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Equine encephalosis (EE) is an arthropod-borne viral disease resembling a mild form of African horse sickness disease, which affects all species of equids. Previously, only EEV serotype 4 (EEV-4) caused sporadic outbreaks of the disease in Israel. In the summer of 2023, EE was clinically diagnosed in horses and donkeys in Israel. For laboratory confirmation, tissue cultures were inoculated with whole-blood samples obtained from sick animals. Five EEV isolates were successfully recovered in tissue and confirmed by conventional RT-PCR and Sanger sequencing of several viral genes. BLAST analysis of genome segment 2 revealed that the isolates belonged to serotype 6. Full-genome sequencing of one representative strain and subsequent phylogenetic analysis demonstrated a close relationship to South African and Indian EEV strains, suggesting possible epidemiological links that warrant further investigation. This observation can indirectly point to a broader geographic circulation of EEV than was previously thought.

Flaviviruses, including Dengue, West Nile, Zika, and Japanese encephalitis viruses, are arthropod-borne RNA viruses that pose an increasing global health threat. This review summarizes the role of nonstructural protein 1 (NS1), a multifunctional glycoprotein found in intracellular and secreted forms, as a key regulator of innate immunity. NS1 modulates several pattern recognition receptor pathways, including TLRs, RLRs, SR-B1-related mechanisms, and inflammasome platforms, thereby altering cytokine and interferon responses. Its effects are virus- and context-dependent. WNV NS1 inhibits TLR3/TRIF signaling, reducing IRF3 activation, type I interferon production, and interferon-stimulated gene expression. In contrast, DENV NS1 is linked to inflammatory signaling, particularly through TLR4. At the cytosolic level, NS1 from DENV, WNV, and ZIKV disrupts RIG-I/MDA5-MAVS signaling and weakens IFN-β induction. NS1 also affects inflammasome pathways: DENV promotes IL-1β release through a CD14-dependent mechanism, ZIKV suppresses cGAS-mediated antiviral signaling, and JEV promotes NLRP3 inflammasome assembly. Overall, NS1 selectively dampens interferon-mediated antiviral defenses while sustaining or enhancing inflammation, contributing to endothelial dysfunction, neuroinflammation, and severe disease.

Flaviviruses, or orthoflaviviruses, are arthropod-borne RNA viruses that pose a significant global health threat and co-circulate in many regions across the world. Neutralizing antibodies against specific pathogenic flaviviruses, such as dengue virus, Zika virus, and West Nile virus, are well-known. However, vaccine and therapeutic development against many flaviviruses remains challenging due to their antigenic diversity and complex humoral responses. Recent studies have reported patient-derived neutralizing antibodies that are active against multiple flaviviruses. Structural characterization of these pan-flavivirus antibodies has identified quaternary epitopes that are conserved across multiple flaviviruses, emphasizing the importance of quaternary epitopes on native flaviviruses, which, in some cases, are also preserved across different virus morphologies. Understanding the basis of quaternary structural epitope recognition can aid in the design of immunogens that elicit broad protection, with a lower risk of infection enhancement. In this review, we discuss mechanistic insights of bnAbs targeting different quaternary epitopes found on pathogenic flaviviruses, and implications for next-generation pan-flavivirus vaccine strategies.

Getah virus (GetV) is an arthropod-borne alphavirus historically recognized as an emerging zoonotic pathogen of veterinary significance, particularly in livestock and equine populations across Asia and parts of the Western Pacific. Over the past several decades, its expanding ecological range, broad mosquito vector competence, and increasing frequency of animal outbreaks have positioned GetV as a growing concern for animal health surveillance, diagnostics, and vaccine development. However, beyond its established role in veterinary virology, a critical and underexplored dimension of GetV biology is its emerging potential in oncolytic virotherapy. Recent discoveries, particularly involving the M1 strain, reveal a striking capacity for tumor-selective replication driven by defects in antiviral innate immune signaling within malignant cells. This property positions GetV-derived platforms as promising candidates for next-generation oncolytic virus development, capable of direct tumor lysis and secondary activation of antitumor immunity. These findings signal a paradigm shift in how traditionally zoonotic alphaviruses may be repurposed for precision oncology. We therefore hypothesize that whilst broad cellular tropism enables Getah virus entry into different kinds of cells, the oncolytic efficacy requires another layer of intracellular permissiveness characterized by tumor-specific innate immune defects. This Perspective synthesizes the current state of knowledge on GetV from both veterinary and translational oncology viewpoints and outlines the dual-use trajectory of the virus from agricultural pathogen to therapeutic bioplatform. We further highlight unresolved questions surrounding mechanisms of tumor selectivity, biosafety and host restriction, genetic stability, immune modulation, and regulatory translational barriers. Addressing these gaps will be essential for advancing GetV-based oncolytic platforms toward clinical applicability. Collectively, GetV represents a compelling example of how emerging zoonotic viruses may be strategically repositioned at the interface of infectious disease surveillance and cancer therapy innovation.

