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Ecological determinants driving orthohantavirus prevalence in small mammals of Europe: a systematic review

One Health Outlook volume 7, Article number: 15 (2025) Cite this article

Abstract

Orthohantaviruses are emerging zoonotic pathogens that cause severe human disease and are considered an emerging public health threat globally. Mammalian orthohantaviruses are naturally maintained in rodent species and occasionally in other mammals. The abundance and density of natural orthohantavirus reservoir species are affected by multi annual and seasonal population cycles, community composition, ecosystem variables and climate. Horizontal transmission between host species is mostly density-driven and occurs via contact with infected host excreta, thus, fluctuations in populations and environmental variables often determine the prevalence of hantavirus in natural hosts. Given the zoonotic potential of hantaviruses, ecological factors influencing their spread and persistence in their natural reservoir and population dynamics influencing horizontal transmission require critical evaluation for human infection risk assessment. The present review paper discusses the impacts of natural host population cycles and ecosystem diversity, environmental conditions, and abiotic factors on the epidemiology of rodent-borne hantavirus infections in Europe. While significant efforts have been made to understand the drivers of hantavirus prevalence in natural hosts, we highlight key challenges in evaluating viral prevalence and assessing the role of environmental and population variables in determining hantavirus prevalence in host species.

Introduction

Orthohantaviruses are emerging zoonotic viruses with a major global impact on public health. As per the most recent taxonomical review, the genus Orthohantavirus is one of the four belonging to the subfamily Mammantavirinae, order Bunyavirales, family Hantaviridae and includes sixty different viruses [1]. Like other Bunyaviridae members, hantaviruses are enveloped and pleomorphic, with genomes comprising three negative-sense, single-stranded RNA segments encoding structural and non-structural proteins. Orthohantaviruses infect wild rodents, specifically species within Muridae (mice), Cricetidae (voles), and Soricidae (shrews) families in Europe. Occasionally, bats may serve as hosts [1].

Upon direct or indirect contact with infected hosts, hantaviruses can infect humans causing a mild-to-severe, sometimes fatal disease [2,3,4]. The presence of the virus within the host, both human and rodent, is concentrated in the kidneys, lungs and, at times, may affect the brain [5,6,7,8]. Chronic viral proliferation within target organs is often asymptomatic in natural hosts due to immune suppression [9,10,11] but several clinical signs may manifest if human infection takes place. Hantavirus replication in humans occurs in macrophages and vascular endothelial cells of lung and kidney tissues and may lead to many symptoms including fever, pain, nausea and in severe cases renal conditions, shock, haemorrhagic manifestations, and haemodialysis [4, 12,13,14,15,16].

Hantavirus species are divided into Old World and New World based on their distribution and pathogenicity. Old World hantaviruses, which are found in Asia and Europe, predominantly cause haemorrhagic fever with renal syndrome (HFRS). New World hantaviruses, located in the Americas, are major causes of haemorrhagic cardio-pulmonary or pulmonary syndrome (HCPS/HPS).

Approximately thirty thousand people are affected each year, however, owing to widespread underreporting, the actual number of affected individuals is likely to be much greater [2, 17, 18]. The highest case numbers occur in the Old World, particularly in China, with over 10,000 cases reported annually between 2004 and 2016 [19], and in Russia, with approximately 7,000 cases per year [20]. In Europe, cases average around 3,000 annually (mean: 3,152 from 2010–2020, ranging from 1,647 cases in 2020 to 4,686 in 2012 [21,22,23]). Scandinavia has the highest case numbers within Europe, followed by Central Europe and the Balkans [21,22,23]. In the Americas, reported cases are much lower, at about 300 annually [4].

Hantavirus transmission primarily occurs through the inhalation of contaminated aerosols derived from the secretions of infected hosts, but may also occur through direct contact with infected host saliva [1, 9, 23,24,25,26,27,28]. Forestry workers, outdoor enthusiasts, and rural inhabitants are generally considered at greater risk due to their prolonged contact with potentially infected hosts and their habitat [19, 29,30,31,32,33,34,35,36].

