Nat Microbiol. 2024 Aug 29. doi: 10.1038/s41564-024-01799-3. Online ahead of print.

ABSTRACT

Fungal fermentation of food and agricultural by-products holds promise for improving food sustainability and security. However, the molecular basis of fungal waste-to-food upcycling remains poorly understood. Here we use a multi-omics approach to characterize oncom, a fermented food traditionally produced from soymilk by-products in Java, Indonesia. Metagenomic sequencing of samples from small-scale producers in Western Java indicated that the fungus Neurospora intermedia dominates oncom. Further transcriptomic, metabolomic and phylogenomic analysis revealed that oncom-derived N. intermedia utilizes pectin and cellulose degradation during fermentation and belongs to a genetically distinct subpopulation associated with human-generated by-products. Finally, we found that N. intermedia grew on diverse by-products such as fruit and vegetable pomace and plant-based milk waste, did not encode mycotoxins, and could create foods that were positively perceived by consumers outside Indonesia. These results showcase the traditional significance and future potential of fungal fermentation for creating delicious and nutritious foods from readily available by-products.

PMID:39209985 | DOI:10.1038/s41564-024-01799-3

Sci Rep. 2024 Aug 30;14(1):20144. doi: 10.1038/s41598-024-70327-4.

ABSTRACT

Our understanding of the spread of yeasts in natural ecosystems remains somewhat limited. The recent momentum of yeast ecology research has unveiled novel habitats and vectors that, alongside human activities, impact yeast communities in their natural environments. Yeasts, as non-airborne microorganisms, rely on animal vectors, predominantly insects. However, the overlooked actor in this interplay is the environmental matrix, a player potentially influencing yeast populations and their vectors. This study aims to delve deeper into the intricate, multi-layered connections between yeast populations and ecosystems, focusing on the interactions between the attributes of the environmental matrix, arthropod diversity, and the mycobiota within a renowned yeast-inhabited framework: the vineyard. To investigate these relationships, we sampled both invertebrate and yeast diversity in six organic and conventional vineyards described in terms of management and landscape composition. We identified 80 different invertebrate taxa and isolated 170 yeast strains belonging to 18 species. Notably, new species-specific yeast-insect associations were observed, including the exclusive association between Candida orthopsilosis and Hymenoptera and between Metschnikowia pulcherrima and Coleoptera. These newly identified potential associations provide valuable insights into insect and yeast physiology, hence holding the promise of enhancing our understanding of yeast and arthropod ecology and their collective impact on overall ecosystem health.

PMID:39209939 | DOI:10.1038/s41598-024-70327-4

Eur Respir J. 2024 Aug 29;64(2):2401133. doi: 10.1183/13993003.01133-2024. Print 2024 Aug.

NO ABSTRACT

PMID:39209466 | DOI:10.1183/13993003.01133-2024

Br J Pharmacol. 2024 Aug 29. doi: 10.1111/bph.17314. Online ahead of print.

ABSTRACT

G protein-coupled receptors (GPCRs) play a crucial role in cell function by transducing signals from the extracellular environment to the inside of the cell. They mediate the effects of various stimuli, including hormones, neurotransmitters, ions, photons, food tastants and odorants, and are renowned drug targets. Advancements in structural biology techniques, including X-ray crystallography and cryo-electron microscopy (cryo-EM), have driven the elucidation of an increasing number of GPCR structures. These structures reveal novel features that shed light on receptor activation, dimerization and oligomerization, dichotomy between orthosteric and allosteric modulation, and the intricate interactions underlying signal transduction, providing insights into diverse ligand-binding modes and signalling pathways. However, a substantial portion of the GPCR repertoire and their activation states remain structurally unexplored. Future efforts should prioritize capturing the full structural diversity of GPCRs across multiple dimensions. To do so, the integration of structural biology with biophysical and computational techniques will be essential. We describe in this review the progress of nuclear magnetic resonance (NMR) to examine GPCR plasticity and conformational dynamics, of atomic force microscopy (AFM) to explore the spatial-temporal dynamics and kinetic aspects of GPCRs, and the recent breakthroughs in artificial intelligence for protein structure prediction to characterize the structures of the entire GPCRome. In summary, the journey through GPCR structural biology provided in this review illustrates how far we have come in decoding these essential proteins architecture and function. Looking ahead, integrating cutting-edge biophysics and computational tools offers a path to navigating the GPCR structural landscape, ultimately advancing GPCR-based applications.

