Prevalence Of Sin Nombre Virus Research Articles

Distribution and prevalence of Sin Nombre hantavirus in rodent species in eastern New Mexico.

Orthohantaviruses are diverse zoonotic RNA viruses. Small mammals, such as mice and rats are common chronic, asymptomatic hosts that transmit the virus through their feces and urine. In North America, hantavirus infection primarily causes hantavirus cardiopulmonary syndrome (HCPS), which has a mortality rate of nearly 36%. In the United States of America, New Mexico (NM) is leading the nation in the number of HCPS-reported cases (N = 129). However, no reported cases of HCPS have occurred within eastern NM. In this study, we assessed the prevalence of Sin Nombre virus (SNV) in rodent assemblages across eastern NM, using RT-qPCR. We screened for potential rodent hosts in the region, as well as identified areas that may pose significant infection risk to humans. We captured and collected blood and lung tissues from 738 rodents belonging to 23 species. 167 individuals from 16 different species were positive for SNV RNA by RT-qPCR, including 6 species unreported in the literature: Onychomys leucogaster (Northern grasshopper mouse), Dipodomys merriami (Merriam's kangaroo rat), Dipodomys ordii (Ord's kangaroo rat), Dipodomys spectabilis (Banner-tailed kangaroo rat), Perognathus flavus (Silky pocket mouse), and Chaetodipus hispidus (Hispid pocket mouse). The infection rates did not differ between sexes or rodent families (i.e., Cricetidae vs. Heteromyidae). Generalized linear model showed that disturbed habitat types positively influenced the prevalence of SNV at sites of survey. Overall, the results of this study indicate that many rodent species in east New Mexico have the potential to maintain SNV in the environment, but further research is needed to assess species specific infectivity mechanisms and potential risk to humans.

Exome sequencing of deer mice on two California Channel Islands identifies potential adaptation to strongly contrasting ecological conditions.

Understanding the forces that drive genotypic and phenotypic change in wild populations is a central goal of evolutionary biology. We examined exome variation in populations of deer mice from two of the California Channel Islands: Peromyscus maniculatus elusus from Santa Barbara Island and P. m. santacruzae from Santa Cruz Island exhibit significant differences in olfactory predator recognition, activity timing, aggressive behavior, morphology, prevalence of Sin Nombre virus, and population densities. We characterized variation in protein‐coding regions using exome capture and sequencing of 25 mice from Santa Barbara Island and 22 mice from Santa Cruz Island. We identified and examined 386,256 SNPs using three complementary methods (BayeScan, pcadapt, and LFMM). We found strong differences in molecular variation between the two populations and 710 outlier SNPs in protein‐coding genes that were detected by all three methods. We identified 35 candidate genes from this outlier set that were related to differences in phenotypes between island populations. Enrichment analyses demonstrated that patterns of molecular variation were associated with biological processes related to response to chemical stimuli and regulation of immune processes. Candidate genes associated with olfaction (Gfy, Tlr2, Vmn13r2, numerous olfactory receptor genes), circadian activity (Cry1), anxiety (Brca1), immunity (Cd28, Eif2ak4, Il12a, Syne1), aggression (Cyp19a, Lama2), and body size (Bc16, Syne1) exhibited non‐synonymous mutations predicted to have moderate to large effects. Variation in olfaction‐related genes, including a stop codon in the Santa Barbara Island population, suggests loss of predator‐recognition traits at the molecular level, consistent with a lack of behavioral aversion to fox feces. These findings also suggest that divergent pathogen prevalence and population density may have influenced adaptive immunity and behavioral phenotypes, such as reduced aggression. Overall, our study indicates that ecological differences between islands are associated with signatures of selection in protein‐coding genes underlying phenotypes that promote success in those environments.

Sin Nombre virus prevalence from 2014–2017 in wild deer mice,Peromyscus maniculatus, on five of the California Channel Islands

Sin Nombre virus (SNV) is a zoonotic virus that is highly pathogenic to humans. The deer mouse, Peromyscus maniculatus, is the primary host of SNV, and SNV prevalence in P.maniculatus is an important indicator of human disease risk. Because the California Channel Islands contain permanent human settlements, receive hundreds of thousands of visitors each year, and can have extremely high densities of P.maniculatus, surveillance for SNV in island P.maniculatus is important for understanding the human risk of zoonotic disease. Despite the importance of surveillance on these heavily utilized islands, SNV prevalence (i.e. the proportion of P.maniculatus that test positive to antibodies to SNV) has not been examined in the last 13-27years. We present data on 1,610 mice sampled for four consecutive years (2014-2017) on five of the California Channel Islands: East Anacapa, Santa Barbara, Santa Catalina, San Nicolas, and San Clemente. Despite historical data indicating SNV-positive mice on San Clemente and Santa Catalina, we detected no SNV-positive mice on these islands, suggesting very low prevalence or possible loss of SNV. Islands historically free of SNV (East Anacapa, Santa Barbara, and San Nicolas) remained free of SNV, suggesting that rates of pathogen introduction from other islands and/or the mainland are low. Although continued surveillance is warranted to determine whether SNV establishes on these islands, our work helps inform current human disease risk in these locations and suggests that SNV prevalence on these islands is currently very low.