Given the high coevolution between viruses and host species, hantaviruses often rely on a single species as the main reservoir [2, 17] although spillover has been extensively reported, the role of non-target hosts remains unclear [9, 37, 38]. In Western Europe, Orthohantavirus puumalaense (PUUV) accounts for over 95% of reported human hantavirus infections [23]. Predominant in Boreal and Continental Europe, PUUV causes “nephropathia epidemica” (NE), a milder, often asymptomatic form of HFRS. Its main reservoir host is the bank vole (Myodes glareolus syn. Chletrionomys glareolus) [11], a common rodent in many forested areas [39]. The second most prevalent hantavirus in Europe, Orthohantavirus dobravaense (DOBV), can cause a severe form of HFRS with up to 12% fatality [2]. DOBV is common in the Balkans and Eastern Europe, with the yellow-necked mouse (Apodemus flavicollis) as its primary host, often found in mature deciduous forests in mountainous areas of Central and Southern Europe. Less frequently recorded hantaviruses in Europe include O. tulaense, O. seoulense, O. hantanense, O. brugesense, and O. asikkalaense, linked to various rodent hosts (Table 1), with few or no human cases reported to date [2, 4, 40, 41]. In the Americas, sigmodontinae-borne hantaviruses cause the most severe cases of hantavirus cardiopulmonary syndrome (HCPS), with fatality rates reaching 60% [42].

Table 1 ICVT currently recognised Orthohantavirus species in Western Europe [1], the main reservoir host and broad geographic distribution
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In Europe, human hantavirus infection is a concerning issue aggravated by the lack of available and effective vaccines, an increasing trend in the number of reported human cases, and an increase in the endemicity of natural host species [2, 3, 17, 23]. This trend is likely intensified by ongoing climate change, which is expected to increase the frequency of rodent-borne zoonosis outbreaks by promoting more frequent population surges [48,49,50,51].

Several studies link human hantavirus cases with location through large-scale climate datasets and virus prevalence surveys in reservoir hosts [48, 50, 52,53,54,55,56,57,58,59,60,61,62]. However, patterns of human cases do not consistently correspond with virus distribution within host populations, and peak prevalence in hosts does not necessarily coincide with peak human incidence [59, 61, 63,64,65]. Predicting and monitoring hantavirus prevalence in hosts is challenging due to factors such as winter survival rates, ecological conditions, and climate, which influence host population dynamics, distribution, and indirect transmission [65,66,67,68,69,70,71]. Moreover, forecasting host population trends across Europe remains difficult, given the scarcity of large-scale data on host abundance and the challenges in obtaining unbiased local data [72].

This review focuses on the environmental, climate and host factors that influence the prevalence of hantavirus in small mammals in Europe. Understanding host population variations, ecological drivers, and the effects of variable interactions on population diversity and indirect transmission is essential for grasping pathogen epidemiology in reservoir hosts, thereby supporting efforts to assess and mitigate human risk.

Methods

The “Preferred Reporting Items for Systematic Reviews and Meta-Analyses” (PRISMA) method was adopted for this review [73]. The searches covered entries from January 2003 to January 2024. The query was applied to four digital databases (CABI Digital Library, PubMed, JSTOR, and SpringerLink) using the Boolean query: Hantavirus AND Europe AND “Small Mammals”. After duplicateremoval (= 51), 364 entries remained.

We included studies using live trapping data from small mammal reservoir hosts, assessing hantavirus prevalence (regardless of species) and analysing environmental or population dynamics factors. Studies focusing on human case data, genetic diversity, non-European reservoir species, or experimental infections were excluded, though relevant conclusions from experimental studies are discussed. Scientific papers in languages other than English were translated using commercially available software. Out of 364 entries, 51 were excluded for lacking relevance to European hantavirus dynamics (see Fig. 1).