Culicoides biting midges are small blood feeding insects responsible for the transmission of important arthropod-borne viruses (arboviruses) such as bluetongue virus (BTV), Schmallenberg virus (SBV) and epizootic hemorrhagic disease virus (EHDV), which cause major losses to livestock production worldwide. Culicoides sonorensis is the primary vector of BTV in North America and one of the few Culicoides species to be colonised and reared in artificial conditions. Gene editing technology has been used to explore virus-vector interactions in other vector groups, particularly within mosquitoes. Despite the availability of a reference genome since 2018, to date there have been no reports of gene editing in C. sonorensis. Here, we report the first instance of gene editing in C. sonorensis, achieved by intrathoracic injection of adult females with Cas9 and sgRNAs targeting the white gene. We generated heritable mutations in the white gene which produced both white eye and red eye phenotypes and went on to establish a homozygous knockout line carrying a single mutation. We observed gene editing efficiencies of up to 12.3%, making this an efficient protocol for genetic manipulation of Culicoides biting midges, opening the door to functional genomics studies and the development of control strategies in these important and understudied disease vectors.

Arthropod-borne viruses are increasingly reported across Europe, with Culex pipiens serving as the main vector of West Nile and Usutu viruses. The C. pipiens complex comprises two ecologically distinct ecotypes, pipiens and molestus, which can hybridise. These ecotypes are thought to differ in habitat preference, with C. p. molestus more frequent in urban environments and C. p. pipiens in natural ones. However, many studies have either not distinguished between these ecotypes or have investigated them without considering a clear landscape gradient. This information is nevertheless important for understanding vector distribution and the potential implications for virus transmission pathways and spillover risk. A season-long survey was conducted from May to September 2025 across 57 sampling sites in Switzerland. Mosquitoes were morphologically identified, and C. pipiens ecotypes were distinguished using molecular analyses. We characterised landscape composition and their scale of effects, as well as meteorological conditions on the sampling dates to determine their influence on the presence and relative proportion of each C. pipiens ecotype. Agricultural landscapes promoted all ecotypes, urbanisation positively influenced C. p. pipiens but not C. p. molestus, and forest cover reduced the presence and relative proportion of hybrids. In addition, temperature was positively correlated with all ecotype presence, whereas rainfall had no detectable effect. The responses to landscape variables differ among C. pipiens ecotypes and across different landscape features. This highlights the complex, context-dependent interactions between the ecology of mosquitoes and the composition of their habitat, which ultimately determine their spatial distribution patterns.

Alphaviruses are arthropod-borne pathogens that cause immune-mediated encephalomyelitis. The prototypic alphavirus, Sindbis virus (SINV), primarily infects neurons in mice, resulting in neurologic disease involving both the brain and spinal cord. Interferon (IFN) regulatory factor (IRF) 7-deficient mice (Irf7-/-) rapidly succumb to SINV infection with extensive immunopathology while wildtype mice experience only mild disease and recover. IRF7 is widely recognized to be the main transcription factor required for the amplification of type I IFN, specifically IFNα, as Irf7-/- mice do not produce IFNα but do express IFNβ. However, based on the current experimental evidence, it is not clear if the severe outcome of SINV infection in Irf7-/- mice is due to the absence of IFNα or heretofore unappreciated noncanonical actions of IRF7. In this study, we demonstrate that the administration of IFNα to Irf7-/- mice early in infection restricted SINV replication and largely rescued the animals from severe disease and mortality but did not alter the nature of CNS inflammation. Further, Cre-Lox-mediated deletion of Irf7 in myeloid cells (Irf7fl/flLyz2-cre mice) resulted in severe disease and lethality despite significantly higher peak levels of IFNα than WT animals, suggesting that the lethal phenotype of Irf7-/- mice was attributed to the myeloid cell-specific loss of IRF7 and not to the loss of IFNα production. Both Irf7-/- and Irf7fl/flLyz2-cre mice had increased levels of monocytes infiltrating into the brain compared to WT, indicating a potential role for IRF7 in the trafficking and activation of myeloid cells. Therefore, while IFNα supplementation may contribute to reducing disease severity by restricting virus replication, disease was ultimately exacerbated by the increased infiltration of inflammatory myeloid cells in Irf7-/- mice.

