Rodent-associated viruses are important zoonotic agents of increasing relevance to public and veterinary health. Muroid rodents occupy diverse natural and human-modified environments, facilitating interactions with humans, livestock and wildlife. However, knowledge of rodent-associated viral diversity and the ecological processes influencing viral maintenance and transmission remains fragmented. This review synthesizes published literature on viral diversity, host-virus associations, research trends, and ecological drivers of viral occurrence in Asian muroid rodents. PubMed and Scopus were systematically searched using terms related to rodents, viruses, and Asian regions. Extracted data included publication characteristics, diagnostic methods, host and virus taxonomy, geography, and ecological metadata. Descriptive analyses, geospatial mapping, and network approaches were applied to identify patterns and knowledge gaps. Of 1,049 records retrieved, 165 studies published between 1968-2025 from 30 Asian countries met the inclusion criteria. These studies documented 106 viral taxa representing 74 genera and 35 families. Research activity increased markedly after 2000 alongside advances in molecular diagnostics and metagenomic sequencing. Studies were concentrated in East and mainland Southeast Asia. Orthohantavirus spp. were the most studied viral group, whereas many other viruses remained poorly characterized. Network analyses identified core murine genera, particularly Rattus, Apodemus, Niviventer, Bandicota and Mus, sharing extensive viral associations. Host age, sex, population density, habitat disturbance, climate, and biodiversity were commonly linked with viral prevalence and dynamics. Despite substantial progress, gaps remain in ecological integration, longitudinal surveillance, and comparative study design. Future research should prioritize standardized, ecologically informed surveillance within an integrated One Health framework to improve zoonotic risk assessment and prevention.

Climate change and the increasing frequency of extreme heat events have heightened the importance of health issues during the summer season. This season is also associated with greater population mobility, outdoor recreational activities, and exposure to biological and environmental risks, all of which require coordinated responses from health systems. Within this context, the Ministry of Health of Chile implemented the summer seasonal illness and emergency preparedness plan 2024-2025, with the goal of strengthening surveillance, intersectoral coordination, and risk communication in response to priority threats to population health.This article describes the design, implementation, and key results of this first national initiative to prepare for diseases occurring during the summer season. The strategy was based on a multilevel governance model that liaised between the central, regional, and local levels of the health system through national coordination meetings, integrated surveillance, strengthening of technical capacities, and public communications. During the season covered by the plan, detection of Aedes aegypti remained confined to areas where it was previously known to occur; 395 outbreaks of foodborne illnesses affecting 2618 people were investigated; 8 cases of hantavirus were reported, with no deaths; and environmental risks and emergencies were monitored, including 4330 forest fires, none of which affected health facilities.This experience demonstrates the feasibility of implementing integrated disease preparedness strategies during the summer season and provides lessons for their consolidation as public policy, including the formalization of coordination mechanisms, the systematic assessment of implementation, and the incorporation of new hazards, such as drowning and injuries associated with recreational water activities.

Emerging respiratory infectious diseases increasingly arise at the human-animal-environment interface and challenge clinicians with rapidly evolving diagnostic, therapeutic, and infection-control decisions. This narrative review summarizes clinically relevant viral and bacterial pathogens that may present as severe respiratory disease, but are easily mistaken for common community-acquired infections during early illness. We focus on zoonotic influenza A viruses, including contemporary H5N1, Middle East respiratory syndrome coronavirus (MERS-CoV), hantaviruses, Nipah virus, and inhalational bacterial threats such as anthrax, pneumonic plague, tularemia, and melioidosis. These infections may progress from non-specific symptoms to severe pneumonia, acute respiratory distress syndrome, shock, neurological complications, disseminated infection, or death. Timely recognition depends on careful assessment of travel, occupational and recreational exposures, animal contact, outbreak signals, and pathogen-specific syndromic clues. Multiplex molecular diagnostics can support early triage and exclusion of common pathogens, but targeted PCR, culture, serology, sequencing, and reference laboratory confirmation remain essential. Management requires prompt supportive care, appropriate isolation, public health notification, and pathogen-directed antimicrobial, antiviral, antitoxin, or prophylactic strategies where available. By integrating clinical presentation, diagnostics, treatment, vaccines, and One Health considerations, this review aims to translate knowledge on emerging infections into practical bedside preparedness.

