Viruses infect plants through wounds or insect vectors and use host cell machinery to replicate their genomes and produce proteins. They move between cells via plasmodesmata or transport streams. Pathogenesis involves implantation, local replication, spread to target organs, and shedding from the plant. Strategies to control plant viruses include eliminating sources and infected plants, controlling vectors, breeding resistance, and using cross-protection methods like satellite RNAs or transgenic expression of antiviral genes. RNA interference is now a primary tool for inducing virus resistance by degrading viral genomes.

1. PATHOGENICITY CONTROL OF PLANT
VIRUSES
Fizza khan
MPhil Biotechnology
Course- Molecular Plant Virology
UNIVERSITY OF AGRICULTURE, FAISALABAD, PAKISTAN

2. PLANT VIRUSES
Viruses are very small (submicroscopic) infectious particles (virions) composed of a protein coat and a
nucleic acid core. They carry genetic information encoded in their nucleic acid, which typically specifies
two or more proteins. Translation of the genome (to produce proteins) or transcription and replication (to
produce more nucleic acid) takes place within the host cell and uses some of the host's biochemical
"machinery". Viruses do not capture or store free energy and are not functionally active outside their host.
They are therefore parasites (and usually pathogens) but are not usually regarded as genuine
microorganisms.
Most viruses are restricted to a particular type of host. Some infect bacteria, and are known as
bacteriophages, whereas others are known that infect algae, protozoa, fungi (mycoviruses), invertebrates,
vertebrates or vascular plants. However, some viruses that are transmitted between vertebrate or plant hosts
by feeding insects (vectors) can replicate within both their host and their vector.
HOW PLANT VIRUSES CAUSE INFECTIONS?
Most plant viruses are transmitted by insect vectors that cause damage to the plant and create an entry point
for pathogens, or that tap into the phloem to feed. Once inside, viruses use the handful of genes in their tiny
genomes to orchestrate the plant cells’ machinery, while evading the plant’s defenses. Below is a
generalized depiction of this infection process for RNA viruses, the most common type of plant virus.
1. Some viruses can infect plants when aphids and other insects tap into the phloem to feed. Such
insect vectors can also pick up virus particles and carry them to new plant hosts.
2. Other viruses infect plant cells through a wound site created by a leaf-munching insect such as a
beetle.

3. 1. Viral capsid shell opens to release the viral genome, which is translated into proteins that direct the
formation of a viral factory from membranes of the endoplasmic reticulum and other organelles.
2. Antiviral proteins, such as those in the Argonaute family, patrol cells for invading pathogens, but
they cannot break into the viral factories.
3. Viral RNA is replicated and exported to the cytoplasm.
4. Viral RNA and newly assembled viral particles move to other cells through plasmodesmata, which
can be widened by virus-encoded movement proteins.
5. Some virus particles enter the plant’s transport streams.
PATHOGENESIS
Pathogenesis is the process by which an infection leads to disease. Pathogenic mechanisms of viral disease
include
1. Implantation of virus at the portal of entry
2. Local replication
3. Spread to target organs (disease sites)
4. Spread to sites of shedding of virus into the environment.
Factors that affect pathogenic mechanisms
1. Accessibility of virus to tissue
2. Cell susceptibility to virus multiplication
3. Virus susceptibility to host defenses. Natural selection favors the dominance of low-virulence virus
strains.
THE EVOLUTION OF PATHOGENICITY
Because parasites must infect hosts for their survival and parasite infection limits host fitness, pathogenicity
in parasites and resistance in hosts are targets for selection. Plants resist disease through a variety of
preformed and induced barriers to infection, and pathogens use virulence factors to overcome plant defenses
and make infection possible. Plant immunity acts at different layers. One layer involves the recognition of
conserved pathogen associated molecular patterns, which triggers basal defenses (PAMP-triggered
immunity, PTI). Another layer of defense involves the recognition of pathogenicity effectors of the parasite
that might have evolved to suppress PTI. Selection on both the resistance proteins that recognize the
pathogenicity effectors and the pathogenicity factors may lead to an antagonistic host–pathogen co-
evolution. Two major models of host–parasite interaction determining the success of infection have been
proposed:
1. The gene-for-gene (GFG) model
2. The matching-allele (MA) model
These two models are with different assumptions and predictions. GFG and MA models have generally
been applied to plant and animal systems, respectively, but they may both be relevant to understanding the
evolution of plant–pathogen interactions.