Fig. 1
figure 1

The PRISMA screening and selection process is illustrated in the figure. Entries on the right indicate the number of articles discarded or included and the reasons for these decisions. Out of 415 entries obtained from search engines, 40 were ultimately selected for this review. The full details and factor breakdown of each selected article are contained in Supplementary Material 1

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Papers were further filtered after the title; abstract and full text were read. Articles were also removed from the selected pool when no statistics-based method was provided even if all other criteria were fulfilled. After applying the selection criteria, 20 scientific journals were selected for inclusion in the review. A further twenty research papers, identified through reference analysis of the selected articles, were considered significant and included in the review. A complete list of the articles included in this review as well as the main effects they describe can be found in Supplementary Material 1.

Results

Of the 40 articles reviewed, 4 examined multiple hantavirus species across different hosts at the same site. Most studies (37/40) analysed biotic and abiotic factors affecting PUUV prevalence and its primary host, the bank vole (Clethrionomys glareolus). Six articles assessed hantavirus prevalence in Apodemus spp. (4 with DOBV and 1 with PUUV antibodies), while four focused on TULV in its main host, the field vole. Based on European climate macro areas, 16 studies analysed data from Boreal Europe and 24 from Continental Europe, with articles from the Balkans (2), Pannonian region (2), and Alpine region (1) included in the Continental group (see Supplementary Material 2).

The analysis highlighted five key focus areas. Twenty-one articles examined host characteristics (e.g., gender, age, reproductive maturity), and another 21 analysed population dynamics, specifically abundance and density. Eight studies addressed abiotic factors, such as local or regional climates. Eleven articles explored habitat characteristics, including vegetation, landscape changes, and masting patterns of deciduous trees (periodic production of seeds, nuts, or fruits by deciduous trees). Finally, seven studies investigated interactions with other species, including non-host rodents and predators (Fig. 2). A graphical summary of factors affecting hantavirus prevalence in hosts is presented in Fig. 3.

Fig. 2
figure 2

Publication timeline and topic covered by articles included in the review. The colours of the cumulative bar chart indicate the main topic. The dotted line represents the number of selected articles published in the year

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Fig. 3
figure 3

Graphical representation of key factors influencing Orthohantavirus prevalence in natural reservoir hosts. These factors include host biology, environmental abiotic and biotic conditions, habitat characteristics, and determinants of viral particle survival outside the host. Symbols indicate the direction of influence: a green plus sign represents a positive effect, a red minus sign indicates a negative effect, and a grey tilde denotes variable influence

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Host factors

Effects of hantavirus on host fitness and behaviour

While usually asymptomatic, hantavirus infections can affect the survival and fitness of carrier hosts. These viruses have co-evolved with their natural hosts, typically causing chronic, subclinical infections that minimally impact short-term fitness [9,10,11]. However, host mortality may increase under certain ecological conditions or when prolonged infection significantly affects fitness [74,75,76]. For example, PUUV-infected bank voles may show lower winter survival than uninfected voles, perhaps due to the energy demands of managing infection under harsh winter conditions and food scarcity [76]. Gender effects on winter survival are unclear, with some studies reporting higher mortality in infected females [75], others in infected males [76], and others only in immature voles regardless of gender [74]. Interestingly, infected hosts may experience increased survival between spring and summer [69]. No mortality changes were observed in infected A. flavicollis [75]. Multiple factors—species, fitness, environmental conditions, and reproductive status— may affect hantavirus infection outcomes, and assessments rely on recapture to evaluate survival, potentially overlooking the effects of dispersal or migration [69, 74,75,76].

Chronic hantavirus infection in bank voles is linked to co-infections with pathogens such as Leptospira spp. and parasitic helminths [77, 78]. PUUV-infected voles are more likely to be co-infected, although whether this is due to individual traits or diminished fitness from infections remains unclear. In contrast, no significant relationship was found between ectoparasite occurrence and DOBV in Apodemus spp. [79].

