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Rivero, R.

Publications and source records attributed to Rivero, R..

10 recordsLinked to original sources

Molecular and ecological determinants of effective reassortment in orthohantaviruses

A central unsolved problem in RNA virus evolution is understanding why some viral reassortants establish and persist while others do not. To answer this question, we reconstructed reassortant histories across 553 viral genomes from seven orthohantavirus species between 1983 and 2024 using phylogenetic reconciliation and molecular dating. We found that the frequency of retained reassortants varied among orthohantaviruses. For example, reassortment ranged from absent in Andes virus to frequent in Dobrava-Belgrade, Sin Nombre, Seoul, Puumala, and Tula viruses, showing that effective reassortment is not a genus-wide constant. Our Bayesian hierarchical models identified local host overlap as the strongest ecological factor associated with viral reassortment, while cross-segment linkage and terminal RNA structure serve as a molecular filter. We found that the probability of reassortment establishment is highest when ecological opportunity is paired with molecular permissiveness, with their interaction term inferred as the strongest signal in our establishment models (posterior probability = 0.97). These results suggest that reassortment in orthohantaviruses is a sequentially filtered evolutionary process in which divergent lineages must first meet in a host through ecological overlap, exchange segments that are molecularly compatible, and do so within a lineage background permissive to establishment in the host population.

evolutionary biology↗

Viral reservoir status in small mammals emerges as a predictable life-history trait after correcting for surveillance bias

Small mammals, particularly rodents and shrews, act as primary reservoirs for Arenaviruses and Hantaviruses, zoonotic pathogens causing substantial global morbidity. However, our understanding of reservoir ecology is obscured by biased surveillance efforts, where sampling preferentially targets synanthropic species and high-income regions. It remains unclear whether observed patterns of reservoir competence, such as the association with synanthropy, are biological realities or artefacts of surveillance bias. We conducted a systematic review and data synthesis of global surveillance efforts (1960-2023), creating a harmonised database of over 590,000 recorded small mammals contributing 716,000 assay results. We then integrated this with macroecological trait data and phylogenetics to model reservoir probability using Bayesian phylogenetic dyadic generalised linear mixed models. We identified substantial taxonomic and geographic biases; surveillance is heavily skewed towards the Palearctic and widespread, large-bodied species, while 46% of host genera remain entirely unsampled. Geographically, surveillance intensity correlates strongly with accessibility and night-light intensity rather than host biodiversity. After statistically correcting for historical sampling volume, we demonstrate that reservoir status is a predictable biological trait. A fast pace of life (e.g., early maturity, large litters) is associated with an increased probability of reservoir status, independent of sampling effort. Synanthropy also remains a strong, independent predictor, indicating that commensal species act as genuine biological amplifiers in modified landscapes. Evolutionary analyses reveal a mosaic of broad lineage-level co-divergence punctuated by frequent, reactive host-switching. By projecting these models globally, we demonstrate that anthropogenic disturbance acts as an ecological filter, fundamentally challenging the assumption that pristine tropical ecosystems represent the highest intrinsic hazard for viral emergence.

ecology↗

Cell-specific dedifferentiation in Arabidopsis thaliana

Single somatic plant cells are capable of dedifferentiation and reversion to totipotency. However, understanding of dedifferentiation remains incomplete, limiting efforts to reprogram plant cell identities with engineered properties. Here, we describe the transcriptional dynamics of 125,091 Arabidopsis thaliana whole seedling protoplasts along a time course of dedifferentiation and varied chemical perturbations using single-cell RNA sequencing. We observed widespread cell-type-specific transcriptional reprogramming concomitant with cell wall digestion, including a guard cell-specific somatic embryogenic-like program initiated by ectopic LEC2 expression. Contrasting cell states between chemical perturbations across real time revealed that phytohormones antagonize cell aging, promote retention of transcriptional diversity, and selectively suppress wound responses. By dissecting time-resolved transcriptional dynamics, we discovered that dedifferentiation is accompanied by the activation of stem-cell and meristematic marker genes and associated with prevalent chromatin remodeling. Despite discovery of a shared regulatory program underlying early dedifferentiation, temporal modeling of diverse somatic cell types uncovered extensive bias in dedifferentiation potential, including epithem-derived dedifferentiated cells, variable dedifferentiation rates, and diversity in early reprogramming outcomes as a major source of in vitro heterogeneity. Taken together, these data showcase how initial somatic cell identity, phytohormone signaling, chromatin remodeling, and reprogramming heterogeneity combine to coordinate the early transcriptional events defining cellular dedifferentiation.

