The Experts below are selected from a list of 1659 Experts worldwide ranked by ideXlab platform
Stephen St Jeor - One of the best experts on this subject based on the ideXlab platform.
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long term patterns of immune investment by wild deer mice infected with Sin Nombre Virus
Physiological and Biochemical Zoology, 2010Co-Authors: Erin M Lehmer, Stephen St Jeor, Mariana G Bego, Christine A Clay, Jeremy D. Jones, Johanna Varner, Denise DearingAbstract:Abstract Immunocompetence of animals fluctuates seasonally, However, there is little consensus on the cause of these fluctuations. Some studies have suggested that these patterns are influenced by changes in reproductive condition, whereas others have suggested that differences result from seasonal variations in energy expenditures. The objective of our study was to examine these contrasting views of immunity by evaluating seasonal patterns of immune response and reproduction in wild populations of deer mice Peromyscus maniculatus exposed to Sin Nombre Virus (SNV). Over three consecutive fall (September, October, November) and three consecutive spring (March, April, May) sampling periods, we used titration enzyme‐linked immunosorbent assay (ELISA) to quantify Virus‐specific antibody production in 48 deer mice infected with SNV. Levels of reproductive hormones were quantified uSing ELISA. SNV antibody titers reached their lowest level during November (geometric mean titer \documentclass{aastex} \usepackage...
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Sin Nombre Virus and rodent species diversity a test of the dilution and amplification hypotheses
PLOS ONE, 2009Co-Authors: Christine A Clay, Stephen St Jeor, Erin M Lehmer, Denise DearingAbstract:Background Species 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 Findings We 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/Significance While 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.
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testing mechanisms of the dilution effect deer mice encounter rates Sin Nombre Virus prevalence and species diversity
Ecohealth, 2009Co-Authors: Christine A Clay, Stephen St Jeor, Erin M Lehmer, Denise DearingAbstract: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 inves- tigated 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 preva- lence: (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.
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contact heterogeneity in deer mice implications for Sin Nombre Virus transmission
Proceedings of The Royal Society B: Biological Sciences, 2009Co-Authors: Christine A Clay, Stephen St Jeor, Erin M Lehmer, Andrea Previtali, Denise DearingAbstract:Heterogeneities within disease hosts suggest that not all individuals have the same probability of transmitting disease or becoming infected. This heterogeneity is thought to be due to dissimilarity in susceptibility and exposure among hosts. As such, it has been proposed that many host–pathogen systems follow the general pattern whereby a small fraction of the population accounts for a large fraction of the pathogen transmission. This disparity in transmission dynamics is often referred to as ‘20/80 Rule’, i.e. approximately 20 per cent of the hosts are responsible for 80 per cent of pathogen transmission. We investigated the role of heterogeneity in contact rates among potential hosts of a directly transmitted pathogen by examining Sin Nombre Virus (SNV) in deer mice (Peromyscus maniculatus). USing foraging arenas and powder marking, we documented contacts between wild deer mice in Great BaSin Desert, central Utah. Our findings demonstrated heterogeneity among deer mice, both in frequency and in duration of contacts with other deer mice. Contact dynamics appear to follow the general pattern that a minority of the population accounts for a majority of the contacts. We found that 20 per cent of individuals in the population were responsible for roughly 80 per cent of the contacts observed. Larger-bodied individuals appear to be the functional group with the greatest SNV transmission potential. Contrary to our predictions, transmission potential was not influenced by breeding condition or sex.
