER), chloroplast, mitochondrion, endosome, and peroxisome are recruited for the formation of VRC-associated membranous structures. Previously, the 6,000-molecular-weight protein (6K) of plant potyviruses was shown to be an integral membrane protein that induces the formation of 6K-containing membranous vesicles at endoplasmic reticulum (ER) exit sites for potyvirus genome replication. Here, we present evidence that the 6K-induced vesicles predominantly target chloroplasts, where they amalgamate and induce chloroplast membrane invaginations. The vesicular transport pathway and actomyosin motility system are involved in the trafficking of the 6K vesicles from the ER to chloroplasts. Viral RNA, double-stranded RNA, and viral replicase components are concentrated at the 6K vesicles that associate with chloroplasts in infected cells, suggesting that these chloroplast-bound 6K vesicles are the site for potyvirus replication. Taken together, these results suggest that plant potyviruses sequentially recruit the ER and chloroplasts for their genome replication.

NONEXPRESSER OF PATHOGENESIS-RELATED GENES 1 (NPR1) is the master regulator of salicylic acid-mediated basal and systemic acquired resistance in plants. Here, we report that NPR1 plays a pivotal role in restricting compatible infection by turnip mosaic virus, a member of the largest plant RNA virus genus Potyvirus, and that such resistance is counteracted by NUCLEAR INCLUSION B (NIb), the viral RNA-dependent RNA polymerase. We demonstrate that NIb binds to the SUMO-interacting motif 3 (SIM3) of NPR1 to prevent SUMO3 interaction and sumoylation, while sumoylation of NIb by SUMO3 is not essential but can intensify the NIb–NPR1 interaction. We discover that the interaction also impedes the phosphorylation of NPR1 at Ser11/Ser15. Moreover, we show that targeting NPR1 SIM3 is a conserved ability of NIb from diverse potyviruses. These data reveal a molecular "arms race" by which potyviruses deploy NIb to suppress NPR1-mediated resistance through disrupting NPR1 sumoylation. Salicylic acid (SA) signaling pathway restricts the compatible infection of potyviruses. Here, Liu et al. show that potyviral NIb interacts with NPR1, the SA receptor in plants, preventing its sumoylation by SUMO3 and subsequent phosphorylation at Ser11/Ser15. This way, NPR1-mediated immunity is suppressed to promote virus infection. [ABSTRACT FROM AUTHOR]

Healthy agroecosystems are dependent on a complex web of factors and inter-species interactions. Flowers are hubs for pathogen transmission, including the horizontal or vertical transmission of plant-viruses and the horizontal transmission of bee-viruses. Pollination by the European honey bee (Apis mellifera) is critical for industrial fruit production, but bees can also vector viruses and other pathogens between individuals. Here, we utilized commercial honey bee pollination services in blueberry (Vaccinium corymbosum) farms for a metagenomics-based bee and plant virus monitoring system. Following RNA sequencing, viruses were identified by mapping reads to a reference sequence database through the bioinformatics portal Virtool. In total, 29 unique plant viral species were found at two blueberry farms in British Columbia (BC). Nine viruses were identified at one site in Ontario (ON), five of which were not identified in BC. Ilarviruses blueberry shock virus (BlShV) and prune dwarf virus (PDV) were the most frequently detected viruses in BC but absent in ON, while nepoviruses tomato ringspot virus and tobacco ringspot virus were common in ON but absent in BC. BlShV coat protein (CP) nucleotide sequences were nearly identical in all samples, while PDV CP sequences were more diverse, suggesting multiple strains of PDV circulating at this site. Ten bee-infecting viruses were identified, with black queen cell virus frequently detected in ON and BC. Area-wide bee-mediated pathogen monitoring can provide new insights into the diversity of viruses present in, and the health of, bee-pollination ecosystems. This approach can be limited by a short sampling season, biased towards pollen-transmitted viruses, and the plant material collected by bees can be very diverse. This can obscure the origin of some viruses, but bee-mediated virus monitoring can be an effective preliminary monitoring approach. [ABSTRACT FROM AUTHOR]