Infected hosts can also exhibit behavioural changes that affect fitness and energy allocation. PUUV-infected female bank voles show age-dependent behavioural shifts during the reproductive season. Young, infected females may be more likely to reach breeding maturity and prioritise litter size and birth frequency, which could compromise long-term immune function and increase pathogen susceptibility [74, 76, 80]. Older females, on the other hand, tend to reduce litter production, likely due to worsened body condition and fitness from prolonged immunological stress [80]. It remains unclear whether this pattern occurs in other small mammal species infected with different hantavirus species [76, 80].

Effects of age on hantavirus prevalence in the host

Most studies suggest that hantavirus prevalence in natural hosts increases with age, using weight or reproductive maturity as indicators [59, 65, 66, 70, 78,79,80,81,82,83,84,85,86,87,88,89,90]. Few studies found age to have no significant effect [76, 91]. Similar age-related patterns have been observed for other pathogens, such as Leptospira spp., and co-infections are frequently reported [66, 77, 92,93,94].

Viral proliferation peaks within the first month after infection, maximising infectivity [24, 28]. Although viremia declines over time, it is never fully eliminated, leading to continued shedding [26, 28, 95]. As hosts age, the likelihood of infection increases due to more frequent encounters with infected conspecifics, more aggressive adult behaviour, and greater opportunities for indirect transmission [26, 65, 70].

Newborn bank voles born to hantavirus-infected females inherit maternal antibodies, providing immunity for up to 80 days [26, 88]. This phenomenon, observed across hantavirus species and hosts (including humans) [96,97,98,99], contributes to seasonal fluctuations in hantavirus prevalence. This vertical transmission contributes to seasonal declines in hantavirus prevalence, as the influx of young, immune individuals during the reproductive period lowers overall viral prevalence [26, 88, 100,101,102].

Effect of the host gender on hantavirus prevalence

Gender influences hantavirus prevalence in small mammal hosts, with males more frequently infected than females, likely due to behavioral and physiological factors during the reproductive season [59, 65, 69, 70, 84, 87, 88, 90, 103, 104]. However, several studies instead found no significant effect of gender on prevalence [66, 75, 76, 79, 81, 82, 86, 89, 92].

During the breeding season, mature males allocate energy to reproductive behaviours, which may lead to immune suppression and facilitate infection [105, 106]. These behaviours, including mate-seeking and territoriality, increase the chances of horizontal transmission by bringing males into frequent contact with females and other males, further spreading the virus [69, 84, 101, 107, 108].

Breeding males also mark their territory with hormonally attractive, infectious urine [25, 74]. This drives investigation by both females and competing males, thus promoting the indirect transmission of the pathogen [25, 27, 109]. The behaviour and susceptibility of adult male bank voles play a pivotal role in hantavirus transmission, with higher infection rates among males likely acting as a primary driver of rapid increases in virus prevalence within the host population [101].

Genetic immunity to hantavirus

Genetic predisposition plays a key role in PUUV susceptibility in bank voles. Specific immune genes or mutations influence infection tolerance, with related individuals being more susceptible or resistant to infection due to shared genetic traits [83, 107, 110,111,112,113]. In several studies, infected hosts from genetically related clusters were observed [84, 113], also likely due in part to communal wintering burrow behaviour [114] that facilitates direct and indirect virus transmission [25].

An experimental study found that bank voles from PUUV-endemic regions had higher antiviral gene expression (e.g., Tnf, Mx2) than those from non-endemic areas [115]. Genes such as Drb (MHC class II), Tlr-4, and Tlr-7 are frequently associated with tolerance strategies in these populations [83, 110, 111, 113, 115, 116].

While immune responses in Central European bank vole populations may reflect postglacial colonisation patterns [117], not all studies agree. For example, a Finnish study found only weak associations between the Mx2 gene and infection, suggesting limited evidence for strong genetic selection [116]. Further research is needed to identify and understand potential hantavirus resistance genes in host species.

Effects of host demography fluctuations

For horizontally transmitted pathogens, such as hantaviruses, elevated host abundances and densities increase the transmission rate due to higher frequency of contact and greater indirect transmission, leading to a swift increase in pathogen prevalence. Most studies in this review confirm a positive correlation between host abundance and hantavirus prevalence [59, 66, 68,69,70, 85, 86, 100, 100, 102, 118, 119]. Other studies have reported a delayed effect of host abundance, where prevalence is significantly linked to host abundance several months earlier [65, 67, 104, 120,121,122], and few found no significant relationship [75, 89, 123], with one even observing a negative impact of current host abundance on seroprevalence [104].

