Virus Genes最新文献

Ungulate tetraparvovirus 1 (UTPV1), or bovine hokovirus, has been described in cattle but remains poorly characterized in Southeast Asia. In this study, we report the first detection and genomic characterization of UTPV1 in water buffalo (Bubalus bubalis) from Vietnam. Skin swab samples were collected from a buffalo with nodular lesions in northern Vietnam in 2024, and total nucleic acids were subjected to metagenomic sequencing. Analysis of Illumina MiSeq reads revealed the presence of both lumpy skin disease virus (LSDV) and UTPV1. The near-complete UTPV1 genome (NIVR-B12-2024) shared 90.7-93.3% nucleotide identity with reference strains but did not cluster with genotypes I or II, instead forming a distinct lineage. Phylogenetic analyses supported its independent position, and recombination detection indicated potential genetic exchange between Asian and South American strains. Several amino acid substitutions were identified in the NS1 protein, suggesting ongoing viral diversification. This study provides the first molecular evidence of UTPV1 in water buffalo and in Vietnam, expanding the recognized host range and geographic distribution of this virus. The findings highlight the value of non-invasive sampling and metagenomic sequencing for livestock surveillance and underscore the need for continued monitoring to evaluate the epidemiological significance and potential health risks of UTPV1 in Southeast Asia.

Getah virus (GETV), a mosquito-borne arbovirus, possesses many susceptible hosts, including pigs, horses, cattle, and blue foxes. Currently, the biological characteristics and pathogenic mechanisms of GETV remain to be investigated. A GETV, isolated from a contaminated Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) live vaccine, was designated as BJ-Swzp-2022. Subsequently, the complete genome of the GETV BJ-Swzp-2022 was sequenced to construct a full-length infectious cDNA clone using T7 RNA polymerase. Transfection of BSR T7/5 cells expressing T7 RNA polymerase with this infectious clone resulted in the rescue of GETV, which exhibited replication and replication characteristics similar to those of the parental virus. Establishing this platform would facilitate understanding the pathogenic mechanisms of GETV and developing novel vaccines.

Figs (Ficus carica L.) are economically important worldwide, valued for both fruit production and ornamental purposes. Due to the widespread use of vegetative propagation, diverse viruses have accumulated in fig germplasm. To date, more than 14 viruses have been described associated to fig trees, including eight members of the family Closteroviridae, although their role in the etiology of fig mosaic disease (FMD) is unclear. Characteristic symptoms of FMD include mosaic and chlorotic spots on the leaves, along with deformation of fruits and leaves. Fig mosaic virus (FMV) is the causal agent of FMD, although at least five closteroviruses have also been associated with FMD, with unclear roles. In this study, leaf samples displaying typical FMD symptoms, including yellow mosaic and mottling, were collected from a fig tree in Iowa, United States. Total RNA was extracted and subjected to high-throughput sequencing (HTS). Analysis of HTS data revealed contigs corresponding to FMV and a putative new member of the family Closteroviridae, tentatively named fig virus C (FiVC). Based on the HTS-derived sequence, we obtained the full-length genome of the putative new closterovirus using RT-PCR and RACE. The complete genome is approximately 17.8 kb long with open reading frames consistent with the genomic organization of closteroviruses. Sequence comparisons and phylogenetic analysis of the RNA-dependent RNA polymerase, heat shock protein 70-like protein, and capsid protein corroborates that FiVC is a new member of the genus Closterovirus, closely related to other fig-infecting viruses. The discovery of this novel closterovirus in a symptomatic fig tree highlights the need for further studies to clarify the roles of multiple viruses in disease development.

Enterovirus A/B is a significant pathogen responsible for a wide range of human diseases. Currently, effective preventive and therapeutic strategies against these viruses remain limited. Timosaponin BII is the active ingredient of a natural product with potential antioxidant and anti-inflammatory properties. This study aims to investigate the antiviral activity of Timosaponin BII and elucidate its underlying mechanism, thereby providing a scientific basis for the development of novel broad-spectrum anti-enterovirus agent. Firstly, systems pharmacology approaches were employed to integrate the potential targets of Timosaponin BII and predict its mechanism of action. Subsequently, the antiviral activity against representative strains of enterovirus A/B (EV-A71 for enterovirus A and CVB3 for enterovirus B respectively) was verified through cell morphology observation and CCK-8 assay in interferon-deficient Vero cells. Finally, the inhibitory effect on viral replication was assessed using a time-course drug addition experiment in non-interferon-deficient HeLa cells, and the inhibitory effect on viral proteins was detected by Western Blot. Timosaponin BII exhibited significant antiviral activity against enterovirus A and B at the cellular level, with EC₅₀ values of 0.54 μM against EV-A71 and 2.59 μM against CVB3 at 48 h post-infection. Quantitative real-time PCR (qRT-PCR) analysis revealed that the levels of EV-A71 and CVB3 viral VP1 RNA in the group treated with Timosaponin BII simultaneously with viral infection were lower than those in the viral infection group. Western blot results showed that Timosaponin BII could reduce the expression level of viral protein. Timosaponin BII, a potential broad-spectrum antiviral agent, exhibits antiviral activity against EV-A71 and CVB3. Its antiviral mechanism may involve the synergistic interaction of multiple targets and signaling pathways.