This article analyzes the cluster of Andes virus infections that occurred aboard the expedition vessel MV Hondius during a transatlantic crossing. Drawing on publicly available information released by the World Health Organization, the European Centre for Disease Prevention and Control, and the US Centers for Disease Control and Prevention, it examines the key characteristics of this event: probable exposure in a natural reservoir area in South America before embarkation, limited human-to-human transmission in a closed maritime environment, difficulties in early case recognition, and the complexity of international contact tracing. The analysis shows that the vessel itself was not the source of the virus, but rather a setting in which public health risks were amplified due to prolonged cohabitation, limited onboard medical resources, and the cross-border mobility of passengers. Finally, the article highlights the importance of stratified contact management, timely reporting, effective international cooperation, and clear risk communication to avoid both underestimation of the risk and unnecessary public panic.

Hantavirus fevers (HF) are caused by pathogenic orthohantaviruses and are classified into two clinical forms: hemorrhagic fever with renal syndrome (HFRS), reported in Eurasia, and hantavirus pulmonary syndrome (HPS), reported in the Americas. HF are characterised by an acute course with predominant involvement of internal organs: HFRS is mainly associated with kidney damage, while HPS is characterised by severe lung injury. Both diseases may also affect the central nervous and endocrine systems. In addition, hantavirus fevers are marked by severe complications during the acute phase and a prolonged recovery period. Currently, there is neither a WHO-approved vaccine nor any effective etiotropic anti-hantavirus therapy. The development of antiviral treatment strategies focuses on preventing orthohantavirus entry into cells or suppressing their intracellular replication. One of the main directions in the search for effective anti-hantavirus therapy is the low-molecular-weight compounds development and testing, many of which have demonstrated pronounced antiviral activity against orthohantaviruses through direct or indirect effects on viral RNA polymerase function. The review shows that new antiviral nucleoside compounds development and study has promising potential, as well as their combined use for effective etiotropic, pathogenetic and symptomatic treatment of hantavirus fevers.

Hantavirus cardiopulmonary syndrome is a potentially fatal respiratory zoonotic infection caused by New World hantaviruses, and it is acquired mostly via inhaling aerosolized excreta from infected rodents. Over the past 30 years, HCPS has expanded beyond its initial foci, and recent events suggest a potential for spread beyond traditionally endemic regions. The disease rapidly progresses from a vague prodrome to acute cardiopulmonary failure with a high fatality rate despite optimum supportive treatment. Pathophysiology involves endothelial failure, increased vascular permeability, acute thrombocytopenia and excessive immunological responses resulting in capillary leak syndrome and cardiogenic shock. It is still hard to clinically suspect early since the prodromal symptoms are vague and mirror common viral infections and respiratory disorders. Diagnostic confirmation needs serological testing or genetic approaches, which are typically unavailable in resource-limited endemic situations, leading to considerable diagnostic delays. Management is generally supportive, with early ICU admission, judicious hydration management, mechanical breathing and cardiopulmonary support including extracorporeal membrane oxygenation in refractory patients. The recent multi-country Andes virus epidemic on a cruise ship in May 2026 highlights the potential for fast worldwide transmission of HCPS outside of usual endemic settings. This review summarizes the current information on the epidemiology, pathophysiology, clinical presentation, diagnostic techniques, and treatment options for HCPS. We also highlight the pressing need for improved global surveillance, rapid point-of-care diagnostics, global awareness among health care workers, and ongoing development of preventive vaccines and effective antiviral therapies to address this significant public health threat.

The Anthropocene era has been characterized by a higher risk of zoonotic viral outbreaks, which often result from a combination of factors, such as climate change, biodiversity loss, land-use patterns, and increased opportunities for human-animal interactions. The current perspective provides an integrated synthesis of how climate change-driven alterations in rodent ecology impact the molecular evolution, transmission dynamics, and emergence of hantaviruses, with an emphasis on the underlying virological mechanisms and their implications for One Health preparedness. Hantaviruses have undergone extensive diversification throughout their evolution and host adaptation and can infect rodents, bats, reptiles, and fish. Rodents serve as the principal natural reservoirs for hantaviruses, with many viral species exhibiting long-term evolutionary associations with specific rodent host species. Climate change has been recognized as one of the key determinants for the emergence of hantavirus outbreaks in different parts of the world. Climate-related factors may facilitate viral amplification through multiple mechanisms, including their impact on evolution, mutation, and reassortment. To conclude, climate change has shaped the ecology, transmission dynamics, and molecular evolution of hantaviruses by altering rodent behavior, their habitats, and the environmental persistence of viral particles. Climate-induced ecological disruption has created opportunities for viral amplification within reservoir hosts and augmented the risk of zoonotic spillover into humans. These insights provide a conceptual framework for anticipating future outbreaks in the context of climate change and support the integration of ecological, virological, and public health surveillance systems. There is an urgent need to ensure that virological preparedness strategies evolve in accordance with changing environmental conditions by strengthening genomic surveillance and integrated One Health frameworks.