The effect of density should be considered within the context of cyclic fluctuations that occur on both multi-annual and seasonal temporal scales, influencing population trends and hantavirus prevalence [124]. In boreal ecosystems, multiannual cyclic peaks occur every three to five years due to predator–prey dynamics [125,126,127,128], whereas in continental ecosystems, peaks appear every two to three years, mainly driven by winter food availability, particularly the seed production of deciduous trees, or mast [48, 58, 124, 129]. These cycles include a “low” phase, a growth phase, and a peak phase, after which populations crash [56, 65, 100, 108, 130].

Seasonal fluctuations further shape small mammal population dynamics. Populations are lowest in winter but increase throughout the reproductive season, peaking in fall. The highest yearly prevalence often occurs at the end of winter, although the intensity of this peak is lower during the “low” phase. The lowest infection prevalence often occurs in early September during the “increase” and “peak” phases, while in the “low” phase, it is usually lowest in early winter, marking the absolute lowest level of hantavirus prevalence. The concept of “virus refugia” [131] may explain how the virus survives during low-density phases by persisting in locations that support viral particle survival outside the host, as discussed further in the chapter titled "Environmental drivers of hantavirus transmission".

Highest hantavirus prevalence in small mammals occurs either in late winter or early in the reproductive season [59, 65,66,67, 70, 84, 86, 88, 90, 102, 108, 122, 132]. During winter, host populations primarily consist of susceptible adults, as the mating season has ended, and maternal antibodies are no longer present. These adults remain active throughout winter without hibernating, showing reduced territoriality and engaging in communal burrowing, behaviours that facilitate horizontal transmission and contribute to elevated hantavirus prevalence [26, 70, 84, 85, 102, 114, 132]. Additionally, the cold winter conditions help viral particles in excreta maintain infectivity, further aiding transmission [25].

In summer and autumn, when reproductive activity peaks, host abundance and density rise, but the proportion of adults decreases as more juveniles enter the population. During the reproductive season, mature individuals engage in mate-seeking, territorial defence, and foraging behaviours, which increase encounters with potentially infected individuals in high-density environments, further facilitating virus transmission [107, 108]. However, high densities in the summer do not always correlate with increased hantavirus prevalence. The influx of temporarily immune juvenile individuals may reduce overall prevalence by increasing the proportion of immune hosts [88, 100, 102, 120]. Nevertheless, transmission rates remain high due to frequent interactions among mature individuals [108], and one study found the highest prevalence overall in the summer [92]. Notably, maternal antibodies in juveniles were not accounted for in this study, which may result in positive antibody results in uninfected individuals.

In autumn, as the reproductive season ends, hantavirus prevalence may increase in the host population [65, 66]. As reproductive effort declines this would lead to an increased proportion of susceptible adults in the population. Combined with higher densities and abundance, transmission is facilitated [80]. Several studies have indeed reported highest hantavirus prevalence in autumn compared to other seasons [63, 85, 104].

The cyclic nature of annual and multi-annual host population fluctuations influences hantavirus transmission. The abundance of susceptible adults in winter is linked to the density of individuals in the preceding autumn, which plays a crucial role in determining hantavirus prevalence at the start of the reproductive season in spring [65, 67, 104, 120]. Unlike the spring peak, the autumn peak lacks density-dependent characteristics, as many juveniles remain protected by maternal antibodies [69, 88]. While some studies found a relationship between population density and autumn seroprevalence [119], others noted that autumn prevalence can be negatively affected by the population density observed in spring [76, 88]. At a fine temporal scale, the lag between population abundance and hantavirus prevalence ranges from 3 to 4 and a half months, decreasing to 2 months during peak phases [65]. This lag coincides with the window of immune protection from maternal antibodies, and the differences in peak timings may be attributed to density-dependent horizontal transmission dynamics.