PMID:39209310 | DOI:10.1111/bph.17314

Life Sci. 2024 Aug 27:123020. doi: 10.1016/j.lfs.2024.123020. Online ahead of print.

ABSTRACT

AIM: Transcriptional regulation of gene expression plays a crucial role in orchestrating complex morphogenetic and molecular events during heart development and function. Mediator complex is an essential multi-subunit protein complex that governs gene expression in eukaryotic cells. Although Mediator subunits (MEDs) work integrally in the complex, individual MED component displays specialized functions. MED27, categorized as an Upper Tail subunit, possesses an as-yet-uncharacterized function. In this study, we aimed to investigate the physiological role of MED27 in cardiomyocytes.

MATERIALS AND METHODS: we generated a Med27 floxed mouse line, which was further used to generate constitutive (cKO) and inducible (icKO) cardiomyocyte-specific Med27 knockout mouse models. Morphological, histological analysis and cardiac physiological studies were performed in Med27 cKO and icKO mutants. Transcriptional profiles were determined by RNA sequencing (RNAseq) analysis.

KEY FUNDINGS: Ablation of MED27 in developing mouse cardiomyocytes results in embryonic lethality, while its deletion in adult cardiomyocytes leads to heart failure and mortality. Similar to the ablation of another Upper Tail subunit, MED30 in cardiomyocytes, deletion of MED27 leads to decreased protein levels of most MEDs in cardiomyocytes. Interestingly, overexpression of MED30 fails to restore the protein levels of Mediator subunits in MED27-deficient cardiomyocytes, demonstrating that the role of MED27 in maintaining the integrity and stability of the Mediator complex is independent of MED30.

SIGNIFICANCE: Our results revealed an essential role of MED27 in cardiac development and function by maintaining the stability of the Mediator core.

PMID:39209248 | DOI:10.1016/j.lfs.2024.123020

Behav Processes. 2024 Aug 27:105092. doi: 10.1016/j.beproc.2024.105092. Online ahead of print.

ABSTRACT

Behavioural contagion is an automatic process through which a behaviour performed by an individual (trigger) is reproduced by an observer (responder) without necessarily replicating the exact motor sequence. It has been linked to inter-individual synchronisation and possibly emotional contagion. Play can convey a positive mood and enhance social bonding, although its contagiousness is understudied. To verify social play contagion presence and modulating factors, we gathered audio-video data on social play, distance and affiliation on a group of savannah African elephants (15 individuals) at Parque de la Naturaleza de Cabarceno (Cantabria, Spain). Social play was contagious as it was more likely started by uninvolved elephants (within 3-min) in Post-Play Condition (PP) - after that other elephants had started playing - than in Matched-control Condition (MC; no previous play). Social play contagion mostly occurred within 30m - probably due to elephants' limited visual acuity - and it was highest between individuals that affiliated the most, with the distance-affiliation interaction having no effect. The most prominent individuals in the social play network were also the most influential in the play contagion network (Eigenvector-centrality measure). Play contagion was socially modulated, thus suggesting it may extend from motor replication to the replication of the underlying affective state.

PMID:39209084 | DOI:10.1016/j.beproc.2024.105092

Bioorg Chem. 2024 Aug 28;152:107736. doi: 10.1016/j.bioorg.2024.107736. Online ahead of print.