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development of an elisa to detect Sin Nombre Virus specific igm from deer mice peromyscus maniculatus
Journal of Virological Methods, 2008Co-Authors: Mariana G Bego, Darcy Bawiec, Deepa Dandge, Benjamin Martino, Denise Dearing, Eric Wilson, Stephen St JeorAbstract:Peromyscus maniculatus (deer mouse) is the primary reservoir for Sin Nombre Virus (SNV). Although the presence of IgG antibodies is often used as a marker of infection, it provides little information on active infections in a population but usually is an indicator of past infections. The presence of IgM antibodies is a much better marker for determining whether active infections are present in a population. A -capture SNV-specific IgM enzyme linked immunosorbent assay (ELISA) was developed. From live-trap and release studies a total of 68 rodent sera were studied for the presence of Sin Nombre Virus-specific IgG and IgM antibodies. In these studies, IgM responses were detected in a number of animals. In some cases early SNV infection was determined through the presence of anti-SNV IgM before IgG antibodies could be detected. From the set of animals analyzed, it was concluded that the IgM response against SNV can persist anywhere from 1 to up to over 2 months, with a median of less than 1 month. Most importantly, it was demonstrated that anti-Sin Nombre Virus IgM is an important tool for detection of early infections in rodents and should be considered as a key diagnostic tool. © 2008 Elsevier B.V. All rights reserved.
Brian Hjelle - One of the best experts on this subject based on the ideXlab platform.
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Occupational Exposure Leading to HantaVirus Pulmonary Syndrome in a Utility Company Employee
2016Co-Authors: Michele Jay, Brian Hjelle, Richard Davis, Michael Ascher, Nicholas H. Baylies, Kevin Reilly, Due VugiaAbstract:HantaVirus pulmonary syndrome is a newly recognized rodent-borne zoonosis. We report a case of hantaVirus pulmonary syndrome in an employee of a California utility company who was probably occupationally exposed to Sin Nombre Virus. Environmental assessment and genetic comparison of the patient's hantaVirus isolates to hantaVirus isolates from rodents trapped at possible sites of exposure suggested that the patient contracted his infection at the work site. The study revealed a close correspondence between the patient's viral genotype and that from a rodent trapped at the work site. This report alerts the public health and medical community to the fact that employees of utility companies and similar industries may be an important risk group in areas where hantaVirus is endemic and emphasizes the need to incorporate strategies for preventing exposure to hantaVirus and other emerging infections into occupational safety protocols. Since hantaVirus pulmonary syndrome (HPS) was discovered during an investigation of an outbreak in the southwestern United States during 1993, sporadic cases have been reported throughout much of the country [1]. Studies show that the vector of Sin Nombre Virus (SNV) in the western United State
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elevated cytokines thrombin and pai 1 in severe hcps patients due to Sin Nombre Virus
Viruses, 2015Co-Authors: Virginie Bondu, Brian Hjelle, Ronald Schrader, Mary Ann Gawinowicz, Paul G Mcguire, Daniel A Lawrence, Tione BurandaAbstract:Sin Nombre HantaVirus (SNV, Bunyaviridae HantaVirus) is a Category A pathogen that causes HantaVirus Cardiopulmonary Syndrome (HCPS) with case fatality ratios generally ranging from 30% to 50%. HCPS is characterized by vascular leakage due to dysregulation of the endothelial barrier function. The loss of vascular integrity results in non-cardiogenic pulmonary edema, shock, multi-organ failure and death. USing Electric Cell-substrate Impedance SenSing (ECIS) measurements, we found that plasma samples drawn from University of New Mexico Hospital patients with serologically-confirmed HCPS, induce loss of cell-cell adhesion in confluent epithelial and endothelial cell monolayers grown in ECIS cultureware. We show that the loss of cell-cell adhesion is sensitive to both thrombin and plasmin inhibitors in mild cases, and to thrombin only inhibition in severe cases, suggesting an increaSing prothrombotic state with disease severity. A proteomic profile (2D gel electrophoresis and mass spectrometry) of HCPS plasma samples in our cohort revealed robust antifibrinolytic activity among terminal case patients. The prothrombotic activity is highlighted by acute ≥30 to >100 fold increases in active plasminogen activator inhibitor (PAI-1) which, preceded death of the subjects within 48 h. Taken together, this suggests that PAI-1 might be a response to the severe pathology as it is expected to reduce plasmin activity and possibly thrombin activity in the terminal patients.
