Jul 2026· Current Microbiology· Vol 83· 0 citations· 81 references
Medicine
TL;DR
This review emphasizes current knowledge on the biology, symptom modulation, molecular mechanisms, ecological roles, and detection strategies of CMV satRNAs, while highlighting their significance in viral evolution and disease epidemiology.
BACKGROUND
Plant viruses have evolved adaptations that enable them to alter host cues, thereby facilitating their replication and efficient transmission by insect vectors. Satellite RNAs (satRNAs), which accompany certain plant RNA viruses and are dependent on them for replication and transmission, can change the progression of pathogenesis and the expression of disease symptoms. This study aimed to analyse how the change in the course of infection by satRNA (exacerbation or mitigation of pathogenesis) impacts the subsequent stages of virus transmission. We hypothesised that satRNAs influence insect behaviour toward infected plants depending on their effect on pathogenesis progress; specifically, a significant disease exacerbation reduces plant attractiveness to aphids, whereas symptom mitigation promotes attraction.
RESULTS
Using peanut stunt virus (PSV) and cucumber mosaic virus (CMV), and their satRNAs, which induce divergent infection symptoms on Nicotiana benthamiana or Solanum lycopersicum plants, olfactometry, electrical penetration graph (EPG) monitoring, virus acquisition and transmission by Myzus persicae were analysed. The results showed that satRNA, naturally associated with the helper virus, that alleviate disease symptoms caused the plants to be more attractive to the insect vectors. On the other hand, the presence of satRNAs leading to symptom exacerbation reduced plant attractiveness and discouraged phloem feeding. However, acquisition effects were host-dependent: while symptom-exacerbating satRNAs generally reduced acquisition, nc-satRNA markedly enhanced CMV acquisition from N. benthamiana. Moreover, virus transmission was significantly reduced only in S. lycopersicum.
CONCLUSIONS
These findings suggest that symptom-attenuating satRNAs have greater capacity to persist in the environment by limiting disease damage in host plants and maintaining plant attractiveness to aphid vectors, thereby facilitating virus acquisition and transmission. In contrast, symptom-exacerbating satRNA variants appear not only to diminish the number of cells available for viral replication due to severe symptoms but also to reduce plant palatability and to impair vector feeding and thus virus transmission, particularly in crop hosts such as S. lycopersicum, which may limit their environmental persistence. Together, these results underscore the epidemiological relevance of satRNA-mediated symptom modulation as a factor shaping virus spread in natural and agricultural settings.
Barbara Wrzesińska-Krupa, Patryk Frąckowiak, M. Budziszewska et al.· BMC Plant Biology· 0 citations
Potyviruses and cucumoviruses (exemplified by cucumber mosaic virus (CMV)) are highly divergent taxa of plant-infecting positive-sense RNA viruses. However, they face similar challenges. They must overcome host antiviral resistance mechanisms, for example, RNA silencing or resistance mediated by the phytohormone salicylic acid, and they must do this across a very diverse range of host species. Although in some hosts potyviruses and CMV are seedborne, they are predominantly transmitted by aphid vectors. Both have acquired mechanisms for subverting host defences, particularly those controlled by jasmonic acid, to manipulate vector behaviour and increase transmission. This article compares how CMV and potyviruses took distinct evolutionary paths to overcome these common challenges. Potyviruses diverged into numerous distinct viral species to exploit different hosts and co-opted many gene products, including P1, HC-Pro, NIa, VPg, 6K2 and NIb, to effector roles. In contrast, CMV strains show less divergence but still exploit wide host ranges, and predominantly use the 2b counter-defence protein for subverting and manipulating host responses.
John P. Carr· Current Opinion in Virology· 0 citations
Virus-induced gene silencing (VIGS) has evolved from a conceptual demonstration of antiviral defense into a pivotal reverse-genetics platform for plant functional genomics. By exploiting engineered DNA- or RNA-based viral vectors, VIGS enables rapid, sequence-specific transcript knockdown through RNA-mediated degradation of target transcripts. Recent refinements in vector design, inoculation strategies, and viral species selection, such as TRV, BSMV, and FoMV, have expanded its application to previously recalcitrant plants, including major crops and emerging weed models. In weeds, functional genomics remains particularly challenging due to high genetic variability, limited genomic resources, and incompatibility with conventional viral vectors and transformation systems. In this context, VIGS provides a tractable approach to investigate genes associated with herbicide resistance, metabolic adaptation, and stress tolerance. Beyond weed biology, its application to studies of immune signaling, hormonal crosstalk, and secondary metabolism highlights VIGS as a versatile biotechnology for elucidating gene function and supporting next-generation strategies in plant improvement and integrated pest management.