ABSTRACT

Novel anticancer strategies reduce side effects on healthy tissues by elevating the lethal abilities of cancer cells. The development of effective particles with good bioavailability and selectivity remains problematic. For undesirable features, green chemistry is used to synthesize the best compounds, or natural-based particles are improved. Photodynamic therapy (PDT), modelled on phthalocyanines (Pcs), still delivers second-generation sensitizers which are complemented with metal ions, such as Zn2+, Al3+, or Ga3+. Gallium octacarboxyphthalocyanine hydroxide (Ga(OH)PcOC), was designed for skin cancer treatment, and was used as a pro-apoptotic and pro-oxidative agent on normal skin cell lines, fibroblasts (NHDF), and keratinocytes (HaCaT), with promising selectivity against melanoma cancer cells (Me45) in vitro. Compared to the previous reported findings, where the ZnPcOC acted on the skin cell lines at higher doses, the sensitivities to the Ga(OH)PcOC allows for an effective reduction of the sensitizer dose. The effective dose, for a novel Ga(OH)PcOC particle, was significantly reduced from 30 µM to 6 µM on Me45 cancer cells, tested using 24 h MTT viability, as well as cytometric pro-oxidative and pro-apoptotic assays. The promising photosensitizer did not reduce viability in normal fibroblasts and keratinocytes without reactive oxygen species (ROS) elevation or apoptosis induction. The improvement to the previous findings is better Ga-based photosensitizer selectivity against the cancer Me45 cells, then observed in Zn-based compounds.

PMID:39208675 | DOI:10.1016/j.bioorg.2024.107736

PLoS One. 2024 Aug 29;19(8):e0309352. doi: 10.1371/journal.pone.0309352. eCollection 2024.

ABSTRACT

Pyrazinamide (PZA) is a key drug in the treatment of Mycobacterium tuberculosis. Although not completely understood yet, the bactericidal mechanism of PZA starts with its diffusion into the cell and subsequent conversion into pyrazinoic acid (POA) after the hydrolysis of ammonia group. This leads to the acidification cycle, which involves: (1) POA extrusion into the extracellular environment, (2) reentry of protonated POA, and (3) release of a proton into the cytoplasm, resulting in acidification of the cytoplasm and accumulation of intracellular POA. To better understand this process, we developed a system of coupled non-linear differential equations, which successfully recapitulates the kinetics of PZA/POA observed in M. tuberculosis. The parametric space was explored, assessing the impact of different PZA and pH concentrations and variations in the kinetic parameters, finding scenarios of PZA susceptibility and resistance. Furthermore, our predictions show that the acidification cycle alone is not enough to result in significant intracellular accumulation of POA in experimental time scales when compared to other neutral pH scenarios. Thus, revealing the need of novel hypotheses and experimental evidence to determine the missing mechanisms that may explain the pH-dependent intracellular accumulation of POA and their subsequent effects.

PMID:39208342 | DOI:10.1371/journal.pone.0309352

PLoS One. 2024 Aug 29;19(8):e0309303. doi: 10.1371/journal.pone.0309303. eCollection 2024.

ABSTRACT

Immunosuppressive drugs are essential for systemic lupus erythematosus (SLE) treatment, but there are concerns about their toxicity. In this study, Arthrospira platensis was used as a resource for screening of the SLE-related bioactive compounds. To discover the potential compounds, a total of 833 compounds of A. platensis C1 were retrieved from the Spirulina-Proteome Repository (SpirPro) database and by literature mining. We retrieved structures and bioassays of these compounds from PubChem database; and collected approved and potential drugs for SLE treatment from DrugBank and other databases. The result demonstrated that cytidine, desthiobiotin, agmatine, and anthranilic acid, from the alga, has Tanimoto matching scores of 100% with the following drugs: β-arabinosylcytosine/cytarabine, d-dethiobiotin, agmatine, and anthranilic acid, respectively. The bioassay matching and disease-gene-drug-compound network analysis, using VisANT 4.0 and Cytoscape, revealed 471 SLE-related genes. Among the SLE-related genes, MDM2, TP53, and JAK2 were identified as targets of cytarabine, while PPARG and IL1B were identified as targets of d-dethiobiotin. Binding affinity between the drug ligands and the algal bioactive compound ligands with their corresponding receptors were similarly comparable scores and stable, examined by molecular docking and molecular dynamic simulations, respectively.