The biodiversity effect in regulating the prevalence of Sin Nombre virus (SNV)

Sin Nombre virus (SNV), a virus that can cause fatal disease among humans, is primarily hosted by the deer mouse, Peromyscus maniculatus . To better understand the biodiversity effect in curbing the prevalence of the SNV infection in the deer mouse population, we analyze the Peixoto & Abramson (2006) “one host, one non-host alien” deterministic model. In this study, we focus on the relationship of carrying capacity and interspecific competition strength of both host and non-host species in relation to the prevalence of the infection. Bifurcation analysis is carried out to examine the dynamics of this eco-epidemiological system. Our results show that the non-host species have a certain degree of influence in suppressing the SNV prevalence, given that the environmental conditions are similar and the interspecific competition strengths are relatively weak between the host and non-host species.

The roles of community diversity and contact rates on pathogen prevalence

The complexity of a community can play a fundamental role in the prevalence of pathogens by altering interactions among hosts and pathogen transmission. Information on the frequency of contacts between individuals and the distribution of contact rates in a population is critical to predicting pathogen prevalence. However, contact rates are notoriously difficult to document especially in small, nocturnal species. We have been documenting the contact rates of deer mice (Peromyscus maniculatus) in nature with respect to infection with Sin Nombre virus (SNV), a zoonotic pathogen, and the biodiversity of the mammalian community. Our long-term field studies, as well as those of others, revealed that prevalence of SNV in deer mice is related to the complexity of the mammalian community such that pathogen prevalence is lower in more diverse communities. Using a combination of techniques, we found evidence that contact rates between deer mice differ with respect to biodiversity. Deer mice in more complex communities had fewer intraspecific interactions than those in less diverse communities. Contact rates of individual deer mice were highly variable with a minority of the deer mice accounting for a majority of the interactions. Infection with SNV was related to risk-taking behavior; animals categorized as “bold” were 3 times more likely to be infected than “shy” deer mice. Results of these studies have implications for pathogen management in wildlife and humans.

Why is the Four Corners a hotspot for hantavirus?

Sin Nombre virus (SNV) is a hantavirus hosted almost exclusively by deer mice (Peromyscus maniculatus) that causes high (∼40%) mortality in humans. Transmission patterns of SNV in natural host populations are not well understood and, as such, represent a knowledge gap that has significant implications for human health. Since its identification in the early 1990s, the Four Corners region of the southwestern United States (i.e. geographic area encompassing southeastern UT, northeastern AZ, southwestern CO and northwestern NM) has remained a “hotspot” for SNV infections in both deer mice and humans; however, the reason for this skewed geographic distribution of SNV remains unclear. Therefore, our objective was to observe regional patterns of SNV prevalence in deer mice along a latitudinal gradient in the Four Corners region and determine the extent to which prevalence is influenced by factors including deer mouse density, small mammal diversity, vegetation cover, plant moisture content, soil pH and soil water content. Although we did not find a significant correlation between SNV prevalence and small mammal species diversity, SNV prevalence and deer mouse density were positively correlated. We found no relationship between soil pH and SNV prevalence; however, there was a strong negative correlation between SNV prevalence and soil water content. We also found strong positive correlations between SNV prevalence and total vegetation cover and between SNV prevalence and plant moisture content. Collectively, our results suggest that SNV prevalence is driven primarily by increased deer mouse densities and that deer mice are more likely to be associated with habitats that have higher plant moisture content, as well as greater total vegetation cover. Our results also indicate that, whereas soil pH is not a direct predictor of SNV prevalence, sites with dry soils at pH levels close to the optimal for SNV (6.9) that also contain high densities of deer mice may be hantavirus “hot spots”.

