Susceptibility Genes to Plant Viruses

Plant viruses use cellular factors and resources to replicate and move. Plants respond to viral infection by several mechanisms, including innate immunity, autophagy, and gene silencing, that viruses must evade or suppress. Thus, the establishment of infection is genetically determined by the availability of host factors necessary for virus replication and movement and by the balance between plant defense and viral suppression of defense responses. Host factors may have antiviral or proviral activities. Proviral factors condition susceptibility to viruses by participating in processes essential to the virus. Here, we review current advances in the identification and characterization of host factors that condition susceptibility to plant viruses. Host factors with proviral activity have been identified for all parts of the virus infection cycle: viral RNA translation, viral replication complex formation, accumulation or activity of virus replication proteins, virus movement, and virion assembly. These factors could be targets of gene editing to engineer resistance to plant viruses

Susceptibility Genes to Plant Viruses

Plant viruses use cellular factors and resources to replicate and move. Plants respond to viral infection by several mechanisms, including innate immunity, autophagy, and gene silencing, that viruses must evade or suppress. Thus, the establishment of infection is genetically determined by the availability of host factors necessary for virus replication and movement and by the balance between plant defense and viral suppression of defense responses. Host factors may have antiviral or proviral activities. Proviral factors condition susceptibility to viruses by participating in processes essential to the virus. Here, we review current advances in the identification and characterization of host factors that condition susceptibility to plant viruses. Host factors with proviral activity have been identified for all parts of the virus infection cycle: viral RNA translation, viral replication complex formation, accumulation or activity of virus replication proteins, virus movement, and virion assembly. These factors could be targets of gene editing to engineer resistance to plant viruses

Host factors against plant viruses

Plant virus genome replication and movement is dependent on host resources and factors. However, plants respond to virus infection through several mechanisms, such as autophagy, ubiquitination, mRNA decay and gene silencing, that target viral components. Viral factors work in synchrony with pro-viral host factors during the infection cycle and are targeted by antiviral responses. Accordingly, establishment of virus infection is genetically determined by the availability of the pro-viral factors necessary for genome replication and movement, and by the balance between plant defence and viral suppression of defence responses. Sequential requirement of pro-viral factors and the antagonistic activity of antiviral factors suggest a two-step model to explain plant–virus interactions. At each step of the infection process, host factors with antiviral activity have been identified. Here we review our current understanding of host factors with antiviral activity against plant viruses

Susceptibility Genes to Plant Viruses

Plant viruses use cellular factors and resources to replicate and move. Plants respond to viral infection by several mechanisms, including innate immunity, autophagy, and gene silencing, that viruses must evade or suppress. Thus, the establishment of infection is genetically determined by the availability of host factors necessary for virus replication and movement and by the balance between plant defense and viral suppression of defense responses. Host factors may have antiviral or proviral activities. Proviral factors condition susceptibility to viruses by participating in processes essential to the virus. Here, we review current advances in the identification and characterization of host factors that condition susceptibility to plant viruses. Host factors with proviral activity have been identified for all parts of the virus infection cycle: viral RNA translation, viral replication complex formation, accumulation or activity of virus replication proteins, virus movement, and virion assembly. These factors could be targets of gene editing to engineer resistance to plant viruses

When Viruses Infect Plants

Just as human beings can catch a cold, plants can also get viral infections. Understanding the mechanisms regulating the interactions between plants and viruses is the first step towards developing better management strategies and using biotechnology methods to immunise plants and engineer genetic resistance to viruses in plants. This is the focus of research by Dr Hernan Garcia-Ruiz and his team based at the University of Nebraska, USA. Viral diseases in plants can cause important economic losses as a result of poor-quality products and lower yield. This impact can particularly seriously affect developing countries which are more likely to be dependent on agricultural production to ensure food security for the population. Additionally, the strict sanitary regulations which are in place to avoid the spread of diseases across countries may limit the international trade of agricultural products, compounding the impact of plant viral infections. Publication @ https://www.scientia.global/dr-hernan-garcia-ruiz-when-viruses-infect-plants/ ebook: https://www.scientia.global/wp-content/uploads/Hernan_Garcia-Ruiz/Hernan_Garcia-Ruiz.pdf audio book: https://www.scipod.global/when-viruses-infect-plants-dr-hernan-garcia-ruiz-university-of-nebraska