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kinetics of immune responses in deer mice experimentally infected with Sin Nombre Virus
Journal of Virology, 2012Co-Authors: Tony Schountz, Joseph Prescott, Fernando Torresperez, William C Black, Mariana Acunaretamar, Shira Feinstein, Brendan K Podell, Staci Peters, Brian HjelleAbstract:Deer mice are the principal reservoir hosts of Sin Nombre Virus, the etiologic agent of most hantaVirus cardiopulmonary syndrome cases in North America. Infection of deer mice results in persistence without conspicuous pathology, and most, if not all, infected mice remain infected for life, with periods of viral shedding. The kinetics of viral load, histopathology, Virus distribution, and immune gene expression in deer mice were examined. Viral antigen was detected as early as 5 days postinfection and peaked on day 15 in the lungs, hearts, kidneys, and livers. Viral RNA levels varied substantially but peaked on day 15 in the lungs and heart, and antinucleocapsid IgG antibodies appeared in some animals on day 10, but a strong neutralizing antibody response failed to develop during the 20-day experiment. No clinical signs of disease were observed in any of the infected deer mice. Most genes were repressed on day 2, suggesting a typical early downregulation of gene expression often observed in viral infections. Several chemokine and cytokine genes were elevated, and markers of a T cell response occurred but then declined days later. Splenic transforming growth factor beta (TGF-β) expression was elevated early in infection, declined, and then was elevated again late in infection. Together, these data suggest that a subtle immune response that fails to clear the Virus occurs in deer mice.
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Sin Nombre Virus infection in field workers colorado usa
Emerging Infectious Diseases, 2010Co-Authors: Fernando Torresperez, Linda Wilson, Sharon K Collinge, Heath Harmon, Chris Ray, Rafael A Medina, Brian HjelleAbstract:We report 2 cases of Sin Nombre Virus (SNV) infection in field workers, possibly contracted through rodent bites. Screening for antibodies to SNV in rodents trapped in 2 seasons showed that 9.77% were seropositive. Quantitative real-time PCR showed that 2 of 79 deer mice had detectable titers of SNV RNA.
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regulatory t cell like responses in deer mice persistently infected with Sin Nombre Virus
Proceedings of the National Academy of Sciences of the United States of America, 2007Co-Authors: Tony Schountz, Joseph Prescott, Katy Mirowskygarcia, Ann C Cogswell, Lauren Oko, Alejandra P Galvez, Brian HjelleAbstract:HantaVirus cardiopulmonary syndrome is a zoonotic illness associated with a systemic inflammatory immune response, capillary leak, noncardiogenic pulmonary edema, and shock in humans. Cytokines, including TNF, IFN-γ, and lymphotoxin, are thought to contribute to its pathogenesis. In contrast, infected rodent reservoirs of hantaViruses experience few or no pathologic changes and the host rodent can remain persistently infected for life. Generally, it is unknown why such dichotomous immune responses occur between humans and reservoir hosts. Thus, we examined CD4+ T cell responses from one such reservoir, the deer mouse (Peromyscus maniculatus), infected with Sin Nombre Virus. Proliferation responses to viral nucleocapsid antigen were relatively weak in T cells isolated from deer mice, regardless of acute or persistent infection. The T cells from acutely infected deer mice synthesized a broad spectrum of cytokines, including IFN-γ, IL-4, IL-5, and TGF-β1, but not TNF, lymphotoxin, or IL-17. However, in T cells from persistently infected deer mice, only TGF-β1 was expressed by all lines, whereas some expressed reduced levels of IFN-γ or IL-5. The Forkhead box P3 transcription factor, a marker of some regulatory T cells, was expressed by most of these cells. Collectively, these data suggest that TGF-β1-expresSing regulatory T cells may play an important role in limiting immunopathology in the natural reservoir host, but this response may interfere with viral clearance. Such a response may have arisen as a mutually beneficial coadaptive evolutionary event between hantaViruses and their rodent reservoirs, so as to limit disease while also allowing the Virus to persist.