The Interplay of Plant and Animal Disease in a Changing Landscape: The Role of Sudden Aspen Decline in Moderating Sin Nombre Virus Prevalence in Natural Deer Mouse Populations

We examined how climate-mediated forest dieback regulates zoonotic disease prevalence using the relationship between sudden aspen decline (SAD) and Sin Nombre virus (SNV) as a model system. We compared understory plant community structure, small mammal community composition, and SNV prevalence on 12 study sites within aspen forests experiencing levels of SAD ranging from <10.0% crown fade to >95.0% crown fade. Our results show that sites with the highest levels of SAD had reduced canopy cover, stand density, and basal area, and these differences were reflected by reductions in understory vegetation cover. Conversely, sites with the highest levels of SAD had greater understory standing biomass, suggesting that vegetation on these sites was highly clustered. Changes in forest and understory vegetation structure likely resulted in shifts in small mammal community composition across the SAD gradient, as we found reduced species diversity and higher densities of deer mice, the primary host for SNV, on sites with the highest levels of SAD. Sites with the highest levels of SAD also had significantly greater SNV prevalence compared to sites with lower levels of SAD, which is likely a result of their abundance of deer mice. Collectively, results of our research provide strong evidence to show SAD has considerable impacts on vegetation community structure, small mammal density and biodiversity and the prevalence of SNV.

Biogeographic and Ecological Regulation of Disease: Prevalence of Sin Nombre Virus in Island Mice Is Related to Island Area, Precipitation, and Predator Richness

The relative roles of top-down and bottom-up forces in affecting disease prevalence in wild hosts is important for understanding disease dynamics and human disease risk. We found that the prevalence of Sin Nombre virus (SNV), the agent of a severe disease in humans (hantavirus pulmonary syndrome), in island deer mice from the eight California Channel Islands was greater with increased precipitation (a measure of productivity), greater island area, and fewer species of rodent predators. In finding a strong signal of the ecological forces affecting SNV prevalence, our work highlights the need for future work to understand the relative importance of average rodent density, population fluctuations, behavior, and specialist predators as they affect SNV prevalence. In addition to illustrating the importance of both bottom-up and top-down limitation of disease prevalence, our results suggest that predator richness may have important bearing on the risk of exposure to animal-borne diseases that affect humans.

Using MODIS satellite imagery to predict hantavirus risk

Aims Sin Nombre virus (SNV), a strain of hantavirus, causes hantavirus pulmonary syndrome (HPS) in humans, a deadly disease with high mortality rate (> 50%). The primary virus host is the deer mouse, and greater abundance of deer mice has been shown to increase the human risk of HPS. Our aim is to identify and compare vegetation indices and associated time lags for predicting hantavirus risk using remotely sensed imagery. Location Utah, USA. Methods A 5-year time-series of moderate-resolution imaging spectroradiometer (MODIS) satellite imagery and corresponding field data was utilized to compare various vegetation indices that measure productivity with the goal of indirectly estimating mouse abundance and SNV prevalence. Relationships between the vegetation indices and deer mouse density, SNV prevalence and the number of infected deer mice at various time lags were examined to assess which indices and associated time lags might be valuable in predicting SNV outbreaks. Results The results reveal varying levels of positive correlation between the vegetation indices and deer mouse density as well as the number of infected deer mice. Among the vegetation indices, the normalized difference vegetation index (NDVI) and the enhanced vegetation index (EVI) produced the highest correlations with deer mouse density and the number of infected deer mice using a time lag of 1.0 to 1.3 years for May and June imagery. Main conclusions This study demonstrates the potential for using MODIS time-series satellite imagery in estimating deer mouse abundance and predicting hantavirus risk. The 1-year time lag provides a great opportunity to apply satellite imagery to predict upcoming SNV outbreaks, allowing preventive strategies to be adopted. Analysis of different predictive indices and lags could also be valuable in identifying the time windows for data collection for practical uses in monitoring rodent abundance and subsequent disease risk to humans.

The Relative Abundance of Deer Mice with Antibody to Sin Nombre Virus Corresponds to the Occurrence of Hantavirus Pulmonary Syndrome in Nearby Humans

Sin Nombre virus (SNV) is the principal cause of hantavirus pulmonary syndrome (HPS) in the United States and deer mice (Peromyscus maniculatus) are its principal rodent host, and thus the natural cycle of the virus is related to the occurrence of HPS. Prevalence of rodent infection appears to be associated with fluctuations in deer mouse populations and, indirectly, with timing and amount of precipitation, a complex of biologic events. Given that rodent population abundances fluctuate, often acutely, it is not unreasonable to assume a direct correlation between the numbers of infected rodents and the number of human infections, unless confounding factors are involved. During a 13-year longitudinal study at a site in southwestern Colorado, we accumulated data regarding deer mice and antibody to SNV and therefore had the opportunity to compare dynamics of deer mouse populations, seroprevalence of antibody to SNV in the rodents, and numbers of HPS cases in Durango and in the State of Colorado as a whole. If abundances of deer mouse populations are directly correlated with occurrence of HPS, it is reasonable to assume that low densities of deer mice and low prevalences of antibody to SNV would lead to fewer human cases than would high densities and high prevalences. Our results substantiate such an assumption and suggest that the risk of acquisition of HPS is likely related to both high numbers of infected deer mice and human activities, rather than being strictly related to prevalence of SNV in the host rodent.