Mechanisms of Silencing Suppression by a Polerovirus P0 Protein

Maize lethal necrosis is an intense viral disease spreading across sub-Saharan Africa. Maize is the staple crop grown in sub-Saharan Africa, but most crops infected with maize lethal necrosis will not survive to harvest. This causes immense economic hardship and starvation within the population. Maize lethal necrosis consists of a combination of two viruses, Maize chlorotic mottle virus (MCMV) and a virus from the genus potyvirus. In a recent study, a Maize yellow dwarf virus-RMV (MYDV-RMV)-like polerovirus, was repeatedly detected in plants with maize lethal necrosis. Poleroviruses have a silencing suppressor, P0 protein, and the mechanism of suppression is poorly understood. In order to understand the mechanisms of silencing suppression, P0 was cloned and tagged. Transient analysis showed it is a strong suppressor of transgene silencing. P0 also restored pathogenicity in trans-complementation assays with two suppressor-deficient viruses, Turnip mosaic virus (TuMV), a potyvirus, and Turnip crinkle virus (TCV), a carmovirus, elucidating that P0 is a suppressor of antiviral silencing. P0 lead to the depletion of secondary small-interfering RNAs (siRNAs) possibly due to the degradation of Argonautes (AGO). P0 was co-expressed with tagged AGO 1, 2, 4, 5, 7, and 10 and caused a drop in all AGOs except AGO 4. Dual suppressor assays show that P0 affects the biogenesis of secondary virus-derived siRNAs. Our results provide novel insights on the mechanism of siRNA silencing suppression by polerovirus P0

Determinants of Virus Variation, Evolution, and Host Adaptation

Virus evolution is the change in the genetic structure of a viral population over time and results in the emergence of new viral variants, strains, and species with novel biological properties, including adaptation to new hosts. There are host, vector, environmental, and viral factors that contribute to virus evolution. To achieve or fine tune compatibility and successfully establish infection, viruses adapt to a particular host species or to a group of species. However, some viruses are better able to adapt to diverse hosts, vectors, and environments. Viruses generate genetic diversity through mutation, reassortment, and recombination. Plant viruses are exposed to genetic drift and selection pressures by host and vector factors, and random variants or those with a competitive advantage are fixed in the population and mediate the emergence of new viral strains or species with novel biological properties. This process creates a footprint in the virus genome evident as the preferential accumulation of substitutions, insertions, or deletions in areas of the genome that function as determinants of host adaptation. Here, with respect to plant viruses, we review the current understanding of the sources of variation, the effect of selection, and its role in virus evolution and host adaptation

Variation Profile of the Orthotospovirus Genome

Orthotospoviruses are plant-infecting members of the family Tospoviridae (order Bunyavirales), have a broad host range and are vectored by polyphagous thrips in a circulative- propagative manner. Because diverse hosts and vectors impose heterogeneous selection constraints on viral genomes, the evolutionary arms races between hosts and their pathogens might be manifested as selection for rapid changes in key genes. These observations suggest that orthotospoviruses contain key genetic components that rapidly mutate to mediate host adaptation and vector transmission. Using complete genome sequences, we profiled genomic variation in orthotospoviruses. Results show that the three genomic segments contain hypervariable areas at homologous locations across species. Remarkably, the highest nucleotide variation mapped to the intergenic region of RNA segments S and M, which fold into a hairpin. Secondary structure analyses showed that the hairpin is a dynamic structure with multiple functional shapes formed by stems and loops, contains sites under positive selection and covariable sites. A ccumulation and tolerance of mutations in the intergenic region is a general feature of orthotospoviruses and might mediate adaptation to host plants and insect vectors

Age-related Resistance in Bell Pepper to \u3ci\u3eCucumber mosaic virus \u3c/i\u3e

We demonstrated the occurrence of mature plant resistance in Capsicum annuum \u27Early Calwonder\u27 to Cucumber mosaic virus (CMV) under greenhouse conditions. When Early Cal wonder plants were sown at 10 day intervals and transplanted to 10-cm square pots, three distinct plant sizes were identified that were designated small, medium and large. Trials conducted during each season showed that CMV accumulated in inoculated leaves of all plants of each size category. All small plants (with the exception of the winter trial) developed a systemic infection that included accumulation of CMV in uninoculated leaves and severe systemic symptoms. Medium plants had a range of responses that included no systemic infection to detection of CMV in uninoculated leaves with the systemically infected plants being either symptomless or expressing only mild symptoms. None of the large plants contained detectable amounts of CMV in uninoculated leaves or developed symptoms. When plants were challenged by inoculation of leaves positioned at different locations along the stem or different numbers of leaves were inoculated, large plants continued to accumulate CMV in inoculated leaves but no systemic infection was observed. When systemic infection of large plants did occur, e.g. when CMV-infected pepper was used as a source of inoculum, virus accumulation in uninoculated leaves was relatively low and plants remained symptomless. A time-course study of CMV accumulation in inoculated leaves revealed no difference between small and large plants. Analyses to examine movement of CMV into the petiole of inoculated leaves and throughout the stem showed a range in the extent of infection. While all large plants contained CMV in inoculated leaves, some had no detectable amounts of virus beyond the leaf blade, whereas others contained virus throughout the length of the stem but with limited accumulation relative to controls