The Andes Virus (ANDV) outbreak reported on May 2, 2026, aboard a luxury vessel departing from Ushuaia, Patagonia, Argentina, was caused by an Orthohantavirus unique in its person-to-person transmissibility in contrast to zoonotic transmission characteristic of better-known hantaviruses. Containment required coordinated international management because passengers and crew embarked and disembarked at several international ports-of-call prior to outbreak recognition, resulting in cross-border transmission potential. Among those who disembarked, several traveled on flights to various destinations. Cases subsequently manifested in multiple countries, including Tristan da Cunha, Spain, France, Switzerland, South Africa, Canada, and The Netherlands. Upon notification, international health authorities implemented containment measures, such as contact tracing, quarantine, and isolation. Uniquely, ANDV poses distinctive risks due to its immediately prodromal presymptomatic transmission potential, initial non-specific flu-like symptoms, prolonged incubation period, conceivable long-term neurologic and endocrinologic sequalae, high case fatality rates (CFRs), and possibility of international dissemination. This report describes the successful management of a multi-national outbreak associated with cruise-ship travel, a setting with unique challenges. It also examines implications and challenges for prehospital, health care facility, and public health systems for future ANDV outbreaks. The event was characterized by delayed recognition, international spread, and complex coordination across multiple jurisdictions and sectors, including medical and public health authorities, policy- and decision-makers, crisis and emergency risk-communication experts, media, logistics, transportation, and security. Rapid implementation of public health measures coupled with clinician implementation of the Identify-Isolate-Inform (3I) model, a clinical framework to detect and prevent the spread of infectious disease, at the prehospital and health care facility levels are critical actions that can contain future ANDV outbreaks.

Mammalian hantaviruses are RNA viruses that cause hantavirus cardiopulmonary syndrome in the Americas and hemorrhagic fever with renal syndrome in Eurasia. The cellular entry mechanisms of most hantaviruses remain poorly defined. To examine entry by phylogenetically distinct hantaviruses identified across Africa, Eurasia, and the Americas, we generated replication-competent recombinant vesicular stomatitis viruses (rVSVs) bearing Gn/Gc proteins from Necoclí, Sangassou, Thottapalayam, Kenkeme, Nova, Oxbow, and Tula viruses. All these Gn/Gc proteins except Kenkeme supported infection of primary human endothelial cells, indicating that endothelial cell entry is permissive for a broader range of hantaviruses than previously appreciated. Except for rVSV-Kenkeme, these rVSVs did not acquire additional mutations beyond pre-engineered rescue-enhancing changes during rescue and passaging. Genetic studies in human cells lacking protocadherin-1 (PCDH1) showed that Necoclí, Tula, and Nova viruses use PCDH1 for efficient infection, although the Nova phenotype was weaker. These three Gn/Gc proteins bound soluble PCDH1 with different apparent avidities, and infection by the corresponding rVSVs was inhibited by soluble PCDH1; Necoclí and Tula, but not Nova, were also blocked by a PCDH1-targeting monoclonal antibody. Authentic Tula virus infection was similarly reduced in PCDH1 knockout endothelial cells. Finally, the broadly reactive anti-Gn/Gc human monoclonal antibody ADI-42898 efficiently neutralized Necoclí, Nova, Sangassou, and Kenkeme rVSVs, but showed weak or undetectable activity against Oxbow, Tula, and Thottapalayam rVSVs. Together, these findings expand the range of hantavirus glycoproteins capable of mediating infection of human endothelial cells, broaden the phylogenetic scope of PCDH1-dependent entry, and identify receptor-targeted and viral glycoprotein-targeted strategies with differential activity.IMPORTANCEMany newly discovered hantaviruses are known only from sequence data, leaving their ability to enter human cells and their receptor usage unresolved. Using a BSL2-compatible recombinant vesicular stomatitis virus (rVSV) system, we show that glycoproteins from several divergent hantaviruses can mediate infection of primary human endothelial cells, indicating that endothelial cell entry is permissive for a broader range of hantaviruses than previously appreciated. We also show that protocadherin-1 (PCDH1), previously linked mainly to New World hantaviruses, is used by Necoclí, Tula, and Nova viruses but not universally across the panel, revealing broader but heterogeneous receptor usage. An authentic Tula virus experiment supports this conclusion beyond the surrogate system. Finally, a broadly reactive anti-Gn/Gc antibody neutralizes several, but not all, of these viruses, highlighting both the promise and the limits of broadly protective countermeasures and the utility of these rVSVs for evaluating entry inhibitors.