Between mosquitoes and birds, West Nile virus (WNV) is a neurotropic flavivirus, an arthropod-borne pathogen involved in an enzootic cycle. Additionally, it can infect both people and horses, leading to severe illness. Since 1999, WNV has spread across North and South America, including Mexico and the Caribbean. It is endemic in several regions of Europe, Africa, the Middle East, and Asia. WNV affects the central nervous system (CNS), causing severe disease in a small percentage of infected individuals, especially in immunocompromised or elderly hosts. This re-emerging pathogen was identified during an outbreak in July 2025 in the Lazio region of Italy, rekindling interest in an area where the virus had not circulated for some time and raising several questions about the WNV vector and its spread. Gammadelta T (γδ T) lymphocytes are innate cells that can respond rapidly and non-specifically to viral infections and other pathogens, thereby linking innate and adaptive immunity. Several studies in mice and humans suggest they play distinct roles in controlling WNV infection by communicating with other immune cells, underscoring their antiviral role, which is essential for containing viral dissemination in the host. This review will discuss recent studies on the role of γδ T cells in viral pathogenesis and in protective immunity during WNV infection.

The Orthobunyavirus genus of arthropod-borne segmented RNA viruses comprises important pathogens including the human-infecting Oropouche virus and ruminant-infecting Schmallenberg virus (SBV). The prototypical Bunyamwera orthobunyavirus (BUNV) possesses envelope-embedded glycoprotein Gn-Gc tripodal spikes, of which the ectodomains mediate virus entry, while endodomains interact with nucleoprotein (NP) enwrapped genome segments driving virion assembly. Interestingly, BUNV Gc head/stalk domains are redundant for virus growth in mammalian cells, consistent with isolations of SBV from ruminants bearing head/stalk deletions. However, these domains appear strictly maintained in orthobunyavirus isolations from arthropods in nature. To investigate the molecular mechanism that underlines this discrepancy, we compared the multiplication characteristics of wildtype BUNV (BUNV-WT) with a Gc head/stalk deleted BUNV (BUNV-∆7). In mammalian cells BUNV-WT and BUNV-∆7 grew to equivalent titres, whereas in insect cells BUNV-∆7 titres were 1000-fold lower and strikingly produced no virions following blood meal infection of Aedes mosquitoes. To understand this insect-specific restriction in virion production, we showed the intracellular abundance of BUNV-WT and BUNV-∆7 Gc and NP components were equivalent, suggesting the deletion impacted post-translational stages of the infection cycle. To explore this, we investigated Gc and ∆7-Gc interactions during BUNV-WT and BUNV-∆7 infections of both insect and mammalian cells by co-immunoprecipitation and multiplex mass spectrometry, revealing ∆7-Gc exhibited markedly reduced NP interactions in insect cells, potentially indicating reduced segment interactions during assembly. We hypothesize that the Gc head/stalk performs an insect cell-specific role in segment recruitment during virion formation, and that maintenance in nature of full-length Gc is due to this essential role in the insect host.