plant biology↗

Epithelial Reprogramming and Transition during Pulmonary Bioengineering

Recent research has emphasized the critical role of cell state transitions in tissue homeostasis. In lung biology, transitional cells are recognized as a feature of tissue-scale processes during both normal physiology and disease. The precise way that transitional cell states emerge and are regulated remains to be determined. Engineered tissues, built in a laboratory through bioengineering approaches, allow detailed study of cellular states that are not commonly found in native biology, and allow opportunities to directly induce and manipulate cellular transitions. The following study explores and characterizes epithelial cell states that emerge via cellular reprogramming in a tissue engineering context. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=172 SRC="FIGDIR/small/701406v1_ufig1.gif" ALT="Figure 1"> View larger version (68K): org.highwire.dtl.DTLVardef@1d456f3org.highwire.dtl.DTLVardef@1989ba5org.highwire.dtl.DTLVardef@127dd7org.highwire.dtl.DTLVardef@3dd7a_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioengineering↗

Comparative susceptibility of Old World and New World bat cell lines to Zika virus: Insights into viral replication and inflammatory responses

BackgroundFrom the first isolation of Zika virus (ZIKV) in Uganda in 1947, ZIKV had primarily been associated with sporadic human cases in Africa and Asia until ZIKV emerged as an epidemic in the Americas in 2015. As ZIKV spread into new geographic regions, it now has the potential to interact with many novel potential host species whose susceptibility to the virus has yet to be determined. Bats, with their ability to fly and live in or near human structures, are plausible ZIKV reservoirs. However, their competence as hosts for ZIKV remains unresolved. In this study, we investigate the immune response of Old World and New World bats to ZIKV infection in vitro. ResultsWe demonstrate that Egyptian Rousette bat (Rousettus aegyptiacus; Old World) cells are susceptible to ZIKV, while we observed little to no ZIKV replication in Jamaican fruit bat (Artibeus jamaicensis) cells. Notably, both the Asian and African ZIKV lineages elicited a strong proinflammatory response in the R. aegyptiacus cell line including upregulation of IL6, CXCL8, and CCL5. These data contrast with the dampened inflammatory response detected in these bats to other viruses. ConclusionsThe findings reveal that R06E cells derived from Egyptian Rousette bats exhibit robust proinflammatory and antiviral responses upon Zika virus (ZIKV) infection, characterized by significant upregulation of proinflammatory cytokines. This suggests that while these cells support productive ZIKV replication, they also mount a strong immune response, challenging the notion of these bats as immune-tolerant reservoirs and indicating a more complex interaction with the virus.

microbiology↗

Protocol for the production of an Arenavirus and Hantavirus host-pathogen database: Project ArHa.

1Arenaviruses and Hantaviruses, primarily hosted by rodents and shrews, represent significant public health threats due to their potential for zoonotic spillover into human populations. Despite their global distribution, the full impact of these viruses on human health remains poorly understood, particularly in regions like Africa, where data is sparse. Both virus families continue to emerge, with pathogen evolution and spillover driven by anthropogenic factors such as land use change, climate change, and biodiversity loss. Recent research highlights the complex interactions between ecological dynamics, host species, and environmental factors in shaping the risk of pathogen transmission and spillover. This underscores the need for integrated ecological and genomic approaches to better understand these zoonotic diseases. A comprehensive, spatially and temporally explicit dataset, incorporating host-pathogen dynamics and human disease data, is crucial for improving risk assessments, enhancing disease surveillance, and guiding public health interventions. Such a dataset (ArHa) would also support predictive modelling efforts aimed at mitigating future spillover events. This paper proposes the development of this unified database for small-mammal hosts of Arenaviruses and Hantaviruses, identifying gaps in current research and promoting a more comprehensive understanding of pathogen prevalence, spillover risk, and viral evolution. 2 Strengths and Limitations of this studyO_LIThis dataset combines detailed spatial and temporal information, providing a unique resource for understanding geographic and temporal trends in Arenavirus and Hantavirus host-pathogen relationships. C_LIO_LIBy explicitly quantifying sampling biases and detection efforts, the dataset allows more robust and accurate asssessments of pathogen prevalence and distribution. C_LIO_LIThe dataset offers a platform for linking ecological data with human health outcomes, supporting the identification of spillover hotspots. C_LIO_LIThe dataset relies on published material, which may vary in terms of detail, accuracy and completeness. Missing or imprecise information may limit the reliability of subsequent analyses. C_LIO_LIThe dataset will be produced as a static resource which could limit its relevance over time as emerging data will not be added. C_LI

microbiology↗

Activation of three targets by a TAL effector confers susceptibility to bacterial blight of cotton