PMID:39208266 | DOI:10.1371/journal.pone.0309303

Science. 2024 Aug 30;385(6712):eadj8691. doi: 10.1126/science.adj8691. Epub 2024 Aug 30.

ABSTRACT

Chromosome-containing micronuclei are a hallmark of aggressive cancers. Micronuclei frequently undergo irreversible collapse, exposing their enclosed chromatin to the cytosol. Micronuclear rupture catalyzes chromosomal rearrangements, epigenetic abnormalities, and inflammation, yet mechanisms safeguarding micronuclear integrity are poorly understood. In this study, we found that mitochondria-derived reactive oxygen species (ROS) disrupt micronuclei by promoting a noncanonical function of charged multivesicular body protein 7 (CHMP7), a scaffolding protein for the membrane repair complex known as endosomal sorting complex required for transport III (ESCRT-III). ROS retained CHMP7 in micronuclei while disrupting its interaction with other ESCRT-III components. ROS-induced cysteine oxidation stimulated CHMP7 oligomerization and binding to the nuclear membrane protein LEMD2, disrupting micronuclear envelopes. Furthermore, this ROS-CHMP7 pathological axis engendered chromosome shattering known to result from micronuclear rupture. It also mediated micronuclear disintegrity under hypoxic conditions, linking tumor hypoxia with downstream processes driving cancer progression.

PMID:39208110 | DOI:10.1126/science.adj8691

Endocrinology. 2024 Aug 29:bqae111. doi: 10.1210/endocr/bqae111. Online ahead of print.

ABSTRACT

Breast cancer is a leading cause of female mortality and despite advancements in personalized therapeutics, metastatic disease largely remains incurable due to drug resistance. The estrogen receptor (ER, ESR1) is expressed in two-thirds of all breast cancer, and under endocrine stress, somatic ESR1 mutations arise in ∼30% of cases that result in endocrine resistance. We and others reported ESR1 fusions as a mechanism of ER mediated endocrine resistance. ER fusions, which retain the AF1 and DNA binding domains, harbor ESR1 exons 1-6 fused to an in-frame gene partner resulting in loss of the ER ligand binding domain (LBD). We demonstrate that in a no-special type (invasive ductal carcinoma (IDC)-NST) and an invasive lobular carcinoma (ILC) cell line, ER fusions exhibit robust hyperactivation of canonical ER signaling pathways independent of estradiol or anti-endocrine therapies. We employ cell line models stably overexpressing ER fusions with concurrent endogenous ER knockdown to minimize endogenous ER influence. Cell lines exhibited shared transcriptomic enrichment in pathways known to be drivers of metastatic disease, notably MYC signaling. Cells expressing the 3' fusion partners SOX9 and YAP1 consistently demonstrated enhanced growth and cell survival. ILC cells expressing the DAB2 fusion led to enhanced growth, survival, and migration; phenotypes not appreciated in the IDC-NST DAB2 model. Herein, we report that cell line activity is subtype-, fusion-, and assay-specific suggesting that LBD loss, the fusion partner, and the cellular landscape all influence fusion activities. Therefore, it will be critical to assess fusion frequency, in the context of the tumor clinicopathology.

PMID:39207954 | DOI:10.1210/endocr/bqae111

mSystems. 2024 Aug 29:e0086824. doi: 10.1128/msystems.00868-24. Online ahead of print.