Effect of tree mast cycle on transmission dynamics

Cyclic increases in mast production, particularly from oak (Quercus spp.) and beech (Fagus spp.) trees, lead to a delayed rise in small mammal abundance and density, subsequently affecting hantavirus transmission [48, 59, 63, 81, 118]. These fluctuations in seed production provide abundant autumn resources, which enhance winter survival [2, 48, 57, 59, 65] and lead to larger spring populations, associated with higher levels of hantavirus prevalence throughout the following year [59, 118]. Small mammal populations are affected by masting at both at patch level and landscape level, with masting events being considered one of the primary causes of multi-annual population fluctuations in continental Europe [48, 63, 118].

Effects of inter-species competition

The richness and diversity of non-susceptible species can suppress hantavirus prevalence in the target host by reducing its density through competition for ecological niches and resources, leading to a decrease in viral transmission [133]. In continental Europe, studies have shown that PUUV prevalence in bank voles declines as the proportion of Apodemus spp. increases [89, 120]. High shrew (Sorex spp.) abundance also negatively impacts hantavirus prevalence in bank voles, as they compete for similar habitats. Over time, an increase in the abundance of other generalist species may result in reduced vole density, lowering the horizontal transmission rate to susceptible individuals [70, 100, 102, 120]. Host densities may also decline in habitats dominated by specialist species, such as grasslands, where field voles outcompete bank voles, reducing host populations and viral transmission [102]. Seasonal effects have also been observed, with a negative impact of small mammal species diversity on bank vole hantavirus prevalence in spring, but not in fall [70].

The “dilution effect” from interspecific competition does not always occur and can vary depending on the location, habitat, and resource availability. For example, studies conducted in Belgium revealed that the prevalence of Apodemus species did not significantly affect bank vole densities or hantavirus prevalence [59, 89]. In contrast, while no substantial impact of other vole or shrew species on PUUV prevalence in bank voles was found, species diversity was linked to changes in bank vole abundance [71]. Additionally, research has also suggested that local small mammal diversity may increase PUUV prevalence in vole hosts, possibly due to interspecific interactions driving more territorial behaviour [123].

Effect of predation

The presence of predators may reduce hantavirus prevalence in host species by inducing behavioural changes or through selective predation of infected individuals. For example, in the presence of foxes (Vulpes vulpes), bank voles alter their behaviour to minimise interactions with conspecifics, decreasing pathogen transmission and reducing overall prevalence within the population [71]. Predators may also reduce prevalence by preferentially targeting infected individuals. In boreal ecosystems, owl species (Aegolius funereus), along with weasels (Mustela nivalis) and foxes, selectively prey on infected voles, affecting hantavirus transmission dynamics [71, 91, 102]. This effect is amplified during high predator density periods in autumn, which decreases infected individuals and overall abundance, leading to a lagged reduction in hantavirus prevalence by spring [65, 67, 104]. The increased predation risk may be due to infected individuals inhabiting suboptimal patches with reduced vegetation cover [68, 107], combined with a loss of immunological fitness induced by the pathogen [74, 76, 80].

Environmental drivers of hantavirus transmission

Outside-host hantavirus particle survival

Viral particle survival outside the host is essential for hantavirus transmission and persistence within host populations. Indirect transmission, primarily via contaminated excreta, is the main pathway for hantavirus spread among reservoir hosts [11]. For PUUV, infectivity in faeces and urine can persist for several days, facilitating aerosol transmission without direct contact [24, 25]. Low temperatures and high moisture enhance viral survival in the environment [25, 134].

Laboratory studies show that particles from O. hantanense remains infective for up to 9 days at 20 °C, while TULV and PUUV persist for 5 days at 23 °C [25, 134]. Under optimal conditions, O. hantanense retains infectivity for up to 96 days at 4 °C [134] but is inactive within 24 h in dry conditions [25, 134].