Arthropod-borne orthobunyaviruses belonging to the Simbu serogroup can cause congenital and neurological disease in livestock. Across Australia, the National Arbovirus Monitoring Program (NAMP) conducts surveillance for veterinary-important arboviruses. Our study complements this broader surveillance framework by investigating the virus-specific transmission patterns of Simbu group viruses (SGVs) present in New South Wales (NSW). To describe the distribution of six SGVs: Akabane, Aino, Douglas, Peaton, Tinaroo, and a recently recognised Shamonda-like virus, we examined 24 years of serological data (2000-2023) from NSW sentinel cattle. The transmission of a Simbu serogroup virus was detected during every monitoring period (October-July), progressing from north to south along the NSW coastline. Inland transmission west of the Great Dividing Range (GDR) was intermittent (2012-2013, 2020, and 2022), when SGV distribution extended across the mountain range or progressed down the western slopes from Queensland. From 2014, repeated seasonal SGV transmission extended to the far south coast of NSW. Peaton virus was the most frequently detected and widely distributed virus. Since testing for the newly detected Shamonda-like virus started in 2019, this virus has been widely detected across coastal NSW and often in herds also infected with Douglas or Peaton viruses. Discrepancies between the ELISA and virus neutralisation test (VNT) results suggest that this virus could have been present in NSW as early as 2012. From 2017, Akabane virus has a sporadic distribution. The distribution for both Aino and Tinaroo viruses was sporadic (2005-2023). These findings highlight the importance of long-term, virus-specific surveillance in identifying emerging variants and detecting exotic incursions.

Chikungunya virus (CHIKV) is an arthropod-borne Alphavirus primarily transmitted by Aedes mosquitoes, causing sudden outbreaks with high morbidity and chronic polyarthritis. Following the US FDA approval of the first CHIKV vaccine in November 2023, concerns remain regarding vaccine efficacy due to the existence of at least three major CHIKV lineages. We conducted an in-silico genomic analysis of the CHIKV E2 glycoprotein to evaluate genetic diversity and evolutionary patterns relevant to vaccine and therapeutic antibody-binding effectiveness. The E2 gene exhibited substantial variation, reflecting high polymorphism and both intra- and inter-lineage differences. The variations detected may reduce antibody-antigen binding affinity, potentially compromising vaccine and therapeutic antibody efficacy. Our findings underscore the importance of incorporating pathogen genetic diversity into vaccine and therapeutic design. Long-term, pan-CHIKV vaccines could offer sustainable, cost-effective protection. Validation through in vitro and in vivo studies, alongside strengthened vector surveillance and control, is recommended to mitigate ongoing outbreaks.

Dengue is the most prevalent arthropod-borne viral disease, caused by infection with the dengue virus (DENV). Severe dengue is characterized by significant vasculopathy involving a proinflammatory and procoagulant state associated with increased vascular permeability. However, the host-virus interactions driving this process remain incompletely elucidated. Monocytes (Mø) are primary target cells during DENV infection and actively release extracellular vesicles, like microparticles (MPs), mediating intercellular communication, contributing to dengue pathogenesis. Here, we evaluated whether MPs released by DENV-infected monocytes represent a previously underappreciated mechanism contributing to dengue-associated vascular dysfunction. The vascular endothelium plays a determining role in the response to injury because it functions as a regulatory interface during hemostasis (coagulation-fibrinolysis-inflammation) and by preserving the endothelial barrier. We found that these vesicles transport viral proteins (E and NS1), exhibit a procoagulant profile that promotes thrombin generation, and enhance endothelial vascular cell (EVC) activation. DENV-infected THP-1 Mø MPs interaction induces a shift toward a procoagulant, proinflammatory, and proadherent phenotype, characterized by increased expression of PAR-1, TF, ICAM-1, and VCAM-1, reflecting the establishment of a sustained HMEC-1 EVC activation that compromises vascular barrier integrity. This leads to increased permeability, a hallmark of DENV-associated vasculopathy and a central event in the progression to severe dengue.