Denise Dearing - One of the best experts on this subject based on the ideXlab platform.
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Appendix A. Sin Nombre Virus prevalence and total deer mice captured at 17 sites that differed in their degree of disturbance caused by off-road vehicles.
2016Co-Authors: Andrea M. Previtali, Erin M Lehmer, Christine A Clay, Jessica M. C. Pearce-duvet, Jeremy D. Jones, Britta A. Wood, Patrick W. Ely, Sean M. Laverty, Denise DearingAbstract:Sin Nombre Virus prevalence and total deer mice captured at 17 sites that differed in their degree of disturbance caused by off-road vehicles
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long term patterns of immune investment by wild deer mice infected with Sin Nombre Virus
Physiological and Biochemical Zoology, 2010Co-Authors: Erin M Lehmer, Stephen St Jeor, Mariana G Bego, Christine A Clay, Jeremy D. Jones, Johanna Varner, Denise DearingAbstract:Abstract Immunocompetence of animals fluctuates seasonally, However, there is little consensus on the cause of these fluctuations. Some studies have suggested that these patterns are influenced by changes in reproductive condition, whereas others have suggested that differences result from seasonal variations in energy expenditures. The objective of our study was to examine these contrasting views of immunity by evaluating seasonal patterns of immune response and reproduction in wild populations of deer mice Peromyscus maniculatus exposed to Sin Nombre Virus (SNV). Over three consecutive fall (September, October, November) and three consecutive spring (March, April, May) sampling periods, we used titration enzyme‐linked immunosorbent assay (ELISA) to quantify Virus‐specific antibody production in 48 deer mice infected with SNV. Levels of reproductive hormones were quantified uSing ELISA. SNV antibody titers reached their lowest level during November (geometric mean titer \documentclass{aastex} \usepackage...
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Sin Nombre Virus and rodent species diversity a test of the dilution and amplification hypotheses
PLOS ONE, 2009Co-Authors: Christine A Clay, Stephen St Jeor, Erin M Lehmer, Denise DearingAbstract:Background Species 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 Findings We 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/Significance While 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.
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testing mechanisms of the dilution effect deer mice encounter rates Sin Nombre Virus prevalence and species diversity
Ecohealth, 2009Co-Authors: Christine A Clay, Stephen St Jeor, Erin M Lehmer, Denise DearingAbstract: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 inves- tigated 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 preva- lence: (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.
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contact heterogeneity in deer mice implications for Sin Nombre Virus transmission
Proceedings of The Royal Society B: Biological Sciences, 2009Co-Authors: Christine A Clay, Stephen St Jeor, Erin M Lehmer, Andrea Previtali, Denise DearingAbstract:Heterogeneities within disease hosts suggest that not all individuals have the same probability of transmitting disease or becoming infected. This heterogeneity is thought to be due to dissimilarity in susceptibility and exposure among hosts. As such, it has been proposed that many host–pathogen systems follow the general pattern whereby a small fraction of the population accounts for a large fraction of the pathogen transmission. This disparity in transmission dynamics is often referred to as ‘20/80 Rule’, i.e. approximately 20 per cent of the hosts are responsible for 80 per cent of pathogen transmission. We investigated the role of heterogeneity in contact rates among potential hosts of a directly transmitted pathogen by examining Sin Nombre Virus (SNV) in deer mice (Peromyscus maniculatus). USing foraging arenas and powder marking, we documented contacts between wild deer mice in Great BaSin Desert, central Utah. Our findings demonstrated heterogeneity among deer mice, both in frequency and in duration of contacts with other deer mice. Contact dynamics appear to follow the general pattern that a minority of the population accounts for a majority of the contacts. We found that 20 per cent of individuals in the population were responsible for roughly 80 per cent of the contacts observed. Larger-bodied individuals appear to be the functional group with the greatest SNV transmission potential. Contrary to our predictions, transmission potential was not influenced by breeding condition or sex.