Persistent viral infectivity is crucial during high-density phases, such as the reproductive season, and prevents virus fadeout during low-density periods [27, 67, 107, 108, 128]. Hosts often interact with contaminated environments during dispersal, foraging, and mating, further facilitating transmission [27, 109]. Climate analyses show that factors promoting viral survival, such as low temperatures and high rainfall, may correlate with hantavirus prevalence in small mammal populations [68, 71, 102, 108, 122]. A negative relationship between bank vole territorial range and population density also supports the role of indirect transmission in maintaining the virus in low-density scenarios [135].

Habitat influence on viral infection and transmission

Forest patches often show higher hantavirus transmission rate and prevalence, serving as refuges for outside-host viral particles due to shade and humidity, while also providing optimal habitats for hosts [68, 107, 131, 132, 136]. Normalized differential vegetation index (NDVI), obtained from satellite imagery, estimates vegetative production and correlates with increased hantavirus prevalence in bank vole populations, using both historical and seasonal data [89, 108].

Densely vegetated areas offer shelter and foraging resources year-round, supporting high small mammal densities and facilitating hantavirus transmission [70, 108, 131]. This effect is particularly pronounced in winter, when increased trophic availability reduces mortality, leading to higher host densities and increased prevalence in spring [67, 87, 104, 123, 131]. Shaded, humid conditions in winter further enhance viral persistence, promoting indirect transmission [25, 70, 123]. In both boreal and continental European ecosystems, the presence of woody debris and hollow areas on the forest floor may increase PUUV prevalence in bank voles [119, 123, 131].

In Boreal ecosystems, forest strand age may influence bank vole populations and hantavirus prevalence. Old forest strands (over 100 years old) have the highest populations, but the highest PUUV prevalence is found in 25-30-year-old stands [70]. A more recent study, using landscape metrics and a larger dataset, found that PUUV prevalence in bank voles was linked to old forest strands, while increased forest cutting was associated with lower hantavirus prevalence [132]. Whether forest strand age affects other species or produces similar results in continental Europe remains unclear.

One article analysed also found that the largest populations and highest prevalence of PUUV were found in moist forest environments [119]. The role of habitat moisture was further emphasized by other authors and linked to indirect transmission [25, 131]. Similarly, another study using large spatial datasets found a significant association between proximity to waterlogged soils and hantavirus prevalence in bank voles [71].

When optimal habitats exceed their carrying capacity, small mammals may disperse to lower-quality neighbouring patches, driven by high population densities and limited resources [137]. This typically occurs during population peaks, when abundance rises rapidly, and available niches become crowded [68]. In fragmented landscapes, this dispersal helps spread hantavirus across patches [107]. Dispersing individuals may acquire the virus either before or during movement, as high densities and competition reduce their fitness and increase the likelihood of infection [25, 27, 107, 109]. Additionally, higher densities and hantavirus prevalence may also be observed in isolated patches, possibly due to dispersal constraints [68, 91].

The link between hantavirus infection and dispersal may result in high prevalence in lower-quality habitats, where individuals allocate more energy to survival than to immune function, increasing susceptibility to the virus [70, 91]. These habitats also have higher mortality rates, which may lead to stochastic fadeout events of the virus or the host population [76, 107, 135]. In contrast, high-quality, vegetated patches maintain hantavirus presence by supporting susceptible hosts and trophic availability, even at low population densities [70, 76, 132].

Effects of climate on hantavirus prevalence

In Continental Europe, studies have shown varying effects of temperature and precipitation on hantavirus prevalence in host populations. Some report a positive relationship between winter temperatures and viral prevalence, likely due to improved small mammal fitness and increased vegetative production, which enhances horizontal transmission [56, 79, 108]. In contrast, other studies suggest that colder temperatures increase viral particle longevity, leading to higher hantavirus prevalence in host [68, 89, 123]. Finally, some studies found no effect of temperature on PUUV prevalence in bank voles [60].

