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Plant Virus Infection Cycle and Synthesis
Virus infection involves several steps: virus entry into the host cell, uncoating of the viral genome, targeting of viral genes to host cell machinery, genome replication, assembly of new viral components, and release of progeny virus. Key proteins like movement proteins and coat proteins facilitate various stages of the infection process by transporting the viral genome and protecting it. The virus life cycle is dependent on hijacking host cell processes and resources for its replication and spread to new cells.
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Plant Virus Infection Cycle and Synthesis
- 2. Virus Infection andSynthesis Proteins that initiate infection Core Protein Assembly
- 3. Table of Contents •Virus Infection • Introduction • Steps • Virus Entry into Host Cell • Uncoating • Targeting • Gene Expression and Genome Replication • Proteins that Intiate Infection • Virus Synthesis • Viral Translational Strategies • Viral Protein Products • Assembly of Viral Components • Steps of Virus Synthesis • Encapsidation/ Coating • Virion Budding and Maturation • Virion Exit Patterns • Spread of Virus • Virus infection life cycle
- 4.
- 5. •Virus is anucleo-protein having RNA or DNA as a genetic material. Infect a limited number of different plant species, few have a wide host range. Can multiply only inside a living cell, using host machinery. •Viruses can die quickly if outside a cell or if the cell dies. e.g., Cucumber mosaic virus •Viruses can retain their ability to infect for years after the infected plant part dies. e.g., Tobacco mosaic virus. Introduction
- 6. •The pathological phenotypesare the result of interference and/or competition for a substantial amount of host resources, which can disrupt host physiology to cause disease. Continued…
- 7. Several different stagesin the virus life cycle are occurring: 1) Penetration 2) Uncoating 3) Targeting 4) Gene expression 5) Genome replication 6) Virion assembly/maturation 7) Release of new infectious virus Steps of Virus Infection
- 8. Compete with hostdefense mechanism •Although lacking an immune system comparable to animals, plants have developed a stunning array of structural, chemical, and protein- based defenses designed to detect invading organisms and stop them before they are able to cause extensive damage. •Pathogens have developed countermeasures that are able to suppress basal resistance in certain plant species. Virus Entry into Host Cell
- 9. Wounds •Virus enters intothe plant through wounds in epidermal cells or through roots. Fig: Virus entry through wounds Mechanical Damage
- 10. •Virus particles directlyin contact with protoplasmic membranes are assembled in host cells by pinocytosis •e.g., •Cow pea mosaic virus Pinocyte
- 11. •Inoculum efficiency formechanically transmissible viruses is increased in presence of abrasive powders on foliage •Abrasive increases frequency of infectable wounds •Requires104 to 105 virus particles applied to leaf surface for each cell infected •e.g., •Potato virus X Mechanical Inoculation
- 12. •Arthropods •Nematodes •Fungi Arthropods •Aphids, whiteflies, leafhoppers,thrips, beetles, mealybugs, mirids, and mites •The hollow, needle-like mouthparts can penetrate the plant cell wall, either by mechanical force and/or with the help of salivary and gut enzymes. •It does not always irreparably damage the plant cell. Vector-Mediated
- 13. Beetle Whitefly Thripes Leafhopper Zoospore Aphid
- 14. •The genome iscompletely released from the capsid during or after penetration. This is known as "uncoating“ •Different experiments indicating uncoating of viral RNA • TMV multiplication detected some hours earlier when inoculation is done by RNA. Uncoating
- 15. •Since almost allDNA viruses replicate in the nucleus of infected cells, they must be targeted there Targeting
- 16. •Viruses contains twotypes of genome: •DNA genome •RNA genome •For DNA genome, the replication cycle can be broken down into the following steps: •Early gene expression •Replication of the viral genome • Late gene expression Gene Expression and Genome Replication
- 17.
- 18. I: is transcriptionof dsDNA usually by host-DdRP II: is transcription of ssDNA to give ds template for I (Gemini viruses) III: is transcription of dsRNA usually by virus coded RdRp (Reoviruses) IV: is replication of +ve stand RNA via –ve stand template by virus coded RdRp; the viral (+) strand is often the template for the early translation (=ve sense RNA viruses) V: is the transcription of -ve sense virus genome by virus coded RdRp ( Tospoviruses) VI: is the reverse transcription of RNA stage of retro and pararetroviruses leading to dsDNA template for mRNA transcription. Fig Legend
- 19. Systemic viral infectionrequires several different steps
- 20. Proteins that initiatethe infection
- 21. NSP- Nuclear shuttleprotein & Mp-Movement Proteins Fig: Genome organization of Begomoviruses
- 22. •NSP is responsiblefor transport of viral DNA from the nucleus into the cytoplasm •Movement protein coordinates the movement of viral DNA across plasmodesmatal boundaries. •Whereas specific point mutations in MP or NSP prevented this migration. Continued…
- 23. Fig: Role ofNSP and MP in movement
- 24. •MP of Abutilonmosaic virus (AbMV) translationally fused to green fluorescent protein or glutathione-S-transferase as reporter proteins •It has been proposed that MP serves as a membrane anchor at the plasma membranes, thus facilitating the movement of the transport complex along these membranes. • Moreover, MP can shuttle between the nuclear envelope and the cellular periphery in order to fulfill its task, because green fluorescent protein-MP was also observed in the vicinity of nuclei in some cells MP for movement across membranes
- 25. •NSP, interacts withthe Arabidopsis (Arabidopsis thaliana) nuclear acetyl transferase AtNSI (nuclear shuttle protein interactor), •This interaction and NSI expression are necessary for cabbage leaf curl virus infection and pathogenicity. NSP as a Pathogenicity Inducer
- 26. Fig: Model forNSP-AtNSI interactions in the nuclei of CaLCuV-infected cells
- 27. •Expression of theTomato Leaf Curl New Delhi Virus NSP from the PVX vector in N. benthamiana resulted in leaf curling that is typical of the disease symptoms caused by ToLCNDV in this species. NSP as Symptom Determinant
- 28. Fig: Symptoms exhibitedby plants following agroinfiltraton with PVX constructs.