Bluetongue (BT) virus (BTV) is an arthropod-borne pathogen that causes substantial economic losses in ruminants globally. Yunnan Province, located in China's tropical and subtropical border region, faces a high risk of BTV circulation. This study monitored BTV vectors, genetically characterized circulating BTV strains, and assessed seroprevalence to inform early warning efforts. In 2025, 46,000 Culicoides midges were collected from three counties, identified, and grouped into 460 pools. Additionally, 5934 cattle serum samples from 17 border counties were tested using C-ELISA. Midge pools were screened by RT-qPCR for BTV nucleic acids and then inoculated into C6/ 36 cells for virus isolation. Whole-genome sequencing and phylogenetic analysis of VP2 and VP5 genes were performed on the isolates. C. oxystoma and C. trithecoides were the dominant midge species at all sites. RT-qPCR identified 11 BTV-positive midge pools, primarily involving C. oxystoma, C. imicola, C. tainanus, and C. jacobsoni. Four BTV isolates were identified as serotypes 1, 4, 5, and 16. Phylogenetic analysis of VP2 and VP5 showed all four strains likely belong to the Eastern topotype and are closely related to historical BTVs from China, Japan, India, and Australia. The overall BTV seroprevalence in cattle was 41.37% (95% confidence interval [CI], 40.12%-42.62%), with significantly higher rates in autumn (58.07%, 95% CI, 56.29%-59.85%) than in spring (24.87%, 95% CI, 23.32%-26.42%). Several BTV serotypes have been detected and isolated from diverse Culicoides in the border regions of Yunnan. Additionally, BTV seroprevalence has been observed in local cattle populations, indicating that this area may represent a significant BTV endemic hotspot. These findings underscore the need for ongoing vector surveillance and early warning systems to prevent BT outbreaks in susceptible livestock.

Chikungunya virus (CHIKV) is an arthropod-borne virus belonging to the genus Alphavirus; it has been increasingly linked to neurological complications. This study aimed to highlight the neurological manifestations of chikungunya virus infection. This retrospective case series was conducted at the Aga Khan University Hospital, Karachi, Pakistan. Adult patients (aged 18 years and above) with typical arboviral prodrome (fever, arthralgias, myalgias) who tested positive for chikungunya IgM antibodies in serum and demonstrated new-onset neurological symptoms were included in the study. The sample size consisted of 18 patients. Descriptive statistics were used to demonstrate demographics and the clinical, radiological, and electrodiagnostic details of participants. Patients with neuro-chikungunya were trichotomized based on the extent of neuroaxis involvement into those with central nervous system (CNS) involvement, those with CNS and peripheral nervous system (PNS) involvement, and those with isolated PNS involvement. This study found heterogenous nervous system involvement in chikungunya virus infection, including the brain, spinal cord, nerve roots, and peripheral nerves in variable combinations. The majority of patients in this cohort had CNS involvement (55%). Patients with widespread neuroaxis involvement tended to have a complicated hospital course leading to intensive care unit admission and even mortality. The widespread neurological involvement seen in this study potentially points towards the possibility that chikungunya virus may affect the entire neuroaxis. Studies focusing on long-term sequelae are needed to ascertain the prognosis of neuro-chikungunya. HINTERGRUND: Das Chikungunya-Virus (CHIKV) ist ein von Arthropoden übertragenes Virus aus dem Genus Alphavirus; es wird vermehrt mit neurologischen Komplikationen in Verbindung gebracht. Die vorliegende Studie fokussiert auf die neurologischen Manifestationen der Chikungunya-Virus-Infektion. Diese retrospektive Fallserie wurde am Aga Khan University Hospital, Karatschi, Pakistan, durchgeführt. Erwachsene Patienten (Mindestalter 18 Jahre) mit typischem arboviralem Prodrom (Fieber, Arthralgien, Myalgien), positivem Test auf Chikungunya-Immunglobulin-M(IgM)-Antikörper im Serum und neu aufgetretenen neurologischen Symptomen wurden in die Studie eingeschlossen. Die Stichprobe umfasste 18 Patienten. Deskriptive statistische Auswertungen wurden angewendet, um demografische Eckdaten sowie klinische, radiologische und elektrodiagnostische Eigenschaften der Teilnehmer darzustellen. Patienten mit Neuro-Chikungunya wurden auf Grundlage des Ausmaßes der Neuroachsenbeteiligung in drei Gruppen eingeteilt: mit Beteiligung des zentralen Nervensystems (ZNS), mit Beteiligung des ZNS und peripheren Nervensystems (PNS) oder mit isolierter PNS-Beteiligung. Die Analyse ergab eine heterogene Beteiligung des Nervensystems bei Chikungunya-Virus-Infektion, einschließlich Gehirn, Rückenmark, Nervenwurzeln und peripherer Nerven in verschiedenen Kombinationen. Die Mehrheit der Patienten dieser Kohorte zeigte eine ZNS-Beteiligung (55%). Bei Patienten mit ausgedehnter Beteiligung der Neuroachse fand sich tendenziell eher ein komplizierter Verlauf im Krankenhaus, der zur Aufnahme auf die Intensivstation und sogar zu Todesfällen führte. Die in der vorliegenden Arbeit gezeigte ausgedehnte neurologische Beteiligung deutet potenziell darauf hin, dass das Chikungunya-Virus die gesamte Neuroachse betreffen kann. In zukünftigen Studien muss der Fokus auf Langzeitfolgen gelegt werden, um die Prognose der Neuro-Chikungunya zu bestimmen.

