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Current knowledge on immune cell interactions with Borrelia burgdorferi (Bb) derives mostly from studies done in vitro and ex vivo, which cannot assess host immunity to natural tick-delivered Bb within the complex architecture of host tissues. We report the first in vivo study on local and systemic immune responses to Bb during tick feeding on a surrogate reservoir host, in comparison with uninfected-tick and subcutaneously delivered Bb. We show that uninfected-tick and tick-transmitted Bb engaged mixed type-1/type-2/type-17 immune responses in the presence of anti-inflammatory IL-10, in contrast to a type-1 response induced by subcutaneously delivered Bb. Analyses of immune responses to tick-transmitted Bb in a reservoir host can enlighten immunity mechanisms that mediate persistence of Bb.

Vector‐borne diseases (VBD) pose a major concern for public health worldwide. Identifying putative vectors and their potential contribution to transmission is a crucial step in understanding vector‐borne disease hazard. However, existing metrics are limited in their utility to inform transmission hazard in zoonotic multi‐vector, multi‐host VBD systems. We present the Vector Potential Index (VPI), a novel metric for evaluating and comparing the potential of blood‐feeding arthropod vectors to contribute to zoonotic VBD transmission. Taking a meta‐analysis approach, the VPI combines vector competence and host use data obtained from scientific literature to assign relative and absolute VPI ranks across species and transmission cycles. Using West Nile virus (WNV) in the eastern United States as a model system, our results demonstrate the ability of VPI to provide a representative assessment of vector species' potential contribution to transmission hazard in the epizootic and enzootic transmission cycles. Most species had low vector potential, and although Aedes species were the most competent WNV vectors in the laboratory, only Culex species were assigned higher VPI ranks. Additionally, the VPI suggests that the contribution of Culex salinarius to WNV transmission in the U.S. may be greater than previously assumed based on assessments of individual parameters. Relative and absolute VPI ranks assigned to species aligned with recent work reviewing their role as vectors in the transmission cycles, indicating that by jointly considering vector competence and host use, the VPI effectively quantifies the species‐specific potential to contribute to WNV transmission hazard in the natural environment, using existing data. We propose the objective and reproducible VPI as a powerful yet simple tool for scientists and public health practitioners, where this trait‐based approach has considerable potential to provide new insights into disease systems and enhance VBD surveillance and intervention strategies. The Vector Potential Index (VPI) is a novel metric for evaluating and comparing the potential of blood‐feeding arthropod vectors to contribute to zoonotic vector‐borne disease transmission. Taking a meta‐analysis approach, the VPI combines vector competence and host use data obtained from scientific literature to assign relative and absolute VPI ranks across species and transmission cycles. We propose the objective and reproducible VPI as a powerful yet simple tool for scientists and public health practitioners, where it has considerable potential to provide new insights into disease systems and enhance vector‐borne disease surveillance and intervention strategies.

Rickettsial pathogens are strictly dependent on the cellular biology of their hosts for survival and replication. Predominantly transmitted by blood-feeding arthropods, these vector-borne pathogens are forced to adapt between the disparate environments of their mammalian host and arthropod vector. To achieve this, the Rickettsial bacteria undergo extensive transcriptional reprogramming, with over 41% of its genes differentially transcribed between mammals and ticks. How the bacterium orchestrates this dramatic transcriptional reprogramming is not understood. The gene encodes a Helix-Turn-Helix DNA-binding protein that is exclusively expressed during tick infection. Herein, we show that is essential for survival in ticks and regulates the transcription of other genes necessary to adapt to the arthropod vector. We demonstrate that Tr1 is a DNA-binding protein that recognizes promoters of tick-specific genes in , including secreted effector , alternate components of the type IV secretion system (T4SS), and membrane proteins. Our findings demonstrate that Tr1 is a master regulator of genes critical for adaptation to the tick.IMPORTANCETick-borne pathogens are a persistent threat to human and animal health worldwide. These pathogens must be capable of surviving in both the arthropod vector and the mammalian hosts to successfully complete their lifecycle. To achieve this, these pathogens reciprocally regulate genes that are specific for either mammalian or tick infection. The mechanism orchestrating this switch remains undefined. In this study, we identify a transcriptional regulator controlling how the tick-borne agent for granulocytic anaplasmosis, , adapts to life in the tick. Disabling this transcriptional switch and the genes it controls renders the bacteria unable to survive in the arthropod vector. Understanding how this central regulator and the genes under its control impact tick infection could lead to interventions that disrupt the cycle of transmission, thereby preventing disease.