4. STRATEGIES TO PROTECT PLANTS
FROM VIRUSES
Prevention, or at least alleviation, of the effects of viruses, involves:
1- Elimination of sources of virus.
2- Elimination of the virus from infected plants.
3- Control of vectors.
4- Breeding for resistance and the use of cross-protection methods.
Each of these approaches to control will be considered.
• SATELLITES AND DI NUCLEIC ACIDS
The ability of some satRNAs to attenuate the symptoms of their helper virus led to their early and
widespread use in spray inoculations of greenhouse and field crops. SatRNAs also protected against the
symptoms of tomato aspermy virus but without causing any reduction in virus replication. This enigma
may be explained by recent observations on the ability of attenuating satRNAs to prevent helper virus CP
from entering the chloroplasts of infected cells. Thus, reduced replication may not be the (sole)
mechanism of satRNA protection. Satellite TRSV also interferes with the replication and disease caused
by another nepovirus, cherry leafroll virus, even though cherry leafroll virus is not a helper virus for
satellite TRSV.
DI RNAs, while common in animal viruses, occur naturally only in members of the Tombusvirus and
Carmovirus groups of plant viruses and represent complicated rearrangements of genomic sequences.
Like satRNAs, they can intensify or ameliorate the symptoms of their helper virus and interfere with its
replication.
• PLANTIBODIES
Plant pathologists have been attracted by the possibility of providing protection against fungal, bacterial,
or viral diseases by expressing an appropriate IgG, Fab2 fragment, or single-chain F, antibody in transgenic
plants. Recent confirmation of the biological activity of an antiphytochrome mouse monoclonal single-
chain F, in transgenic tobacco supports this overall strategy. However, the level of transgene expression
is usually low and problems have been encountered with expression levels of full-length heavy chains in
many transformed lines. "The jury is still out" deciding on the utility of this strategy for plant protection!
• ANTISENSE RNA AND RIBOZYMES
Transgenic plants expressing antisense RNAs to other regions of the CMV genome were generally not
resistant to CMV infection (116), except one line that paradoxically had low transcript levels. Until
recently, therefore, transgenic protection using antisense RNA against RNA virus target sequences
remained largely unproven. However, an exclusively cytoplasmic RNA-virus replication cycle, high
genome-sense RNA copy numbers, and association with proteins at all stages of replication suggest that

5. a simple antisense antiviral strategy is unlikely to be successful. Antisense inhibition of plant nuclear gene
expression is well-documented, supporting some utility against viruses with a nuclear phase in their
replication cycle-for example, geminiviruses, caulimoviruses, or badnaviruses.
Ribozymes are small RNA molecules derived from satellite TRSV, or certain viroids and viroid-like satRNAs,
which are capable of highly specific catalytic cleavage of RNA. Ribozymes can be visualized as
6"warheaded" antisense RNAs; however, the length and base composition of the two arms will affect the
hybridization on/off rates at a given temperature and, hence, the kinetics and efficiency of RNA cleavage.
Although much success has been achieved in vitro, progress in vivo has been markedly slower.
• LATENT SUICIDE GENES
When a plant cell is transformed to express a low, constitutive level of antisense RNA for a highly
phytotoxic protein with a minus-sense plant viral subgenomic RNA promoter at its 3'-end, then infection
by the cognate virus will, during the production of progeny plusstrands and subgenomic RNAs, transcribe
the nonsense RNA into mRNA, allowing expression of the phytotoxin and killing that cell. By use of the
PVX subgenomic RNA promoter and diphtheria toxin mRNA, transgenic tobaccos showed a 20-fold
reduction in PVX concentration in upper, systemic leaves, and the PVX-inoculated leaves turned yellow
and fell off 6-7 days after inoculation. This general approach may be of questionable utility in the field but
can provide a useful and sensitive probe for transcriptional activity.
• RNAi
RNA mediated silencing technology has now become the tool of choice for induction of virus resistance in
plants. A significant feature of this technology is the presence of double-stranded RNA (dsRNA), which is
not only the product of RNA silencing but also the potent triggers of RNA interference (RNAi). Upon RNA
induction, these dsRNA are diced into short RNA fragments termed as small interfering RNAs (siRNA),
which are hallmarks of RNAi.
Virus resistance is achieved usually through the antiviral pathways of RNA silencing, a natural defense
mechanism of plants against viruses. The experimental approach consists of isolating a viral genome itself
and transferring it into the genome of a susceptible plant. Integrating a viral gene fragment into a host
genome does not cause disease. Instead, the plant`s natural antiviral mechanism that acts against a virus
by degrading its genetic material in a nucleotide sequence in specific manner via a cascade of events
involving numerous proteins, including ribonucleases, an enzyme that cleave RNA. This enzyme activated
and then target degradation of the genome of an invader virus protects plants from virus infection.

6. Reference
Www.the-scientist.com/how-viruses-attack-plants
https://www.ncbi.nlm.nih.gov/books/NBK8149/
https://www.sciencedirect.com/science/article/S1567134820300472
https://www.atsu.edu/faculty/chamberlain/website/tritzmed/LECTS/MECHANIS.HTM
https://www.microbiologyresearch.org/docserver/fulltext/92/12/2691_vir034603.pdf?expires=1587479
719&id=id&accname=guest&checksum=63A09E95344728634A836577FAB1FF37
https://www.ncbi.nlm.nih.gov/articles/PMC46254/
https://www.intechopen.com/books/functional-genomics/how-rna-interference-combat-viruses-in-
plants