Influenza A(H1N1)pdm09 viruses pose a significant disease burden on children worldwide, with high rates of hospitalization and substantial morbidity and mortality. Outpatient < 18 years of age with upper respiratory infections (URIs) were enrolled through active surveillance at Shanxi Children's Hospital (SCH) between 7/1/2024 and 6/30/2025. Nasal swabs were collected for the detection of influenza virus and other respiratory pathogens by PCR-based methods. Influenza strains were obtained through in vitro culture, and their antigenic characterization were determined by hemagglutinin-inhibition (HI) assay. Genetic analyses were conducted using next-generation sequencing (NGS), while the fluorescence neuraminidase inhibition assay (FNIA) was employed to ascertain antiviral resistance. A total of 987 throat swab samples were collected. A(H1N1)pdm09 was the main pathogens causing URIs in children during the 2024-2025 influenza season and belongs to the 6B.1A.5a.2a evolutionary branch along with vaccine strains. Four novel HA and six NA non-synonymous substitutions were identified in pH1N1, which are related to antigenic drift and varying degrees of drug resistance, respectively. Three S137P-R142K-V152I-substituted strains were identified as low reactive strains, and strains with T188I, S247N, G249E, I264T, M314I, and K331R substitutions did not demonstrate a significant escalation in drug resistance. Despite the absence of drug-resistant A(H1N1)pdm09 strains in children, the emergence of low-response strains, attributable to mutations associated with antigen drift, necessitates continuous genomic monitoring to ensure preparedness for future seasonal influenza outbreaks.

The rapid evolutionary dynamics of avian influenza viruses (AIVs) enable frequent genetic drift and reassortment, posing ongoing challenges to both poultry and public health. In this study, we report the isolation of an H4N6 virus strain (Duck/Qom/02-663/2024) from a commercial duck farm in Iran. BLAST analysis indicated that, while the surface glycoproteins and nucleoprotein closely matched those of other H4N6 viruses, the remaining gene segments were more closely related to other subtypes, suggesting a potentially reassortant virus. Phylogenetic analysis classified the isolate within the Eurasian lineage. These findings underscore the importance of continuous surveillance of AIVs in both wild and domestic bird populations.

Dengue is a major public health problem that affects millions of people globally. The present study used microarray data to identify differentially expressed genes (DEGs) during dengue clinical conditions. The microarray datasets GSE84331, GSE18090, GSE43777, and E-MTAB-3162 were downloaded and analyzed using statistical analysis (Unpaired t-test). This was followed by Machine Learning (ML) and Deep Learning (DL) techniques with recursive feature elimination and genetic algorithms implemented to identify the potential biomarkers. Further, functional enrichment, platelet signaling, and protein-protein interaction (PPI) network analysis were performed to explore the potential diagnostic markers associated with dengue. Among all ML/DL models, the Random Forest algorithm outperformed on baseline data and identified 27 DEGs in the dengue fever (DF) vs. control (C) group and 13 DEGs in filtered data of the severe dengue (SD) vs. DF group. Likewise, the Support Vector Machine with Genetic Algorithm (SVM-GA) hybrid model outperformed the SD vs. C group and identified 79 DEGs. Based on the analysis, the study identified seven hub genes such as PIK3R1, GATA3, ZFPM, SKAP1 (involved in hemostasis, platelet activation, aggregation, and production), TP63, ZBTB20, and ZEB2 (abnormal hard palate morphology) for dengue diagnosis. Further, the hub genes may facilitate the development of reliable diagnostic potential; their prognostic utility requires further validation in larger, more diverse cohorts.

One challenge in utilizing the Measles virus (MV) for cancer therapy is the number of virus particles required, nearly a million times greater than the amount reported for vaccination. This study aims to design and develop a cell line with increased production capacity to supply the required amounts of MV in oncolytic virotherapy. The sphingosine kinase 1 (SphK1) gene was inserted into a pIRES2-EGFP plasmid and transiently transfected into four cell lines: MRC-5, HEK293, Vero, and A549. Fluorescent light intensity was measured using flow cytometry, and the MV production titer was determined using the TCID50 method. Transient transfection of pIRES2-EGFP-SphK1 was associated with increases in MV yield of approximately 3 logs in HEK293, 2 logs in Vero and A549, and 1 log in MRC-5 cells compared to controls and has impacted the morphology of MRC-5 cells. The top 100 genes co-expressed with SphK1 were identified with the ARCHS4 RNA-seq data resource, and functional enrichment with EnrichR suggested involvement in interleukin and cytokine signaling, extracellular matrix organization, and stress responses. The observed results indicate that augmenting the expression of the SphK1 gene may enhance MV production and influence cellular behavior, although effects appear to be cell line-dependent. A better understanding of cell-specific S1P signaling and cytoskeletal regulation could assist in optimizing cell lines for scalable virotherapy production.

Human retroviruses such as HIV-1 and HTLV-1 hijack host cellular mechanisms for their replication, survival, and pathogenesis, often causing profound genomic instability. This review explores the dual role of homologous recombination (HR), explicitly mediated by the recombinase RAD51, in the context of retroviral infections. RAD51 is central to high-fidelity repair of DNA double-strand breaks, yet its activity is manipulated differently by HIV-1 and HTLV-1. In HIV-1 infection, RAD51 expression is elevated by viral proteins like Tat and Vpr, promoting DNA repair and enhancing viral transcription through interactions with NF-κB, thereby supporting viral persistence. Conversely, HTLV-1 suppresses RAD51-mediated HR via viral proteins such as p30 and Tax, promoting error-prone DNA repair pathways that contribute to oncogenesis. These contrasting effects may underscore RAD51's functional plasticity as both a facilitator of viral replication and a potential antiviral restriction factor. Furthermore, the therapeutic modulation of RAD51 activity-especially in combination with PARP inhibitors offers promising avenues for treating retrovirus-associated malignancies such as adult T-cell leukemia/lymphoma. This review highlights RAD51 as a pivotal connection in the interplay between genome stability and retroviral pathobiology.