Erin M Lehmer - One of the best experts on this subject based on the ideXlab platform.
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evaluating the impacts of coinfection on immune system function of the deer mouse peromyscus maniculatus uSing Sin Nombre Virus and bartonella as model pathogen systems
Journal of Wildlife Diseases, 2018Co-Authors: Erin M Lehmer, Kathryn Lavengood, Mason Miller, Jacob Rodgers, Steven D FensterAbstract:ABSTRACT: Simultaneous infections with multiple pathogens can alter the function of the host's immune system, often resulting in additive or synergistic morbidity. We examined how coinfection with the common pathogens Sin Nombre Virus (SNV) and Bartonella sp. affected aspects of the adaptive and innate immune responses of wild deer mice (Peromyscus maniculatus). Adaptive immunity was assessed by measuring SNV antibody production; innate immunity was determined by measuring levels of C-reactive protein (CRP) in blood and the complement activity of plasma. Coinfected mice had reduced plasma complement activity and higher levels of CRP compared to mice infected with either SNV or Bartonella. However, antibody titers of deer mice infected with SNV were more than double those of coinfected mice. Plasma complement activity and CRP levels did not differ between uninfected deer mice and those infected with only Bartonella, suggesting that comorbid SNV and Bartonella infections act synergistically, altering the i...
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Appendix A. Sin Nombre Virus prevalence and total deer mice captured at 17 sites that differed in their degree of disturbance caused by off-road vehicles.
2016Co-Authors: Andrea M. Previtali, Erin M Lehmer, Christine A Clay, Jessica M. C. Pearce-duvet, Jeremy D. Jones, Britta A. Wood, Patrick W. Ely, Sean M. Laverty, Denise DearingAbstract:Sin Nombre Virus prevalence and total deer mice captured at 17 sites that differed in their degree of disturbance caused by off-road vehicles
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how can hantaViruses kill humans but leave deer mice unaffected an evaluation of the immune response of deer mice to Sin Nombre Virus
Bios, 2012Co-Authors: Nellie Mclean, Tony Schountz, Joni Ghachu, Lacey Hart, Colleen Obrien, Kimberly Wright, Ashley Kelly, Edlin Molinar, Cathy Hartney, Erin M LehmerAbstract:Sin Nombre Virus (SNV) causes hantaVirus pulmonary syndrome (HPS) in humans, a disease with high (∼36%) mortality. Deer mice (Peromyscus maniculatus) are the primary host of SNV and, unlike humans, deer mice infected with SNV have few overt signs of disease. The reasons for such mild infections in deer mice have not been well studied; however, this information may be useful in uncovering therapies that could reduce human HPS mortality. Therefore, the objective of this study was to evaluate the immune response of deer mice to SNV by examining their patterns of white blood cell production. We quantified the number of lymphocytes, eoSinophils, basophils, neutrophils, and monocytes produced by wild deer mice in both the early and late stages of SNV infection. Deer mice captured in the early season had greater basophil, lymphocyte, and eoSinophil levels compared to deer mice captured in the late season. Conversely, monocyte levels were greater in deer mice captured in the late season. SNV infection status appeared to influence production of both neutrophils and monocytes, with SNV-infected mice having greater neutrophil levels but lower monocyte levels than uninfected mice. Collectively, the results seem to support the notion that immune stressors faced by wild deer mice shift from early to late season, and these differences are reflected by differential leukocyte production that occurs across seasons. Furthermore, our results indicate some potential differences between wild deer mice and lab-bred deer mice, as well as some possible similarities between wild deer mice and humans in their immune responses to SNV infection.
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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
Ecohealth, 2012Co-Authors: Erin M Lehmer, Nellie Mclean, Joni Ghachu, Lacey Hart, Colleen Obrien, Ashley Kelly, Julie E Korb, Sara P Bombaci, Edlin Jaramolinar, Kimberly WrightAbstract: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 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.