The arthropod-borne chikungunya virus poses a re-emerging global health threat, causing millions of cases worldwide. Neurological complications induced by chikungunya virus are being increasingly reported in vulnerable populations, including infants and young children. However, the mechanisms by which chikungunya virus invades the central nervous system and drives prolonged neurological dysfunction remain poorly defined. Studying neurological chikungunya virus infection has been limited by the lack of an immunocompetent, neurodevelopmentally appropriate small-animal model that reliably develops central nervous system infection and neurological disease by infection routes analogous to natural transmission. Following a screen of ten Collaborative Cross mouse strains, we identified four-to-six-week-old CC041 mice as an immunocompetent, neurodevelopmentally appropriate model that consistently exhibits chikungunya virus neuroinvasion and clinical signs consistent with neurological disease following peripheral inoculation. Central nervous system infection in CC041 mice was dependent on the chikungunya viral strain used, despite comparable viral replication at the inoculation site, and occurred at physiologically relevant inoculation doses without enhancement at higher doses. Comparative analyses with neuroinvasion-resistant C57BL/6J mice demonstrated that susceptibility to neuroinvasion in CC041 mice was associated with enhanced dissemination beyond the site of inoculation, prolonged serum viral load, and lower peripheral type I interferon levels early in infection. In vivo imaging using a reporter chikungunya virus confirmed rapid viral spread and early brain localization in CC041 mice, in contrast to the restricted peripheral infection observed in C57BL/6J mice. Examination of viral antigen expression by immunohistochemistry revealed regionally variable viral localization in the brain, with central nervous system infection occurring independently of virus-induced blood-brain barrier disruption or experimental macrophage depletion. Furthermore, CC041 mice developed clinical signs consistent with neurological disease that persisted beyond the period when infectious virus was detected in the brain. Together, these findings establish CC041 mice as a tractable, immunocompetent model for studying chikungunya virus-associated neurological disease following peripheral infection.

Arthropod-borne viruses (arboviruses) cause a wide range of acute and chronic diseases and represent a growing global health burden. Although some vaccines exist, antiviral therapies remain limited. Identifying host restriction factors may enable new therapeutic strategies. We previously showed that bacterial effector proteins can serve as tools to uncover innate immune defenses. Here, we used a bacterial effector screen in bat cells to identify host factors restricting the arboviruses Sindbis virus (SINV) and O'nyong'nyong virus (ONNV). Several effectors enhanced infection by both viruses. However, we found the Shigella flexneri-encoded E3 ubiquitin ligase IpaH2 to selectively promote SINV replication. IpaH2 enhanced SINV infection across multiple mammalian cell lines, suggesting that it targets a conserved antiviral mechanism, and this effect required IpaH2 E3 ubiquitin ligase activity. Screening of putative IpaH2 host targets identified via ubiquitin-activated interaction trap (UBAIT) assays revealed the host factors ATP-binding cassette sub-family F member 3 (ABCF3) and Plakophilin-2 (PKP2) to play roles in restricting SINV infection. While ABCF3 broadly restricted multiple viruses, PKP2 specifically limited SINV replication, indicating a virus-specific restriction factor. These findings demonstrate that bacterial effector screening can identify both broadly acting and virus-specific host defenses, providing insight into antiviral mechanisms and potential therapeutic targets.