ABSTRACT

Pollution can negatively impact aquatic ecosystems, aquaculture operations, and recreational water quality. Many aquatic microbes can sequester or degrade pollutants and have been utilized for bioremediation. While planktonic and benthic microbes are well-studied, host-associated microbes likely play an important role in mitigating the negative impacts of aquatic pollution and represent an unrealized source of microbial potential. For example, aquatic organisms that thrive in highly polluted environments or concentrate pollutants may have microbiomes adapted to these selective pressures. Understanding microbe-pollutant interactions in sensitive and valuable species could help protect human well-being and improve ecosystem resilience. Investigating these interactions using appropriate experimental systems and overcoming methodological challenges will present novel opportunities to protect and improve aquatic systems. In this perspective, we review examples of how microbes could mitigate negative impacts of aquatic pollution, outline target study systems, discuss challenges of advancing this field, and outline implications in the face of global changes.

PMID:39207151 | DOI:10.1128/msystems.00868-24

mBio. 2024 Aug 29:e0087324. doi: 10.1128/mbio.00873-24. Online ahead of print.

ABSTRACT

Microorganisms with simplified genomes represent interesting cell chassis for systems and synthetic biology. However, genome reduction can lead to undesired traits, such as decreased growth rate and metabolic imbalances. To investigate the impact of genome reduction on Escherichia coli strain DGF-298, a strain in which ~ 36% of the genome has been removed, we reconstructed a strain-specific metabolic model (iAC1061), investigated the regulation of gene expression using iModulon-based transcriptome analysis, and performed adaptive laboratory evolution to let the strain correct potential imbalances that arose during its simplification. The model notably predicted that the removal of all three key pathways for glycolaldehyde disposal in this microorganism would lead to a metabolic bottleneck through folate starvation. Glycolaldehyde is also known to cause self-generation of reactive oxygen species, as evidenced by the increased expression of oxidative stress resistance genes in the SoxS iModulon. The reintroduction of the aldA gene, responsible for one native glycolaldehyde disposal route, alleviated the constitutive oxidative stress response. Our results suggest that systems-level approaches and adaptive laboratory evolution have additive benefits when trying to repair and optimize genome-engineered strains.

IMPORTANCE: Genomic streamlining can be employed in model organisms to reduce complexity and enhance strain predictability. One of the most striking examples is the bacterial strain Escherichia coli DGF-298, notable for having over one-third of its genome deleted. However, such extensive genome modifications raise the question of how similar this simplified cell remains when compared with its parent, and what are the possible unintended consequences of this simplification. In this study, we used metabolic modeling along with iModulon-based transcriptomic analysis in different growth conditions to assess the impact of genome reduction on metabolism and gene regulation. We observed little impact of genomic reduction on the regulatory network of E. coli DGF-298 and identified a potential metabolic bottleneck leading to the constitutive activity of the SoxS iModulon. We then leveraged the model's predictions to successfully restore SoxS activity to the basal level.

PMID:39207109 | DOI:10.1128/mbio.00873-24

Malays J Pathol. 2024 Aug;46(2):259-278.

ABSTRACT

INTRODUCTION: Leukaemia is the most common cancer in children, however, there is still a big gap in knowledge about the genomic alterations in childhood acute myeloid leukaemia (AML) compared to adult AML. Relapsed AML remains as a leading cause of cancer deaths among children. This study aims to understand the molecular mechanisms of relapsed AML by elucidating the mutational landscape before and during relapse.

MATERIALS AND METHODS: Whole genome sequencing was performed on matched samples collected at diagnosis, remission and relapse from three patients of de novo childhood AML. Sanger sequencing was performed for validation in 47 patients' samples, followed by functional analysis.

RESULTS: Overall, we identified 312 somatic mutations including synonymous single nucleotide variants (SNVs), missense SNVs, deletions and insertion frameshifts, stopgains and splice sites. After prioritisation, only 46 variants were present at diagnosis (13-17 mutations per patient) and 49 variants at relapse (12-20 mutations per patient). Out of 81 variants, there were 35 new variants detected at relapse but not present at diagnosis. Six potential driver mutations (KIT, CDC73, HNF1A, RBM10, ZMYM4 and ETV6) were identified in predicting relapse for the 3 patients, with recurrent mutations of the ETV6 gene in 2 patients. Functional analysis of the ETV6 mutation showed that ETV6 lost its tumour suppressive function when both mutant ETV6 p.P25fs and ETV6 p.N75fs were tested in vitro.