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the relationship between seasonal stressors and innate immunity in wild deer mice chronically infected with Sin Nombre Virus
2012Co-Authors: Sherry A Paddock, Alena G Simpkiss, Nellie Mclean, Erin M LehmerAbstract:HantaViruses are found throughout the world, but the Sin Nombre strain is highly prevalent in the Southwest region of the United States. Sin Nombre Virus (SNV) is a rodent-borne zoonotic pathogen that causes HantaVirus Pulmonary Syndrome (HPS) in humans, a disease with exceptionally high (~40%) mortality rates. The primary reservoir for SNV is the deer mouse (Peromyscus maniculatus). Once infected with SNV, deer mice remain infected for life but exhibit few symptoms. Despite these apparently asymptomatic infections, the extent to which SNV infection impacts the ability of deer mice to respond to other pathogens is unknown. Likewise, it is unknown how the immune response to SNV changes across seasons within individual deer mice. Fluctuations in immunocompetence could have important implications for human health, as deer mice with suppressed immune systems are more likely to shed SNV in urine and feces, thus increaSing the risk of human infection. Therefore, the objective of our study was to determine whether deer mice differentially allocate immune resources during seasonally stressful periods, like reproduction. As part of this study, we conducted a capture-mark-recapture study in which we live-trapped three populations of deer mice monthly from April to November 2011. Upon capture, we collected blood samples from individual deer mice and recorded basic demographic information (reproductive status, sex, age, body mass, presence of ectoparasites). In the lab we used blood samples to screen for infection with SNV. We determined innate immunocompetence by culturing deer mouse serum with E-coli and quantifying the number of E-coli colonies killed by antibacterial agents within the serum. Our results indicated that the immunocompetence of deer mice infected with SNV is compromised due to seasonal stressors. This suggests when confronted with other pathogens, infected deer mice will have a weakened immune response in comparison to their non-infected counterparts.
C. J. Peters - One of the best experts on this subject based on the ideXlab platform.
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Evidence Against Person-to-Person Transmission of HantaVirus to Health Care Workers
2016Co-Authors: Charles R. Vitek, Thomas G Ksiazek, Robert F. Breiman, James C. Mclaughlin, Edith T. Uml, Kurt B. Nolte, Arnold Loera, Mack C. Sewell, C. J. PetersAbstract:Unusual, primarily pulmonary, manifestations of hantaviral illness occurring in the southwestern United States raised the possibilityof person-to-person transmission of a recently recognized hantavi-rus, Sin Nombre Virus. To determine whether such transmission had occurred among health care workers (HCWs) exposed to patients with confirmed hantaVirus pulmonary syndrome, we evaluated HCWs who had cared for patients with hantaVirus pulmonary syndrome or who had processed specimens from these patients. Information about exposure to these patients and about recent illnesses was obtained via a standardized questionnaire. Serum specimens were tested for IgM and IgG antibodies to hantaViruses with use of ELISAs. Of the 396 HCWs, 266 (67%) reported that they had been exposed to patients with hantaVirus pulmonary syndrome or to their body fluids or that they had processed laboratory specimens from these patients. Although 108(27%) of the HCWs reported fever, myalgias, or respiratory illnesses during the 3 months before the serum specimens were obtained, hantaVirus antibodies were not detected in any HCW. These data suggest that person-to-person transmission of Sin Nombre Virus is unlikely to occur in health care settings. An investigation of a cluster of cases of adult respiratory distress syndrome occurring in the spring of 1993 among pre
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Sin Nombre Virus glycoprotein trafficking
Virology, 2003Co-Authors: Christina F Spiropoulou, C. J. Peters, Cynthia S Goldsmith, Trevor Shoemaker, Richard W CompansAbstract:Abstract Sin Nombre Virus (SNV) is a major representative of the New World hantaViruses and the most common cause of hantaVirus pulmonary syndrome (HPS) with high mortality in North America. Unlike other members of the family Bunyaviridae which mature in the Golgi complex, New World hantaViruses have been previously reported to mature at the cell surface. For family Bunyaviridae Viruses, retention of the viral glycoproteins at the Golgi complex is thought to be responsible for their Golgi maturation. In our studies, the majority of SNV glycoproteins, G1 and G2, was localized in the Golgi complex when expressed from a full-length GPC clone or in SNV-infected cells, in agreement with data for other members of the family Bunyaviridae, including the Old World hantaViruses. However, the SNV glycoproteins could also be detected at the cell surface at advanced posttransfection or postinfection time points. G1 expressed in the absence of G2 did not accumulate in the Golgi, but remained predominantly associated with the endoplasmic reticulum (ER). Overexpressed amounts of apparently misfolded G1 were aggregated in a subcellular compartment likely to represent the aggresome. Unexpectedly, an additional major pool of G1 was detected intracellularly in SNV-infected and GPC-expresSing transfected cells, by uSing a SNV G1-specific Fab antibody. This pool of G1 is predominantly localized in late endosomes–lysosomes.