- 29. CP-Coat Protein •For efficientsystemic spread •Translation of viral RNA •Targeting viral genome to site of replication •Suppression of RNA silencing TMV CP •Required for phloem loading step
- 30. SPMV CP (Satellite panicummosaic virus coat protein) •Satellite panicum mosaic virus coat protein effectively protect its cognate RNA from deleterious events •Enhances the performance of plant virus gene vectors. e.g., in Nicotiana benthamiana •SPMV CP directly or indirectly promotes spread of heterologous viruses in compatible host systems.
- 31. Fig: Potato virusX (PVX)-derived gene vectors carrying the satellite panicum mosaic virus coat protein gene (SPCP). Fig: Representative upper non-inoculated leaves that were previously inoculated with inoculation buffer (Mock), infectious transcripts of PVX-E1S empty vector (PVX), or a PVX vector carrying the SPMV CP gene in an minus-sense (PVX-SPCP−) or coding (PVX-SPCP+) orientation.
- 32. •DNA β satellitesare symptom-modulating, single-stranded DNA that require the helper begomovirus for replication, spread in plant tissues, and plant-to-plant transmission by the whitefly vector of begomoviruses •The DNA β satellite component encodes an essential pathogenicity protein (βC1) DNA β satellites
- 33. •Plants infected withPVX-βC1 produced severely distorted stems and leaves •Indicating that βC1 protein expression, when removed from the context of the AYVV genome, can have a marked effect on development. •N. benthamiana plants containing a dimeric DNA β transgene produced severe developmental abnormalities, vein-greening, and cell proliferation in the vascular bundles. Continued…
- 34. Fig: Expression ofβC1 protein from PVX vector
- 35.
- 36. Modifications in TranslationSystem of Virus-infected cells Modifications of initiation factors i.e. eIF2 nad eIF4 •Covalent modifications, especially phosphorylation •Association with regulatory partners •Interactions with virus-encoded subunits
- 37. Viral Translational Strategies •Scanning •Leakyscanning •Non-AUG initiation – CUG and GUG codon identified. •CAP-independent initiation •Frame shifting •Read-through •Shunt – Skip 5’ UTR Region and reaches initial codon •Hopping – 50 nucleotides are bypassed, rare event.
- 39. Viral Protein Products •Viral proteins that are components of the mature assembled virus particles and are produced by late genes are called as viral structural proteins i.e. • Nucleocapsid core proteins (gag proteins) • Viral non-structural proteins are ones that are not packaged in the mature virus particle and are only found in the infected cells and are produced by early genes.
- 40. Continued… • Most virusesencode a limited number of gene products therefore, they are dependent on the cell not only for biosynthesis of the macromolecules that constitute the virus particles, • But also for the pre-existing intracellular sorting mechanisms that the virus utilizes to achieve delivery of those macromolecules to the sites of virion assembly.
- 41.
- 42. Potyvirus polyprotein: Cleavageof the polyprotein by host and viral proteases releases the mature viral proteins.
- 43. Assembly of ViralComponents
- 44. Steps of VirusSynthesis • Movement of components to assembly site(s) in the nucleus and/or cytoplasm • Assembly of proteins • Incorporation of the nucleic acid genome • Intracellular movement of viral or subviral particles • Exit from the cell • Virion maturation (in some cases).
- 45. Encapsidation/ Coating • Proteinmonomers can aggregate in solution in various ways depending upon: • pH • Ionic strength, and • Temperature • During the replication of many viruses, hundreds to thousands of proteins assemble around the viral nucleic acid to form a protein shell called a capsid.
- 47.
- 48. Capsid Types • Helical:Helical capsids are usually formed from one protein that interlocks to form a helix-like structure around the viral genome. • Icosahedral: An icosahedron is a twenty-sided object, that is almost spherical. • Prolate: This is an icosahedron elongated along the fivefold axis and is a common arrangement of the heads of bacteriophages.
- 49. Continued… • Complex: Mostlyfound in non-animal viruses; are divided into two groups: • Viruses without identifiable capsids. • Viruses whose capsids are attached with additional structures.
- 50.
- 51. Virion Budding andMaturation
- 52. Budding Sites • Golgicomplex • ER-Golgi Complex Compartment • Cellular Membranes • Plasma membranes • Virions bud off in the form of vesicles or in the form of capsids depending on their formulation
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- 54.
- 55. Process •In order tocause infection in neighboring cells, plant viruses spread from the initially infected cells to the rest of the plant in several distinct stages. •First, after first viral genome replication cycles have been completed, the progeny viruses moves intracellularly from the sites of replication to plasmodesmata (PD) •The virus then transverses the PD to spread intercellularly (cell-to-cell movement). Long-distance movement of virus occurs through phloem sieve tubes. •The processes of plant virus movement especially cell to cell movement are controlled by specific viral movement proteins (MPs).
- 56. Spread of VirusIn a Plant
- 57. Virus Infection LifeCycle
- 58. Barley Yellow DwarfVirus (BYDV) Life Cycle
- 59. BYDV Life cycle(In Detail)
Editor's Notes
- #29 N. Benthamiana plants were inoculated with PVX and NSP/PVX Leaves were agroinfiltrated with NSP/PVX (C;right leaf), NSPUT/PVX (C, middle leaf), and NSPdm30C/PVX (C, Left leaf)