Sin nombre virus and rodent species diversity: a test of the dilution and amplification hypotheses.

BackgroundSpecies diversity is proposed to greatly impact the prevalence of pathogens. Two predominant hypotheses, the “Dilution Effect” and the “Amplification Effect”, predict divergent outcomes with respect to the impact of species diversity. The Dilution Effect predicts that pathogen prevalence will be negatively correlated with increased species diversity, while the Amplification Effect predicts that pathogen prevalence will be positively correlated with diversity. For many host-pathogen systems, the relationship between diversity and pathogen prevalence has not be empirically examined.Methodology/Principal FindingsWe tested the Dilution and Amplification Effect hypotheses by examining the prevalence of Sin Nombre virus (SNV) with respect to diversity of the nocturnal rodent community. SNV is directly transmitted primarily between deer mice (Peromyscus maniculatus). Using mark-recapture sampling in the Spring and Fall of 2003–2005, we measured SNV prevalence in deer mice at 16 landscape level sites (3.1 hectares each) that varied in rodent species diversity. We explored several mechanisms by which species diversity may affect SNV prevalence, including reduced host density, reduced host persistence, the presence of secondary reservoirs and community composition. We found a negative relationship between species diversity and SNV prevalence in deer mice, thereby supporting the Dilution Effect hypothesis. Deer mouse density and persistence were lower at sites with greater species diversity; however, only deer mouse persistence was positively correlated with SNV prevalence. Pinyon mice (P. truei) may serve as dilution agents, having a negative effect on prevalence, while kangaroo rats (Dipodomys ordii), may have a positive effect on the prevalence of SNV, perhaps through effects on deer mouse behavior.Conclusions/SignificanceWhile previous studies on host-pathogen systems have found patterns of diversity consistent with either the Dilution or Amplification Effects, the mechanisms by which species diversity influences prevalence have not been investigated. Our study indicates that changes in host persistence, coupled with interspecific interactions, are important mechanisms through which diversity may influence patterns of pathogens. Our results reveal the complexity of rodent community interactions with respect to SNV dynamics.

Testing Mechanisms of the Dilution Effect: Deer Mice Encounter Rates, Sin Nombre Virus Prevalence and Species Diversity

Species diversity has been shown to decrease prevalence of disease in a variety of host-pathogen systems, in a phenomenon termed the Dilution Effect. Several mechanisms have been proposed by which diversity may decrease prevalence, though few have been tested in natural host-pathogen systems. We investigated the mechanisms by which diversity influenced the prevalence of Sin Nombre virus (SNV), a directly transmitted virus in deer mice (Peromyscus maniculatus). We monitored both intra and interspecific encounters of deer mice using foraging arenas at five sites in the Great Basin Desert with disparate levels of species diversity to examine two potential mechanisms which may contribute to the dilution of SNV prevalence: (1) reduced frequency of encounters between deer mice, or (2) reduced duration of contacts between deer mice. We also investigated the relationship between deer mouse density and these mechanisms, as density is often predicted to influence both inter and intraspecific encounters. Results of our study indicate that frequency of intraspecific interactions between deer mice was reduced with increased diversity. Species diversity did not impact average duration of encounters. Density was correlated with absolute, but not relative rates of encounters between deer mice, suggesting that encounters may be influenced by factors other than density. Our study indicates that species diversity influences the dynamics of SNV by reducing encounters between deer mice in a trade-off between intra and interspecific interactions.