Xanthomonas spp. employ transcription activator-like effectors (TALEs) to promote pathogenicity by activating host susceptibility (S) genes. Cotton GhSWEET10 is an S gene targeted by a TALE in an early isolate of Xanthomonas citri pv. malvacearum (Xcm), but not by recent field Xcm isolates. To understand the pathogenicity shift in Xcm and its adaptation to cotton, we assembled the whole genome and the TALE repertoire of three recent Xcm Texas field isolates. A newly evolved TALE, Tal7b, activated different GhSWEET genes, GhSWEET14a and GhSWEET14b. Simultaneous activation of GhSWEET14a and GhSWEET14b resulted in pronounced water-soaked lesions. Transcriptome profiling coupled with TALE-binding element prediction identified a pectin lyase as an additional Tal7b target, quantitatively contributing to Xcm virulence alongside GhSWEET14a/b. CRISPR-Cas9-based gene editing supported the function of GhSWEETs as S genes in cotton bacterial blight and the promise of disrupting the TALE-binding site in these genes to control the disease. Collectively, our findings elucidate the rapid evolution of TALEs in Xanthomonas field isolates and highlight the virulence mechanism wherein TALEs induce multiple S genes simultaneously to promote pathogenicity.

plant biology↗

Organ Boundary Circuits Regulate Sox9+ Alveolar Tuft Cells During Post-Pneumonectomy Lung Regeneration

Tissue homeostasis is controlled by cellular circuits governing cell growth, organization, and differentation. In this study we identify previously undescribed cell-to-cell communication that mediates information flow from mechanosensitive pleural mesothelial cells to alveolar-resident stem-like tuft cells in the lung. We find mesothelial cells to express a combination of mechanotransduction genes and lineage-restricted ligands which makes them uniquely capable of responding to tissue tension and producing paracrine cues acting on parenchymal populations. In parallel, we describe a large population of stem-like alveolar tuft cells that express the endodermal stem cell markers Sox9 and Lgr5 and a receptor profile making them uniquely sensitive to cues produced by pleural Mesothelium. We hypothesized that crosstalk from mesothelial cells to alveolar tuft cells might be central to the regulation of post-penumonectomy lung regeneration. Following pneumonectomy, we find that mesothelial cells display radically altered phenotype and ligand expression, in a pattern that closely tracks with parenchymal epithelial proliferation and alveolar tissue growth. During an initial pro-inflammatory stage of tissue regeneration, Mesothelium promotes epithelial proliferation via WNT ligand secretion, orchestrates an increase in microvascular permeability, and encourages immune extravasation via chemokine secretion. This stage is followed first by a tissue remodeling period, characterized by angiogenesis and BMP pathway sensitization, and then a stable return to homeostasis. Coupled with key changes in parenchymal structure and matrix production, the cumulative effect is a now larger organ including newly-grown, fully-functional tissue parenchyma. This study paints Mesothelial cells as a key orchestrating cell type that defines the boundary of the lung and exerts critical influence over the tissue-level signaling state regulating resident stem cell populations. The cellular circuits unearthed here suggest that human lung regeneration might be inducible through well-engineered approaches targeting the induction of tissue regeneration and safe return to homeostasis.

systems biology↗

Characterization of environmental effects on flowering and plant architecture in an everbearing strawberry F1-hybrid by meristem dissection and gene expression analysis

Floral transition in the cultivated everbearing strawberry is a hot topic because these genotypes flower perpetually and are difficult to maintain in a non-flowering state. However, it has rarely been studied using morphogenetic and molecular analyses simultaneously. We therefore examined morphogenetic effects and the activation of genes involved in floral induction and initiation in seedlings of an everbearing F1-hybrid. Seedlings were grown at 12, 19, and 26{degrees}C under 10-h SD and 20-h LD conditions. We observed a strong environmental influence on meristem development and a FLOWERING LOCUS T1 (FaFT1)-SUPPRESSOR OF OVEREXPRESSION OF CONSTANS1 (FaSOC1) pathway similar to that in the everbearing woodland strawberry. The everbearing cultivar showed typical features of a quantitative LD plant, flowering earlier under LD than SD conditions at all temperatures. We also found that floral induction is facilitated by FaFT1 upregulation under LD conditions, while FaSOC1 upregulation in the apex leads to photoperiod-independent floral initiation. Moreover, we confirmed the strawberry meristem identity gene FRUITFULL (FaFUL) can also be used as an early indicator of floral initiation in EB cultivars. This study also highlights the advantages of using seed-propagated F1-hybrids for genetic studies because are genetically identical, and not biased by a previous flowering history.

plant biology↗