Orbivirus palyamense belongs to the group of arthropod-borne viruses often referred to as Palyam serogroup viruses (PALV), which include Chuzan virus (CHUV), D'Aguilar virus (DAGV), and Bunyip Creek virus (BCV). Several members of this serogroup have been implicated in congenital abnormalities with gross lesions in brain tissues. CHUV causes congenital abnormalities in cattle, whereas other serotypes show variable pathogenicity, with DAGV being sporadically associated with congenital abnormalities and BCV showing no clear disease causality. To elucidate the mechanisms underlying these clinical differences at the cellular level, we established a novel immortalized bovine cerebral-derived cell line (IKBC), as an in vitro model. An RNA sequencing analysis revealed that IKBC cells exhibited neuroepithelial-like properties with the partial expression of immature neuron markers and some mesenchymal-like features consistent with an epithelial-mesenchymal transition-like state. Infection assays demonstrated that CHUV exerted stronger cytopathic effects and tended to replicate more efficiently in IKBC cells than DAGV and BCV. The expression of type I interferon and more downstream interferon-stimulated genes (ISGs) in IKBC cells was more strongly and weakly induced, respectively, by CHUV infection than by DAGV or BCV infection. To assess strain-specific differences, comparisons among CHUV strains revealed that those isolated during large-scale outbreaks more weakly induced the expression of ISGs than strains from sporadic occurrences, suggesting that viral immunosuppressive properties contributed to the magnitude of the epidemics. Overall, IKBC cells provide unique models for investigating the characteristics and pathogenesis of PALV in cattle.

Scorpion venom is a complex mixture containing toxic peptides, free amino acids, enzymes, nucleotides, lipids, amines, mucoproteins and other bioactive components. It has been reported to exhibit a range of medicinal properties, including anticancer, antithrombotic, anticoagulant, fibrinolytic, analgesic, antitumor and antiepileptic effects. This study aimed to evaluate the anticancer effects of crude venom from Odontobuthus doriae on the Michigan Cancer Foundation-7 (MCf-7) breast cancer cell line. 2×104 MCF-7 cancer cells were cultured in T25 flasks containing Dulbecco's Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and 1% penicillin-streptomycin. After overnight incubation, the culture medium was replaced with different concentrations of crude venom (0.2, 0.48, 0.97, 1.95, 3.9, 7.81, 15.62, 31.25, 62.5, 125, 250, 500 μg/mL). The cytotoxic effects were assessed using the MTT reduction assay at 24, 48 and 72 hours post-treatment, performed in triplicate. Absorbance was measured at 570 nm using an ELISA reader. A concentration-dependent decrease in cell viability was observed. A statistically significant difference in cytotoxicity was observed between the 24 hour and the 48/72-hour treatments, while no significant difference was noted between the 48 and 72 hour time points. The IC50 values were calculated to be 4.775 μg/mL (24 h), 31.87 μg/mL (48 h), and 3.543 μg/mL (72 h). The crude venom of O. doriae exhibits significant cytotoxic effects against MCF-7 breast cancer cells in a dose- and time-dependent manner, suggesting its potential as a natural anticancer agent.

Biogeography can illuminate spatial patterns of intraspecific morphological variation along environmental gradients. We evaluated whether body size in the common vampire bat (Desmodus rotundus) varies with climate and elevation across Colombia using 1076 museum and field specimens (1921-2023). Field specimens originated from diverse environmental conditions, including sites with mean annual temperatures ranging from 8.94 to 28.94 °C, annual precipitations from 515 to 7132 mm, and elevations from 4.6 to 3476 m a.s.l. Forearm length, a proxy for body size, was analysed with regression models, including Colombian department as a random effect. Linear models showed that forearm length decreased with mean annual temperature (females: R 2 = .023, β = -.143, P = .006; males: R 2 = .044, β = -.173, P = 1.03 × 10-5) and increased with elevation (females: R 2 = .038, β = .001, P = 3.66 × 10-4; males: R 2 = .039, β = .001, P = 3.35 × 10-5), with an overall decrease of .19 mm per 1°C across all individuals. In contrast, linear mixed-effects models found no significant effects of temperature, elevation, precipitation, or latitude. These contrasting results suggest data limitations and that patterns detected by simpler models disappear when accounting for the spatial structure of the sampling. We argue that temperature is not a robust predictor of body size in D. rotundus. Our findings advance the biogeography of D. rotundus and provide a foundation for the uncertainty of climate change effects on bat morphology.