The Role of Heterogeneity in the Persistence and Prevalence of Sin Nombre Virus in Deer Mice

Many diseases persist at a relatively low prevalence, seemingly close to extinction. For a chronic disease in a homogeneous population, reducing the transmission rate by a fraction proportional to the prevalence would be sufficient to eradicate the disease. This study examines how higher prevalence of the Sin Nombre virus in male deer mice (Peromyscus maniculatus) might contribute to disease persistence. Analyzing data from over 2,000 individual mice captured in 19 sites over 4 years, we found prevalences of 18.5% in males and 8.8% in females. By examining recaptures, we determined that males are more likely to contract the infection because of higher susceptibility or higher encounter rates. Comparing across 86 sampling periods, we found a higher proportion of males when population densities were low. A capture-recapture analysis indicates that males live longer than females. A mathematical model based on the measured parameters and population size trajectories suggests that the combined heterogeneity in encounters, susceptibility, and mortality may buffer the disease from extinction by concentrating disease in the subgroup most likely to transmit the disease. This buffering effect is not significantly stronger in a fluctuating population, indicating that these forms of heterogeneity might not be the key for disease persistence through host population bottlenecks.

Differential regulation of pathogens: the role of habitat disturbance in predicting prevalence of Sin Nombre virus

Deer mice (Peromyscus maniculatus) are the primary reservoir for Sin Nombre virus (SNV), a North American hantavirus that causes disease with high mortality in humans. Recent studies have proposed that habitat disturbance affects prevalence of SNV in deer mice; however, the outcomes proposed in these studies are in opposition to each other. Our objectives were to test these divergent hypotheses by: (1) measuring SNV infection in deer mice within a patchwork of disturbance; and (2) evaluating the relationships between SNV prevalence, population density and demography as possible mechanisms. In 2003 and 2004, we sampled 1,297 deer mice from 17 sites with varying levels of disturbance in the Great Basin Desert. Across sites and years, SNV prevalence varied from 0.0 to 38.9%. We found a negative relationship between SNV prevalence and disturbance. Although we found no direct relationship between SNV prevalence and deer mouse density, we found that density was highest on sites with the lowest levels of disturbance. The number of deer mice that survived across seasons (e.g., trans-seasonal survivors) differed across levels of disturbance and was greatest on our least disturbed study sites [Formula: see text] moderate on sites with intermediate levels of disturbance (x = 5.61%) and zero on highly disturbed sites. On low-disturbance sites, a greater proportion of trans-seasonal survivors were SNV seropositive (28.80%) compared to the intermediate-disturbance sites (16.67). Collectively, our results indicate that habitat disturbance plays a predictive role in SNV prevalence, with highly disturbed sites having reduced long-term survival of deer mice, including survival of infected individuals.

PERSISTENTLY HIGHEST RISK AREAS FOR HANTAVIRUS PULMONARY SYNDROME: POTENTIAL SITES FOR REFUGIA

Interannual variation in the number of cases of human disease caused by hantaviruses in North America has been hypothesized to reflect environmental changes that influence rodent reservoir populations. This hypothesis postulates that when cases are rare reservoir populations are geographically restricted in patches of suitable habitat. Identifying these sites, which is needed to test the hypothesis, has proven to be a challenge. Satellite imagery of the U.S. Southwest has shown associations among the likelihood of human hantaviral disease and increases in the rodent populations, as well as increased prevalence of Sin Nombre virus (SNV) in rodent populations. In this study we characterize local areas that had environmental signatures that persisted as predicted highest risk sites for human disease through much of the 1990s. These areas represent a small percentage (0.3%) of the region. Exploratory analyses indicate that these areas were not randomly distributed, but were associated with certain landscape characteristics. Characteristics of elevation, slope, aspect, and land cover were associated with persistent high risk. Using multivariate Poisson regression to control for confounding effects, sites with deciduous- or mixed-forest land cover on moderate to steep slopes (>5 degrees) above 2130 m elevation were associated with increasing numbers of years at highest risk. These are candidate locations for refugia. Sites associated with cleared ground or shrubland were less often associated with high risk compared to reference conditions. The seasonal patterns of vegetation growth in persistently high-risk areas were compared to matched locations using MODIS (moderate resolution imaging spectroradiometer) NDVI (normalized difference vegetation index) during a time of a severe drought in the region from 2002 to 2004. Despite the drought and regardless of land cover, the NDVI in persistently highest risk areas had an early onset, with significantly higher levels of green vegetation that lasted longer than at comparable sites. These observations identify locations that can be monitored for the abundance of P. maniculatus and presence of SNV. If these sites are refugia, we predict they will be occupied by infected deer mice when other monitored sites are unoccupied.

Population dynamics of the deer mouse (Peromyscus maniculatus) and Sin Nombre virus, California Channel Islands.

Hantavirus pulmonary syndrome, first documented in 1993, is caused by Sin Nombre virus (SNV), which is carried by the Peromyscus species. In 1994, high SNV antibody prevalence was identified in deer mice from two California Channel Islands. We sampled two locations on three islands to estimate mouse population density and SNV prevalence. Population flux and SNV prevalence appear to vary independently.