CONCLUSION: This study has uncovered the mutational landscape in three local childhood AML patients and contributes to a better understanding of the molecular mechanisms of relapsed AML.

PMID:39207003

J Cell Sci. 2024 Aug 15;137(16):jcs261386. doi: 10.1242/jcs.261386. Epub 2024 Aug 29.

ABSTRACT

Intermediate filaments (IFs) comprise a large family of versatile cytoskeletal proteins, divided into six subtypes with tissue-specific expression patterns. IFs have a wide repertoire of cellular functions, including providing structural support to cells, as well as active roles in mechanical support and signaling pathways. Consequently, defects in IFs are associated with more than 100 diseases. In this Cell Science at a Glance article, we discuss the established classes of IFs and their general features, their functions beyond structural support, and recent advances in the field. We also highlight their involvement in disease and potential use as clinical markers of pathological conditions. Finally, we provide our view on current knowledge gaps and the future directions of the IF field.

PMID:39206824 | DOI:10.1242/jcs.261386

Circ Res. 2024 Aug 29. doi: 10.1161/CIRCRESAHA.124.324829. Online ahead of print.

NO ABSTRACT

PMID:39206552 | DOI:10.1161/CIRCRESAHA.124.324829

Front Microbiol. 2024 Aug 14;15:1446595. doi: 10.3389/fmicb.2024.1446595. eCollection 2024.

ABSTRACT

Acinetobacter baumannii is an opportunistic human pathogen which can use host-derived L-carnitine as sole carbon and energy source. Recently, an L-carnitine transporter (Aci1347) and a specific monooxygense (CntA/CntB) for the intracellular cleavage of L-carnitine have been characterized. Subsequent conversion of the resulting malic semialdehyde into the central metabolite L-malate was hypothesized. Alternatively, L-carnitine degradation via D-malate with subsequent oxidation into pyruvate was proposed. Here we describe the in vitro and in vivo reconstitution of the entire pathway, starting from the as yet uncharacterized gene products of the carnitine degradation gene operon. Using recombinantly purified enzymes, enantiomer-specific formation of D-malate by the NAD(P)+-dependent malic semialdehyde dehydrogenase (MSA-DH) is demonstrated. The solved X-ray crystal structure of tetrameric MSA-DH reveals the key catalytic residues Cys290 and Glu256, accessible through opposing substrate and cofactor funnels. Specific substrate binding is enabled by Arg166, Arg284 and Ser447 while dual cofactor specificity for NAD+ and NADP+ is mediated by Asn184. The subsequent conversion of the unusual D-malate reaction product by an uncharacterized NAD+-dependent malate dehydrogenase (MDH) is shown. Tetrameric MDH is a β-decarboxylating dehydrogenase that synthesizes pyruvate. MDH experiments with alternative substrates showed a high degree of substrate specificity. Finally, the entire A. baumannni pathway was heterologously reconstituted, allowing E. coli to grow on L-carnitine as a carbon and energy source. Overall, the metabolic conversion of L-carnitine via malic semialdehyde and D-malate into pyruvate, CO2 and trimethylamine was demonstrated. Trimethylamine is also an important gut microbiota-dependent metabolite that is associated with an increased risk of cardiovascular disease. The pathway reconstitution experiments allowed us to assess the TMA forming capacity of gut microbes which is related to human cardiovascular health.

PMID:39206375 | PMC:PMC11353897 | DOI:10.3389/fmicb.2024.1446595

iScience. 2024 Jul 20;27(8):110544. doi: 10.1016/j.isci.2024.110544. eCollection 2024 Aug 16.

