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Silva, J. M. F.

Publications and source records attributed to Silva, J. M. F..

4 recordsLinked to original sources

Genetic shifts in viral populations: how sudden vs gradual changes in host species composition affect the stability and dynamics of genetic variability in viral populations

Sudden and gradual changes in host species composition --transitioning from more permissive to less permissive hosts-- have been shown to influence viral fitness, virulence, and rates of molecular evolution. In this study, we analyzed the roles of stochasticity and selection using previously published time-series data from evolving populations of Sindbis virus under different rates of host replacement. First, an approximate Markov model within the Wright-Fisher diffusion framework revealed a reduction in effective population size by approximately half in scenarios involving sudden host changes. These scenarios were also associated with fewer and generally weaker beneficial mutations. Second, genetic distance analysis between populations at consecutive time points indicated that populations undergoing gradual host changes evolved steadily until the original host was no longer present. Distances to the ancestral sequence in these cases exhibited occasional leapfrog phenomena, where the rise of certain haplotypes is not predictable based solely on their relatedness to previously dominant ones. In contrast, populations exposed to sudden host changes displayed less stable compositions and diverged from the ancestral sequence at a more constant rate. Third, we observed that allele frequencies distribution followed a power law consistent with Taylors law. Both treatments exhibited high levels of allele aggregation with significant fluctuations, where neutral, beneficial, and deleterious alleles could be distinguished by their general behavior and their position on Taylors plot. Finally, we found evidence that the host replacement regime influences the temporal distribution of mutations across the genome.

evolutionary biology↗

System and transcript dynamics of cells infected with severe acute respiratory syndrome virus 2 (SARS-CoV-2)

Statistical laws arise in many complex systems and can be explored to gain insights into their structure and behavior. Here, we investigate the dynamics of cells infected with severe acute respiratory syndrome virus 2 (SARS-CoV-2) at the system and individual gene levels; and demonstrate that the statistical frameworks used here are robust in spite of the technical noise associated with single-cell RNA sequencing (scRNA-seq) data. A biphasic fit to Taylors power law was observed, and it is likely associated with the larger sampling noise inherent to the measure of less expressed genes. The type of the distribution of the system, as assessed by Taylors parameters, varies along the course of infection in a cell type-dependent manner, but also sampling noise had a significant influence on Taylors parameters. At the individual gene level, we found that genes that displayed signals of punctual rank stability and/or long-range dependence behavior, as measured by Hurst exponents, were associated with translation, cellular respiration, apoptosis, protein-folding, virus processes, and immune response. Author summaryViruses replicate within susceptible cells by exploiting the cellular machinery. Consequently, cells initiate defenses against the virus and signal other cells, notably immune cells. This ongoing battle prompts significant alterations in the cells gene expression patterns throughout the infection process. In this study, we apply statistical principles from complex systems theory to analyze gene expression data from individual cells infected with SARS-CoV-2. Our research aims to elucidate how viral infection impacts cells at both systemic and individual gene levels. Our primary findings are twofold: (i) the virus influences the distribution of gene transcripts over the course of infection, varying depending on cell type. (ii) As the infection progresses, numerous genes associated with critical cellular functions and immunity exhibit signs of punctual instability and/or autocorrelation, indicating their response to viral infection at various stages of the process.

systems biology↗

Date palm virus A: first plant virus found in date palm trees

In this work, a novel ssRNA (+) viral genomic sequence with gene organization typical of members of the subfamily Quinvirinae (family Betaflexiviridae) was identified using high throughput sequencing data of date palm obtained from the Sequence Read Archive database. The viral genome sequence consists of 7860 nucleotides and contains five ORFs encoding for the replication protein (Rep), triple gene block proteins 1, 2, 3 (TGB 1, 2 and 3) and coat protein (CP). Phylogenetic analysis based on the Rep and the CP amino acid sequences showed the closest relationship to garlic yellow mosaic-associated virus (GYMaV). Based on the demarcation criteria of the family Betaflexiviridae, this new virus, provisionally named date palm virus A (DPVA), could constitute a member of a novel genus. However, considering that DPVA and GYMaV share the same genomic organization and that they cluster together on the Rep phylogenetic analysis, they could also constitute a novel genus together, highlighting the necessity of a revision of the taxonomic criteria of the family Betaflexiviridae.

plant biology↗

Heterogeneity in the response of different subtypes of Drosophila melanogaster enteroendocrine cells to viral infections

Single cell RNA sequencing (scRNA-seq) offers the possibility to monitor both host and pathogens transcriptomes at the cellular level. Here, public scRNA-seq data from Drosophila melanogaster have been used to compare the differences in replication strategy and cellular response between two viruses, Thika virus (TV) and D. melanogaster Nora virus (DMelNV) in enteroendocrine cells (EEs). TV and DMelNV exhibited different patterns of replication and for TV, accumulation varied according to cell subtype. Cells infected with TV underwent down-regulation of genes that represent bottlenecks in the fruit fly interactome, while cells infected with DMelNV went through a down-expression of translation-related genes that represent both hubs and bottlenecks in the host interactome. In contrast, flies infected with DMelNV show only a systemic level down-regulation of bottleneck genes. Here, we use scRNA-seq to highlight the differences and commonalities between cellular response to TV and DMelNV and between cellular and systemic response to DMelNV.

systems biology↗