
Aeromonas hydrophila is an opportunistic pathogen of fish, humans, and livestock, and has a severe negative impact on aquaculture development. Phage therapy is considered an alternative strategy for controlling bacterial infections and contamination. In this study, a novel phage, Aeromonas hydrophila BMBAH1, was isolated. Transmission electron microscopy showed that phage BMBAH1 had a long tail and an icosahedral head. Biological characterization indicated that phage BMBAH1 remained highly active across a broad range of temperatures and pH values, exhibiting long-term and significant inhibitory effects on host bacteria at an optimal multiplicity of infection (MOI) of 0.1. The genome of phage BMBAH1 is 237 kb in length with a guanine-cytosine (GC) content of 44.3%, and it was identified as a typical jumbo phage and predicted to contain 241 open reading frames (ORFs). Whole-proteome-based phylogenetic analysis, gene-sharing network analysis, and core protein clustering consistently indicated that phage BMBAH1 belongs to the family Chimalliviridae . However, phage BMBAH1 exhibited low intergenomic similarity to previously isolated phages, with values of approximately 30%. These results support the designation of phage BMBAH1 as the representative member of a candidate novel viral genus, designated Southlakevirus . Our findings expand the diversity of A. hydrophila phages and provide a promising genetic resource for further exploring biological characteristics of jumbo phages and developing biocontrol strategies.
Tahyna virus (TAHV) is a neglected mosquito-borne Orthobunyavirus pathogenic to humans. In Italy, TAHV was first recorded in Friuli Venezia-Giulia and then repeatedly in Emilia Romagna Region (Northern Italy). This study was set up to verify the presence of TAHV in Central Italy and to identify its potential vectors. Mosquito surveillance was conducted from April to November 2025, using 78 CDCCO₂ traps across Latium and Tuscany Regions. A total of 17,728 Culicidae was captured, including 9237 specimens of four potential vector Aedes species (Aedes albopictus, Aedes caspius, Aedes detritus, and Aedes vexans). Aedes caspius was the dominant species, showing a marked abundance peak from late-summer to early-autumn. Additionally, a high density of Ae. vexans, a primary TAHV vector species in Europe, was recorded in Arezzo province, Eastern Tuscany. A total of 356 pools of the Aedes species, made up of 6600 specimens, was screened for TAHV by real-time and conventional PCR. TAHV was detected in one pool of Ae. caspius collected in Grosseto province, Southern Tuscany. This study provides the first report of TAHV in Central Italy, identifying the southernmost detection in the Country to date.
Capturing nanoscale biological objects in nanochannels depends strongly on surface geometry and interfacial interactions. However, the spatial and temporal limitations of atomistic simulations prevent the direct representation of a complete rabies virion. In this study, we used molecular dynamics simulations to examine the force-driven retention of a reduced rabies-virus model with a characteristic size of approximately 4 nm in a water-filled platinum nanochannel with non-ideal surface roughness. The simulated construct was developed from reported rabies-virus structural information but did not reproduce the complete morphology, envelope, genomic content, or biological functionality of an intact virion. The atomic interactions were described using DREIDING and Universal Force Field parameters, the TIP3P water model, the embedded atom method for Pt–Pt interactions, and Lennard-Jones and Coulombic terms for interfacial interactions. After 10 ns of canonical equilibration at 300 K, the system underwent a 20 ns force-driven production stage. Roughness sizes of 35, 37, 40, and 43 Å were investigated. Among the four simulated configurations, the 40 Å roughness case produced the largest maximum density (0.187 atom/ų), the lowest maximum velocity (0.006 Å/ps), the largest retained surface-mesh volume (31,118 ų), and the most negative reduced-model–Pt interaction energy (−469.91 kcal/mol). The simulation-defined retained fraction for the reduced construct reached 95% at 20 ns. The weaker responses at 43 Å indicated a non-monotonic dependence on roughness size within this model and the investigated geometries. These results characterized the force-driven behavior of a specific 4-nm construct under the stated simulation conditions; they did not establish roughness-dependent capture behavior for intact rabies virions or predict experimental device performance.
Aeromonas hydrophila is an opportunistic pathogen of fish, humans, and livestock, and has a severe negative impact on aquaculture development. Phage therapy is considered an alternative strategy for controlling bacterial infections and contamination. In this study, a novel phage, Aeromonas hydrophila BMBAH1, was isolated. Transmission electron microscopy showed that phage BMBAH1 had a long tail and an icosahedral head. Biological characterization indicated that phage BMBAH1 remained highly active across a broad range of temperatures and pH values, exhibiting long-term and significant inhibitory effects on host bacteria at an optimal multiplicity of infection (MOI) of 0.1. The genome of phage BMBAH1 is 237 kb in length with a guanine-cytosine (GC) content of 44.3%, and it was identified as a typical jumbo phage and predicted to contain 241 open reading frames (ORFs). Whole-proteome-based phylogenetic analysis, gene-sharing network analysis, and core protein clustering consistently indicated that phage BMBAH1 belongs to the family Chimalliviridae. However, phage BMBAH1 exhibited low intergenomic similarity to previously isolated phages, with values of approximately 30%. These results support the designation of phage BMBAH1 as the representative member of a candidate novel viral genus, designated Southlakevirus. Our findings expand the diversity of A. hydrophila phages and provide a promising genetic resource for further exploring biological characteristics of jumbo phages and developing biocontrol strategies.
Zika virus (ZIKV) infection can cause severe neurological complications, particularly when antiviral immune responses are impaired. Here, we investigated how type I interferon (IFN-I) signaling influences the cellular inflammatory response and immunopathology in the central nervous system (CNS) during ZIKV infection. ZIKV infection induced early IFN-α and IFN-β expression in the CNS of wild-type (WT) mice. In contrast, mice lacking the IFN-I receptor (IFNAR−/−) exhibited higher CNS viral loads, severe clinical symptoms, weight loss, increased mortality, and histopathological alterations characterized by extensive leukocyte accumulation and ZIKV antigen detection. Flow cytometry and UMAP analysis revealed that IFN-I signaling restrains leukocyte accumulation in the CNS. IFNAR−/−mice showed increased accumulation of myeloid and lymphoid cells, including inflammatory monocytes, monocyte-derived dendritic cells, and activated CD4+ and CD8+ T cells, whereas WT mice displayed limited leukocyte accumulation. Loss of IFN-I signaling was associated with elevated levels of pro-inflammatory cytokines (IL-6, IL-1β, TNF, and IFN-γ), chemokines (CCL2, CCL4, and CCL5), and inducible nitric oxide synthase (iNOS). Notably, CNS-resident microglia from IFNAR−/− mice were highly susceptible to cell death, including among ZIKV antigen-negative cells, suggesting that inflammatory signals generated during infection may contribute to injury in uninfected microglia. In contrast, myeloid cells were predominantly ZIKV antigen-positive but remained largely viable. CD45− non-leukocyte cells constituted the major ZIKV antigen-positive population in the CNS and displayed resistance to cell death, indicating that this compartment may represent an important cellular population associated with ZIKV antigen detection during acute infection. Together, these findings demonstrate that IFN-I signaling is essential for controlling ZIKV replication, restraining neuroinflammation, and limiting CNS immunopathology. Its absence leads to increased viral burden, dysregulated immune cell accumulation, and severe neurological disease.