Viruses can hijack autophagosomes as the nonlytic release vehicles in cultured host cells. However, how autophagosome-mediated viral spread occurs in infected host tissues or organs in vivo remains poorly understood. Here, we report that an important rice reovirus, rice gall dwarf virus (RGDV) hijacks autophagosomes to traverse multiple insect membrane barriers in the midgut and salivary gland of leafhopper vector to enhance viral spread. Such virus-containing double-membraned autophagosomes are prevented from degradation, resulting in increased viral propagation. Mechanistically, viral nonstructural protein Pns11 induces autophagy and embeds itself in the autophagosome membranes. The autophagy-related protein 5 (ATG5)-ATG12 conjugation is essential for initial autophagosome membrane biogenesis. RGDV Pns11 specifically interacts with ATG5, both in vitro and in vivo. Silencing of ATG5 or Pns11 expression suppresses ATG8 lipidation, autophagosome formation, and efficient viral propagation. Thus, Pns11 could directly recruit ATG5-ATG12 conjugation to induce the formation of autophagosomes, facilitating viral spread within the insect bodies. Furthermore, Pns11 potentially blocks autophagosome degradation by directly targeting and mediating the reduced expression of N-glycosylated Lamp1 on lysosomal membranes. Taken together, these results highlight how RGDV remodels autophagosomes to benefit viral propagation in its insect vector. Author summary: Numerous plant viruses replicate inside the cells of their insect vectors. Here, we demonstrate that the progeny virions of rice gall dwarf virus in leafhopper vector are engulfed within virus-induced double-membraned autophagosomes. Such autophagosomes are modified to evade degradation, thus can be persistently exploited by viruses to safely transport virions across multiple insect membrane barriers. Viral nonstructural protein Pns11 induces the formation of autophagosomes via interaction with ATG5, and potentially blocks autophagosome degradation via mediating the reduced expression of N-glycosylated Lamp1 on lysosomal membranes. For the first time, we reveal that a nonstructural protein encoded by a persistent plant virus can induce an incomplete autophagy to benefit viral propagation in its insect vectors. [ABSTRACT FROM AUTHOR]

Summary: Autophagy is an evolutionarily conserved pathway in eukaryotes that delivers unwanted cytoplasmic materials to the lysosome/vacuole for degradation/recycling. Stimulated autophagy emerges as an integral part of plant immunity against intracellular pathogens.In this study, we used turnip mosaic virus (TuMV) as a model to investigate the involvement of autophagy in plant RNA virus infection.The small integral membrane protein 6K2 of TuMV, known as a marker of the virus replication site and an elicitor of the unfolded protein response (UPR), upregulates the selective autophagy receptor gene NBR1 in a UPR‐dependent manner. NBR1 interacts with TuMV NIb, the RNA‐dependent RNA polymerase of the virus replication complex (VRC), and the autophagy cargo receptor/adaptor protein ATG8f. The NIb/NBR1/ATG8f interaction complexes colocalise with the 6K2‐stained VRC. Overexpression of NBR1 or ATG8f enhances TuMV replication, and deficiency of NBR1 or ATG8f inhibits virus infection. In addition, ATG8f interacts with the tonoplast‐specific protein TIP1 and the NBR1/ATG8f‐containing VRC is enclosed by the TIP1‐labelled tonoplast. In TuMV‐infected cells, numerous membrane‐bound viral particles are evident in the vacuole.Altogether these results suggest that TuMV activates and manipulates UPR‐dependent NBR1‐ATG8f autophagy to target the VRC to the tonoplast to promote viral replication and virion accumulation. [ABSTRACT FROM AUTHOR]

To establish infection, plant viruses are evolutionarily empowered with the ability to spread intercellularly. Potyviruses represent the largest group of known plant‐infecting RNA viruses, including many agriculturally important viruses. To better understand intercellular movement of potyviruses, we used turnip mosaic virus (TuMV) as a model and constructed a double‐fluorescent (green and mCherry) protein‐tagged TuMV infectious clone, which allows distinct observation of primary and secondary infected cells. We conducted a series of deletion and mutation analyses to characterize the role of TuMV coat protein (CP) in viral intercellular movement. TuMV CP has 288 amino acids and is composed of three domains: the N‐terminus (amino acids 1–97), the core (amino acids 98–245), and the C‐terminus (amino acids 246–288). We found that deletion of CP or its segments amino acids 51–199, amino acids 200–283, or amino acids 265–274 abolished the ability of TuMV to spread intercellularly but did not affect virus replication. Interestingly, deletion of amino acids 6–50 in the N‐terminus domain resulted in the formation of aberrant virions but did not significantly compromise TuMV cell‐to‐cell and systemic movement. We identified the charged residues R178 and D222 within the core domain that are essential for virion formation and TuMV local and systemic transport in plants. Moreover, we found that trans‐expression of the wild‐type CP either by TuMV or through genetic transformation‐based stable expression could not rescue the movement defect of CP mutants. Taken together these results suggest that TuMV CP is not essential for viral genome replication but is indispensable for viral intercellular transport where only the cis‐expressed CP is functional. [ABSTRACT FROM AUTHOR]