Bacteria in the genus Borrelia are primarily spread by ticks and cause either Lyme borreliosis or relapsing fever. Substantial work has demonstrated the degree to which rodents and songbirds can contribute to the enzootic cycles and dispersal of these human diseases, but comparatively less attention has been paid to the role of wild bats, particularly in temperate regions. We here report human-relevant findings from a two-year, seasonal survey of migratory Mexican free-tailed bats ( Tadarida brasiliensis ) in Oklahoma, USA. We tested nearly 400 bats and identified Borrelia puertoricensis , a relapsing fever species that could infect humans. Importantly, this represents the first detection of Borrelia puertoricensis in bats and only the second detection in wild vertebrate hosts, expanding the known host range of this emerging tick-borne pathogen. Given the known migratory routes of Mexican free-tailed bats, our results have implications for the role that bats may play in tick-borne pathogen dispersal in North America.

Vector-borne and zoonotic diseases (VBZDs) remain a critical global health challenge, disproportionately affecting low- and middle-income countries and driving significant morbidity, mortality, and economic loss. This review synthesizes emerging evidence on nano-enabled smart drug delivery system (SDDS) within the One Health framework, emphasizing their role in advancing targeted therapy, controlled release, and theranostics for VBZD management. Nano-enabled platforms such as liposomes, polymeric nanoparticles, nanogels, metal–organic frameworks, and biomimetic carriers are designed for stimuli-responsive and site-specific delivery, enhancing therapeutic precision, lowering dosing frequency, and reducing the risk of drug resistance. Controlled-release formulations of agents such as artemisinin derivatives, amphotericin B, and ivermectin have demonstrated superior efficacy in the treatment of malaria and leishmaniasis, and in vector control applications. Targeted delivery strategies extend beyond human therapies to address viral reservoirs, infected macrophages, and arthropod vectors, highlighting the cross-species applications central to One Health. Theranostic innovations combine imaging and therapy to enable early disease detection, real-time monitoring, and the design of adaptive treatment strategies. Applications span human, animal, and environmental domains, from nanovaccines and veterinary antimicrobials to nanoparticle-based larvicides and biosensors for vector surveillance. Future directions underscore the integration of AI-driven nanodesign, scalable and eco-friendly synthesis, and harmonized regulatory frameworks to increase accessibility in resource-limited settings. Although clinical trials are limited, ongoing translational efforts indicate the transformative potential of nanomedicine in VBZD control. Ultimately, integrating nano-enabled SDDS into a One Health framework provides a sustainable and collaborative approach to reduce the global burden of zoonotic and vector-borne diseases.

The lytic cycle of Toxoplasma gondii is critical for parasite dissemination and disease progression in the host. Calcium signaling plays a crucial role in driving these processes; however, the molecules that control calcium storage and release remain poorly understood. The endoplasmic reticulum, likely the largest calcium reservoir in T. gondii , has been understudied in the context of calcium signaling. Here, we uncover a direct link between ER redox regulation and calcium homeostasis, showing that ER redox activity can influence calcium signaling events that govern microneme protein maturation and secretion, parasite invasion, and replication. Our findings indicate that redox-dependent calcium regulation in the ER contributes to control of the parasite lytic cycle and reveals a previously unrecognized mechanism that may influence parasite virulence.

Toxoplasmosis is a disease of worldwide distribution, causing high morbidity and mortality in humans, as well as heavily impacting animal health and the economy. Toxoplasma gondii, the causative agent, is an intracellular parasite with a complex life cycle whose completion entails asexual, pre-sexual, and sexual stage conversions. Pre-sexual and sexual differentiation take place only within the intestinal epithelium of felines. Recently, several transcriptional factors and epigenetic components crucial to trigger parasite stage transitions within the cat have been identified, allowing, through precise genetic manipulation, obtaining pre-sexual stages known as merozoites in vitro. Through conditional depletion of two pre-sexual stage-specific gene silencing transcription factors, AP2XII-1 and AP2XII-2, we have characterized the interplay between cell division and the sequence of events leading up to differentiation of tachyzoites into merozoites. We explored genome duplication, assembly of daughter cells, karyokinesis, and cytokinesis, characterizing the differential cell division modes and kinetics undergone by critical structures along the differentiation axis. Building onto the pre-existing body of knowledge, primarily describing the underpinnings of these forms of division by transmission electron microscopy, our work contributes previously unexplored temporal and spatial resolution to the transitions between endodyogeny and endopolygeny, providing a conceptual framework for understanding and exploring T. gondii’s route of sexual differentiation.IMPORTANCESexual development in Toxoplasma gondii is essential for transmission, but remains poorly understood, largely because pre-sexual stages are restricted to the feline intestine and have only recently become experimentally accessible. Here, we leverage an in vitro differentiation system to resolve how parasites transition toward merozoite formation at the cellular level. By combining expansion microscopy, stage-specific markers, and quantitative analyses, we define the temporal sequence of nuclear division and daughter cell assembly during merogony, addressing longstanding ambiguity regarding division modes in these stages. Our findings reveal that parasites can adopt alternative division strategies emerging from a polyploid intermediate, highlighting an unexpected degree of flexibility in how cell division is executed during differentiation. Beyond refining this developmental framework, this work establishes a foundation for future mechanistic studies of pre-sexual biology and provides broader insight into the diversity of eukaryotic cell division strategies.