Hantavirus pulmonary syndrome (HPS) carries a case fatality rate of 35%-40% and has no approved pharmacologic treatment. Its pathophysiology is rooted in the plasma compartment: cytokines, viral antigens, immune complexes, and platelet-binding glycoproteins circulate as drivers of immunopathologic endothelial injury, noncardiogenic pulmonary edema, and cardiogenic depression. Therapeutic plasma exchange (TPE) achieves bulk clearance of plasma-borne mediators and is established by the American Society for Apheresis (ASFA) for numerous indications that share an analogous mechanistic rationale. This commentary argues that the immunopathology of HPS maps onto the therapeutic targets of TPE, that any intervention would need to be timed to the early cardiopulmonary phase, and that the coagulopathic dimension of the disease provides a mechanistic argument for incorporating plasma into the replacement strategy. We deliberately situate this rationale against the uneven record of TPE in diseases of comparable pathophysiology, in which the intervention has been effective in some settings and without demonstrable benefit in others. The recent Andes virus outbreak aboard the cruise ship MV Hondius, which produced a multinational cluster of severe cardiopulmonary cases, prompted us, as transfusion medicine and apheresis physicians, to articulate this hypothesis. We emphasize that these arguments are mechanistic and hypothesis-generating rather than evidence-based: no clinical data yet support TPE in HPS, and systematic outcome reporting, ideally through a multicenter case series, would be required before any conclusion about efficacy could be drawn.

Andes hantavirus (ANDV) is a rodent-borne orthohantavirus associated with hantavirus cardiopulmonary syndrome in southern South America. Its maintenance and spillover risk depend on the ecology of its principal reservoir, Oligoryzomys longicaudatus, and on environmental changes that alter habitat availability, host abundance, and human-rodent interfaces. We developed a mechanistic eco-epidemiological model that couples effective habitat cover to an SIR framework for ANDV transmission in O. longicaudatus. Habitat degradation and compensatory restoration modify rodent carrying capacity, natality, and the force of infection, which depends on infected host load relative to instantaneous ecological capacity. We derived the habitat equilibrium, the basic reproduction number R0, and the time-dependent effective reproduction number Re(t) and evaluated infection-burden and threshold indicators across degradation-restoration scenarios. The analysis shows that R0 is independent of equilibrium habitat cover because susceptible abundance scales with carrying capacity at the disease-free equilibrium. In contrast, Re(t), cumulative incidence, and infected load depend on transient habitat-mediated crowding. Restoration increases reservoir abundance and absolute infection burden, whereas degradation can reduce abundance while increasing crowding-driven transmission pressure and prolonging supercritical windows. These results identify ecological conditions under which habitat change may intensify reservoir infection pressure and guide One Health surveillance at human-rodent interfaces.

Hemorrhagic fever with renal syndrome (HFRS), caused by Seoul orthohantavirus (SEOV) and Hantaan orthohantavirus (HTNV), remains a neglected rodent-borne zoonosis with persistent residual spillover risk in low-incidence regions of China. This study assessed human HFRS occurrence and small-mammal hantavirus surveillance signals in small-mammal hosts across Zhejiang Province, China, in 2025. Reported human cases were obtained from the National Notifiable Disease Surveillance System, and animal host surveillance was conducted at five designated monitoring sites. A total of 107 HFRS cases were reported, occurring year-round with peaks in June and December and showing spatial heterogeneity, presenting a predominance of males, adults aged ≥40 years, and farmers. Animal host surveillance captured 617 small mammals (566 rodents and 51 shrews) from 15,457 valid trap-nights, with Apodemus agrarius (30.31%) and Rattus norvegicus (29.98%) as the dominant species. Sixteen animals were positive for hantavirus RNA and/or antibody, including 12 for hantavirus RNA and 6 antibody-positive animals; two were positive for both markers. Positive animals were detected in multiple species, including Niviventer confucianus, R. norvegicus, Rattus losea, A. agrarius, Suncus murinus, and Rattus tanezumi. Human incidence, small-mammal density, host species composition, and hantavirus-positive rates were not fully concordant across surveillance sites. Our findings reveal sustained cryptic orthohantavirus circulation in low-endemic Zhejiang, highlighting that integrated human-reservoir One Health surveillance is indispensable for precise spillover risk prediction and targeted zoonotic disease intervention.