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satellite imagery characterizes local animal reservoir populations of Sin Nombre Virus in the southwestern united states
Proceedings of the National Academy of Sciences of the United States of America, 2002Co-Authors: Gregory E Glass, C. J. Peters, Terry L Yates, Joshua B Fine, Timothy M Shields, John B Kendall, Andrew G Hope, Cheryl A Parmenter, Thomas G Ksiazek, Jonathan A PatzAbstract:The relationship between the risk of hantaviral pulmonary syndrome (HPS), as estimated from satellite imagery, and local rodent populations was examined. HPS risk, predicted before rodent sampling, was highly associated with the abundance of Peromyscus maniculatus, the reservoir of Sin Nombre Virus (SNV). P. maniculatus were common in high-risk sites, and populations in high-risk areas were skewed toward adult males, the subclass most frequently infected with SNV. In the year after an El Nino Southern Oscillation (ENSO), captures of P. maniculatus increased only in high-risk areas. During 1998, few sites had infected mice, but by 1999, 18/20 of the high-risk sites contained infected mice and the crude prevalence was 30.8%. Only 1/18 of the low-risk sites contained infected rodents, and the prevalence of infection was lower (8.3%). Satellite imagery identified environmental features associated with SNV transmission within its reservoir population, but at least 2 years of high-risk conditions were needed for SNV to reach high prevalence. Areas with persistently high-risk environmental conditions may serve as refugia for the survival of SNV in local mouse populations.
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Sin Nombre Virus snv ig isotype antibody response during acute and convalescent phases of hantaVirus pulmonary syndrome
Emerging Infectious Diseases, 2000Co-Authors: Pavel Bostik, C. J. Peters, Pierre E. Rollin, Thomas G Ksiazek, Jorn Winter, Francois Villinger, Sherif R Zaki, Aftab A AnsariAbstract:Serum samples from 22 hantaVirus pulmonary syndrome (HPS) patients were tested for Sin Nombre Virus (SNV)-reactive antibodies. In the acute phase of HPS, 100% and 67% of the samples tested positive for SNV-specific immunoglobulin (Ig) M and IgA, respectively. Among the Virus-specific IgG antibodies, the most prevalent were IgG3 (in 97% of samples), followed by IgG1 (70%), IgG2 (30%), and IgG4 (3%).
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acute Sin Nombre hantaVirus infection without pulmonary syndrome united states
Emerging Infectious Diseases, 1999Co-Authors: Paul Kitsutani, Joni C Young, Ali S Khan, Robert W Denton, Curtis L Fritz, Robert A Murray, Randall L Todd, John W Pape, Wyatt J Frampton, C. J. PetersAbstract:HantaVirus pulmonary syndrome (HPS) occurs in most infections with Sin Nombre Virus and other North American hantaViruses. We report five cases of acute hantaVirus infection that did not fit the HPS case definition. The patients had characteristic prodromal symptoms without severe pulmonary involvement. These cases suggest that surveillance for HPS may need to be expanded.