RNA silencing is a fundamental, evolutionarily conserved mechanism that regulates gene expression in eukaryotes. It also functions as a primary immune defense in microbes, such as viruses in plants. In addition to RNA silencing, RNA decay and RNA quality-control pathways are also two ancestral forms of intrinsic antiviral immunity, and the three RNA-targeted pathways may operate cooperatively for their antiviral function. Plant viruses encode viral suppressors of RNA silencing (VSRs) to suppress RNA silencing and facilitate virus infection. In response, plants may activate a counter-counter-defense mechanism to cope with VSR-mediated RNA silencing suppression. In this review, we summarize current knowledge of RNA silencing, RNA decay, and RNA quality control in antiviral defense, and highlight the mechanisms by which viruses compromise RNA-targeted immunity for their infection and survival in plants. RNA silencing, RNA decay, and RNA quality control are three major RNA degradation pathways that target redundant/damaged/detrimental cellular and exogenous RNAs in plants. Virus infection may activate RNA degradation pathways. RNA silencing is the most important line of defense that restricts virus infection. Viruses have evolved diverse mechanisms to suppress RNA silencing. The best effective mechanism is to express VSRs. In response, plants may activate a countersuppression mechanism. RNA decay may function as an antiviral defense, possibly through concerted actions of RNA silencing. Viruses can repress RNA decay to promote viral proliferation. RNA quality control may recognize specific features of certain plant RNA viruses to restrict virus infection. Many viruses have also evolved strategies to escape or avoid this degradation pathway. [ABSTRACT FROM AUTHOR]

Background: Virus infection induces the activation and suppression of global gene expression in the host. Profiling gene expression changes in the host may provide insights into the molecular mechanisms that underlie host physiological and phenotypic responses to virus infection. In this study, the Arabidopsis Affymetrix ATH1 array was used to assess global gene expression changes in Arabidopsis thaliana plants infected with Plum pox virus (PPV). To identify early genes in response to PPV infection, an Arabidopsis synchronized single-cell transformation system was developed. Arabidopsis protoplasts were transfected with a PPV infectious clone and global gene expression changes in the transfected protoplasts were profiled. Results: Microarray analysis of PPV-infected Arabidopsis leaf tissues identified 2013 and 1457 genes that were significantly (Q ≤ 0.05) up- (≥ 2.5 fold) and downregulated (≤ -2.5 fold), respectively. Genes associated with soluble sugar, starch and amino acid, intracellular membrane/membrane-bound organelles, chloroplast, and protein fate were upregulated, while genes related to development/storage proteins, protein synthesis and translation, and cell wall-associated components were downregulated. These gene expression changes were associated with PPV infection and symptom development. Further transcriptional profiling of protoplasts transfected with a PPV infectious clone revealed the upregulation of defence and cellular signalling genes as early as 6 hours post transfection. A cross sequence comparison analysis of genes differentially regulated by PPV-infected Arabidopsis leaves against uniEST sequences derived from PPV-infected leaves of Prunus persica, a natural host of PPV, identified orthologs related to defence, metabolism and protein synthesis. The cross comparison of genes differentially regulated by PPV infection and by the infections of other positive sense RNA viruses revealed a common set of 416 genes. These identified genes, particularly the early responsive genes, may be critical in virus infection. Conclusion: Gene expression changes in PPV-infected Arabidopsis are the molecular basis of stress and defence-like responses, PPV pathogenesis and symptom development. The differentially regulated genes, particularly the early responsive genes, and a common set of genes regulated by infections of PPV and other positive sense RNA viruses identified in this study are candidates suitable for further functional characterization to shed lights on molecular virus-host interactions. [ABSTRACT FROM AUTHOR]

Potyviruses represent the largest group of known plant RNA viruses and include many agriculturally important viruses, such as Plum pox virus, Soybean mosaic virus, Turnip mosaic virus, and Potato virus Y. Potyviruses adopt polyprotein processing as their genome expression strategy. Among the 11 known viral proteins, the nuclear inclusion protein b (NIb) is the RNA-dependent RNA polymerase responsible for viral genome replication. Beyond its principal role as an RNA replicase, NIb has been shown to play key roles in diverse virus–host interactions. NIb recruits several host proteins into the viral replication complexes (VRCs), which are essential for the formation of functional VRCs for virus multiplication, and interacts with the sumoylation pathway proteins to suppress NPR1-mediated immunity response. On the other hand, NIb serves as a target of selective autophagy as well as an elicitor of effector-triggered immunity, resulting in attenuated virus infection. These contrasting roles of NIb provide an excellent example of the complex co-evolutionary arms race between plant hosts and potyviruses. This review highlights the current knowledge about the multifunctional roles of NIb in potyvirus infection, and discusses future research directions. [ABSTRACT FROM AUTHOR]

Plants have evolved sophisticated surveillance and defense mechanisms against constant attacks by different types of microbial pathogens including viruses. Nucleotide-based RNA silencing and receptor-based innate immunity constitute the primary plant defense to viral infection. To establish their infections, plant viruses have also evolved virulence strategies to suppress host defenses. This ever-lasting co-evolutionary arms race between the plant hosts and viruses has shaped today's multifaceted defense and counter-defense layout. A better understanding of this process will certainly assist in the development of new plant varieties with enhanced durable resistance and novel approaches to control viral pathogens for sustainable agriculture. In this addendum, we briefly review the current knowledge of the plant immune response to viral infection and discuss defense and counter-defense strategies. [ABSTRACT FROM PUBLISHER]