In Boreal Europe, winter temperature outcomes are influenced by regional factors. Prolonged snow cover provides thermal insulation, encouraging hosts to reduce activity outside burrows, which may increase horizontal transmission within these sheltered environments [122]. Conversely, in areas with little snow, exposure to harsher winter conditions may cause higher mortality rates, indirectly lowering hantavirus prevalence [53].

Regarding precipitation, some studies found no significant correlation with hantavirus prevalence [68, 71], while others linked winter [108], annual [60, 79], or spring rainfall [90] to increased viral prevalence in host populations. However, a few authors observed that higher winter and spring precipitation negatively affected bank vole density, thus reducing hantavirus prevalence [68]. In Boreal ecosystems, temperature and precipitation during November were associated with PUUV prevalence in bank voles the following spring [122]. Habitat humidity and water bodies also play a role in viral prevalence [60, 71], likely by improving viral survival in moist environments [25]. Further investigation is needed to better understand the timing of rainfall and host sampling frequencies [71].

Conclusion

Humans are increasingly exposed to rodent-transmitted zoonoses, with growing endemicity, more frequent outbreaks, and the breakdown of human-animal barriers. A review of the ecological factors affecting hantaviruses in European reservoir species is of public health importance, as it sheds light on viral transmission dynamics and fluctuations, helping to reduce human risk.

This review examines the complex interactions underlying hantavirus prevalence in rodent populations in Europe. Key drivers include host demographic patterns, which influence transmission among susceptible individuals, as well as environmental factors that prolong indirect transmission, affect host density, and enhance survival. Densely vegetated environments provide optimal conditions for both the virus and its hosts, increasing viral infectivity while offering shelter and resources that boost host fitness and density.

Predicting hantavirus fluctuations in host populations may be possible by monitoring mast years, as food abundance directly affects small mammal winter survival and correlates with higher viral prevalence in spring. With climate change leading to more frequent mast years and milder winters, coupled with a loss of species richness, hantavirus distribution and prevalence are expected to increase across Europe. This review calls for further research, especially on climate and habitat factors, which have produced conflicting results in previous studies. Additionally, preserving small mammal biodiversity and natural predator–prey dynamics can help mitigate infection peaks by reducing intraspecific interactions and promoting selective predation of infected individuals.

Data availability

Not applicable.

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Acknowledgements

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Funding

This activity was part of the National Biodiversity Future Center (NBFC), Project funded under the National Recovery and Resilience Plan (NRRP), Mission 4 Component 2 Investment 1.4—Call for tender No. 3138 of 16 December 2021, rectified by Decree n.3175 of 18 December 2021 of Italian Ministry of University and Research funded by the European Union – NextGenerationEU (Project code CN_00000033).

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Authors and Affiliations

  1. Department of Agricultural, Food, Environmental and Animal Sciences (DI4A), University of Udine, Via Sondrio 2/A, Udine, Italy

    Daniele Fabbri & Paola Beraldo

  2. National Biodiversity Future Center (NBFC), Piazza Marina 61, Palermo, Italy

    Daniele Fabbri, Valentina Tagliapietra & Paola Beraldo

  3. Research Centre for Emerging Infections and Zoonoses, University of Veterinary Medicine, Bünteweg 2, Hannover, Germany

    Monica Mirolo, Martin Ludlow & Albert Osterhaus

  4. Research and Innovation Centre, Fondazione Edmund Mach, San Michele All’ Adige, Via Edmund Mach 1, Trento, Italy

    Valentina Tagliapietra

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  1. Daniele Fabbri
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Contributions

DF concept and design, writing, and data acquisition. MM concept, writing, and review. VT review. ML review. AO review. PB project coordinator, design and review.

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Correspondence to Daniele Fabbri.

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Albert Osterhaus is the Editor-in-Chief and Martin Ludlow is an Associate Editor for One Health Outlook and were not involved in the peer review of this paper. The authors declare no other conflicts of interest.

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Fabbri, D., Mirolo, M., Tagliapietra, V. et al. Ecological determinants driving orthohantavirus prevalence in small mammals of Europe: a systematic review. One Health Outlook 7, 15 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s42522-025-00136-w

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One Health Outlook

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