É. F. Capelari, Márcia Margis-Pinheiro, A. Merotto Júnior et al.· Genetics and Molecular Biolo...· 0 citations
Plant viral symptoms are not merely passive consequences of infection but can represent adaptive strategies for enhancing transmission. The molecular mechanisms and ecological consequences of such virus-induced symptoms, particularly in perennial crops such as kiwifruit, require exploration. Here, in field experiments, we discovered a kiwifruit infected with a novel virus, Actinidia yellow ringspot virus (AYRSpV), which exhibits severe yellowing symptoms and significantly increases the attractiveness of pollinating insects such as bees and aphids during the flowering season. Given that AYRSpV is pollen-transmissible, this visual manipulation may facilitate the pollinator-mediated spread of the virus. We further explored whether the AYRSpV coat protein (CP) is a key virulence determinant that interacts with and targets the chlorophyll metabolic enzyme magnesium protoporphyrin IX methyltransferase (ChlM) for degradation, leading to a significant reduction in chlorophyll content and systemic leaf yellowing. Knockout of kiwifruit ChlM recapitulated the yellowing phenotype and further enhanced plant susceptibility to AYRSpV. Our study elucidates a pathway whereby a viral CP protein directly disrupts chlorophyll biosynthesis to induce leaf yellowing. Furthermore, we reveal a strategy wherein the virus exploits this symptom as a visual signal to manipulate pollinator behavior, thus creating a ‘symptom-mediated transmission’ loop. These findings provide a comprehensive understanding of the molecular and ecological mechanisms driving the spread of an emerging kiwifruit virus.
Ruotong Wang, Jierou Li, Xiaoling Li et al.· Horticulture Research· 0 citations
Nematodes are ubiquitous metazoans that occupy diverse ecological niches, exposing them to a wide range of viruses and positioning them as both viral hosts and vectors. Free-living nematodes, particularly Caenorhabditis elegans and Caenorhabditis briggsae, provide powerful genetic models for studying antiviral immune mechanisms. Natural infections with noda-like viruses have revealed powerful antiviral defense strategies in Caenorhabditis species, including RNA interference, the Intracellular Pathogen Response, Signal Transducers and Activators of Transcription (STAT)-like transcriptional regulation, terminal RNA uridylation, and structural barriers to viral entry and egress. These mechanisms demonstrate robust antiviral mechanisms independent of canonical interferon signaling while relying on conserved principles of viral RNA recognition, signal amplification, and coordinated transcriptional responses. Beyond free-living species, parasitic nematodes harbor a diverse and largely unexplored virome. Plant-parasitic nematodes host multiple RNA viruses and act as vectors for economically and agriculturally important plant pathogens, while animal-parasitic nematodes carry persistent viral infections that may influence the immune responses and disease outcomes of their animal hosts. Evidence for functional antiviral RNA interference in parasitic nematodes suggests partial conservation of immune mechanisms, although functional data remain limited. Together, these findings define current knowledge of viral infections and antiviral responses in nematodes and emphasize the need for deeper mechanistic studies, particularly in parasitic species, where the molecular basis of viral recognition and immune defense remains poorly characterized.
Dustin T. Howard, V. Lažetić· Frontiers in Bioscience· 0 citations
Specific targeting of host genes by plant viruses leads to the induction of distinct disease symptoms with devastating consequences for agriculture. However, it i unknown whether plants have evolved genes to specifically inhibit development of viral disease symptoms. Here we identified the causal gene of two Arabidopsis thaliana mutants that develop prominent systemic necrosis after infection with both wild-type cucumber mosaic virus (CMV) and its mutant (CMV-Δ2b) defective in the suppression of antiviral RNA interference (RNAi). We found that Antiviral RNAi 5 (AVI5) is in a large chromosomal deletion of both Arabidopsis mutants. We demonstrate that AVI5 acts to inhibit CMV-Δ2b viral accumulation in the antiviral RNAi pathway by promoting the biogenesis of the virus-derived small interfering RNAs (vsiRNAs) before host amplification of vsiRNAs. We further show that systemic necrosis symptom associated with cell death and a reactive oxygen species burst is induced by CMV infection and potently inhibited by AVI5. Unlike its suppression of virus accumulation, however, AVI5 inhibits development of systemic necrosis symptom without reducing viral titers or inducing antiviral RNAi. Together, our study demonstrates that Arabidopsis plants have evolved a dual functional gene for antiviral protection to inhibit viral infection and symptom development by distinct mechanisms.