ABSTRACT

Pancreatic neuroendocrine tumors (PanNETs) represent well-differentiated endocrine neoplasms with variable clinical outcomes. Predicting patient outcomes using the current tumor grading system is challenging. In addition, traditional systemic treatment options for PanNETs, such as somatostatin analogs or cytotoxic chemotherapies, are very limited. To address these issues, we characterized PanNETs using integrated proteogenomics and identified four subtypes. Two proteomic subtypes showed high recurrence rates, suggesting clinical aggressiveness that was missed by current classification. Hypoxia and inflammatory pathways were significantly enriched in the clinically aggressive subtypes. Detailed analyses revealed metabolic adaptation via glycolysis upregulation and oxidative phosphorylation downregulation under hypoxic conditions. Inflammatory signature analysis revealed that immunosuppressive molecules were enriched in immune hot tumors and might be immunotherapy targets. In this study, we characterized clinically aggressive proteomic subtypes of well-differentiated PanNETs and identified candidate therapeutic targets.

PMID:39206147 | PMC:PMC11350455 | DOI:10.1016/j.isci.2024.110544

Viruses. 2024 Jul 30;16(8):1221. doi: 10.3390/v16081221.

ABSTRACT

Most mathematical models that assess the vectorial capacity of disease-transmitting insects typically focus on the influence of climatic factors to predict variations across different times and locations, or examine the impact of vector control interventions to forecast their potential effectiveness. We combine features of existing models to develop a novel model for vectorial capacity that considers both climate and vector control. This model considers how vector control tools affect vectors at each stage of their feeding cycle, and incorporates host availability and preference. Applying this model to arboviruses of veterinary importance in Europe, we show that African horse sickness virus (AHSV) has a higher peak predicted vectorial capacity than bluetongue virus (BTV), Schmallenberg virus (SBV), and epizootic haemorrhagic disease virus (EHDV). However, AHSV has a shorter average infectious period due to high mortality; therefore, the overall basic reproduction number of AHSV is similar to BTV. A comparable relationship exists between SBV and EHDV, with both viruses showing similar basic reproduction numbers. Focusing on AHSV transmission in the UK, insecticide-treated stable netting is shown to significantly reduce vectorial capacity of Culicoides, even at low coverage levels. However, untreated stable netting is likely to have limited impact. Overall, this model can be used to consider both climate and vector control interventions either currently utilised or for potential use in an outbreak, and could help guide policy makers seeking to mitigate the impact of climate change on disease control.

PMID:39205195 | DOI:10.3390/v16081221

Viruses. 2024 Jul 26;16(8):1207. doi: 10.3390/v16081207.

ABSTRACT

Bats are natural hosts of a wide variety of viruses, including adenoviruses. European bats are known to carry mastadenoviruses categorized as species B (widespread in European Vespertilionidae bats) and whose taxonomy has not been clarified. We examined fecal samples from Vespertilionidae bats (five species) captured in central Russia and found that 2/12 (16%) were positive for mastadenoviruses. The partial genome of the mastadenovirus was assembled from Pipistrellus nathusii, representing the bat adenovirus species B. The complete genome (37,915 nt) of a novel mastadenovirus was assembled from Nyctalus noctula and named BatAdV/MOW15-Nn19/Quixote. Comparative studies showed significant divergence of the Quixote genome sequence from European bat mastadenoviruses, while the only known virus showing low similarity was the isolate WA3301 from an Australian bat, and together they formed a subclade that separated from other BatAdVs. Phylogenetic and comparative analysis of the protein-coding genes provided evidence that Quixote is related to a novel species within the genus Mastadenovirus, provisionally named "K" (as the next available letter for the species). Phylogenetic analyses revealed that some earlier viruses from Western European bats, for which only partial DNA polymerase genes are known, are most likely members of the tentatively named species "K". Thus, at least two species of mastadenovirus are circulating in bats throughout Europe, from western to eastern areas.

PMID:39205181 | DOI:10.3390/v16081207