Mosquito-borne flaviviruses replicate in physiologically and biochemically distinct host environments in humans and mosquitoes, providing a unique window into conserved and host-specific mechanisms shaping viral infection efficiencies and outcomes. This review focuses specifically on intracellular factors, including proteins, metabolites, innate immune effectors, and stress sensors in human and mosquito cells that collectively regulate the flaviviral life cycle and host cell survival, with specific emphasis on dengue virus. We discuss both conserved dependencies and species-specific differences in receptor usage, membrane remodeling, RNA translation, and replication strategies that influence viral dynamics across hosts. We further highlight how host metabolism, innate immune sensing, and stress response pathways drive divergent outcomes in virus-infected cells. In mammalian cells, rapid viral replication activates interferon-mediated antiviral responses that limit viral infection, but also lead to cytopathic effects and apoptosis. In contrast, mosquito cells support persistent, non-cytopathic infection mediated by RNA interference-dependent control of viral replication, coupled with antioxidant and anti-apoptotic defenses that maintain cellular homeostasis. This comparative perspective integrates insights from mammalian and mosquito systems to illustrate how host environments shape flaviviral infection, host susceptibility, and infection outcomes. Identifying these intracellular determinants of infection and persistence will be critical for defining host susceptibility, understanding barriers to cross-species transmission, and predicting viral emergence potential.

Background The long-term impact of COVID-19-associated public health interventions on zoonotic and vector-borne infectious diseases (ZVBs) remains uncertain. This study sought to examine the changes in ZVBs in China during the COVID-19 pandemic and predict their future trends. Methods Monthly incidents of seven ZVBs (Hemorrhagic fever with renal syndrome [HFRS], Rabies, Dengue fever [DF], Human brucellosis [HB], Leptospirosis, Malaria, and Schistosomiasis) were gathered from January 2004 to July 2023. An autoregressive fractionally integrated moving average (ARFIMA) by incorporating the COVID-19-associated public health intervention variables was developed to evaluate the long-term effectiveness of interventions and forecast ZVBs epidemics from August 2023 to December 2025. Results Over the study period, there were 1,599,647 ZVBs incidents. HFRS and rabies exhibited declining trends, HB showed an upward trajectory, while the others remained relatively stable. The ARFIMA, incorporating a pulse pattern, estimated the average monthly number of changes of − 83 (95% confidence interval [CI] − 353–189) cases, − 3 (95% CI − 33–29) cases, − 468 (95% CI − 1531–597) cases, 2191 (95% CI 1056–3326) cases, 7 (95% CI − 24–38) cases, − 84 (95% CI – 222–55) cases, and − 214 (95% CI − 1036–608) cases for HFRS, rabies, DF, HB, leptospirosis, malaria, and schistosomiasis, respectively, although these changes were not statistically significant besides HB. ARFIMA predicted a decrease in HB cases between August 2023 and December 2025, while indicating a relative plateau for the others. Conclusions China's dynamic zero COVID-19 strategy may have exerted a lasting influence on HFRS, rabies, DF, malaria, and schistosomiasis, beyond immediate consequences, but not affect HB and leptospirosis. ARFIMA emerges as a potent tool for intervention analysis, providing valuable insights into the sustained effectiveness of interventions. Consequently, the application of ARFIMA contributes to informed decision-making, the design of effective interventions, and advancements across various fields.

Effective control of tick-borne disease begins by first understanding how ticks acquire, harbor, and transmit pathogens. Over their lifetime, ticks encounter many sources of oxidative stress-inducing stimuli. Here, we explore the factors contributing to oxidative stress in ticks-including blood digestion, pesticide exposure, and pathogen infection-and then discuss how ticks counter this stress by employing antioxidant defenses. We highlight how non-tick-borne pathogens manipulate the host antioxidant response for survival and speculate that tick-borne pathogens may be acting similarly in the arthropod. We conclude by conjecturing that the robust antioxidant defenses that ticks have evolved to withstand the stress associated with hematophagy may also be inadvertently supporting the pathogens they carry.