Dynamics of Puumala hantavirus infection in naturally infected bank voles (Clethrinomys glareolus)

Бернштейн, А. Д.; Apekina, N. S.; Mikhailova, Tatiana; Myasnikov, Yu. A.; Khlyap, L. A.; Korotkov, Yu. S.; Gavrilovskaya, Irina N.

doi:10.1007/s007050050654

Cited by 135 publications

(174 citation statements)

References 32 publications

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“…Assuming that host populations are made of individuals of different intrinsic quality (e.g., ability to fight infection), another possible hypothesis is that the probability of maturation is higher in infected than in noninfected bank voles because only the few ''high-quality'' individuals could afford the costs of fighting PUUV infection and going through the maturation process (Vaupel and Yashin, 1985;Van Noordwijk and Dejong, 1986). It is also possible that the physiologic or behavioral changes prior to the maturation process in rodents (Lambin and Yoccoz, 2001) already increase the risk of infection or the susceptibility of some individuals (Bernshtein et al, 1999;Klein and Calisher, 2007). Alternatively, hosts may alter their lifehistory traits in order to compensate for the negative effects of parasitism.…”

Section: Discussionmentioning

confidence: 99%

“…Because maternal antibodies are transferred to offspring by infected dams, detection of PUUV immunoglobulin G (IgG) antibody in juvenile bank voles cannot be used alone as an indication of infection (Bernshtein et al, 1999). Therefore, the juvenile cohort was removed from the dataset.…”

Section: Capture-mark-recapture Datamentioning

confidence: 99%

“…Two simplifying assumptions were made: 1) Once an individual is found PUUV IgG antibody positive, it will remain so for the rest of its life (Bernshtein et al, 1999). Hence, transitions from state 2 to states 1 and 3, from state 3 to state 2, and from state 4 to state 3 were set to zero.…”

Section: Analysis Frameworkmentioning

confidence: 99%

“…Allocation models predict that hosts infected with parasites, where impact of infection increases with time, should preferentially allocate resources to reproduction (Gandon et al, 2001). Reproductive activity has indeed been associated with increased infection probability in many hantavirushost studies (Bernshtein et al, 1999;Escutenaire et al, 2002;Douglass et al, 2007;Previtali et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

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Impact of Puumala Virus Infection on Maturation and Survival in Bank Voles: A Capture-Mark-Recapture Analysis

Tersago

Crespin

Verhagen

et al. 2012

Journal of Wildlife Diseases

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ABSTRACT:Many zoonotic diseases are caused by rodent-borne viruses. Major fluctuations in the transmission of these viruses have been related to large changes in reservoir host population numbers due to external factors. However, the impact of the pathogen itself on the demography of its reservoir host is often overlooked. We investigated the impact of Puumala virus (PUUV) on survival and reproductive maturation probability of its reservoir host, the bank vole (Myodes glareolus). Three years (2004-06) of data from nine independent sites in southern Belgium were collected and analyzed with a capture-mark-recapture (CMR) method that includes statistical correction for the variation in capture probability of voles. A multistate model based on four states of reproductive activity and PUUV immunoglobulin G (IgG) antibody status was used to estimate survival and probability of transition from one reproductive or infection state to another. Although survival estimates for reproductively active voles were similar between infected and noninfected individuals, PUUV infection in reproductively inactive voles decreased mean monthly survival by 14%. PUUV infection was associated with a threefold increase in the probability of reproductive maturation in bank voles. Moreover, the probability of PUUV IgG seroconversion was three times higher for reproductively active voles compared to reproductively inactive voles. Our model indicates that PUUV infection may alter bank vole population dynamics by affecting both survival and maturation in its host. Additional studies, using CMR methodology with shorter time intervals between trapping sessions and possibly a longer duration, are needed to confirm these findings.

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Section: Discussionmentioning

confidence: 99%

Section: Capture-mark-recapture Datamentioning

confidence: 99%

Section: Analysis Frameworkmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Impact of Puumala Virus Infection on Maturation and Survival in Bank Voles: A Capture-Mark-Recapture Analysis

Tersago

Crespin

Verhagen

et al. 2012

Journal of Wildlife Diseases

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“…Infection in deer mice is chronic; however, it has been speculated that infectiousness may be greatest during early stages of infection when viremia is high (Botten et al, 2000;Botten et al, 2003). For hantaviruses in general, the number of recently infected animals is an indicator of the epizootic intensity (Bernshtein et al, 1999;Safronetz et al, 2006). With SNV, viral shedding in urine and saliva (critical sources for transmission to humans) may also be highest during early stages of infection (Safronetz et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Seasonal Variation in Sin Nombre Virus Infections in Deer Mice: Preliminary Results

Dearing

Previtali

Jones

et al. 2009

Journal of Wildlife Diseases

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ABSTRACT:The proportion of deer mice (Peromyscus maniculatus) with recently acquired Sin Nombre virus (SNV) infections is an indicator of epizootic intensity and may be key in predicting outbreaks of hantavirus cardio-pulmonary syndrome in humans. We investigated whether incidence of recent infections was related to season, sex, reproductive status, or habitat disturbance. In May and September, 2006, we sampled 912 deer mice at six sites in Utah. We determined SNV antibody prevalence and estimated the number of recent infections with an avidity enzyme-linked immunosorbent assay. Antibody prevalence in adults (n5735) was 22%, and putative maternal antibody prevalence in juveniles (n5177) was 7%. Sampling period explained a significant amount of the variance in the probability of recent infections, which were two times more common in May versus September. Additionally, prevalence of high-avidity maternal antibodies (i.e., from dams with older infections) in juveniles did not correspond to the antibody avidity patterns in adult females. In May, no juveniles had high-avidity antibodies compared to adult females (49%); in September, avidity could not be measured in juveniles because none were seropositive, despite large sample sizes (n584) and an 11% seroprevalence in adult females. Based on the results, coupled with those from the literature, we speculate that the majority of new infections may occur predominantly in the spring and that SNV may impair reproductive output of females.

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Preliminary insights into the genetics of bank vole tolerance to Puumala hantavirus in Sweden

Rohfritsch

Galan

Gautier

et al. 2018

Ecology and Evolution

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Natural reservoirs of zoonotic pathogens generally seem to be capable of tolerating infections. Tolerance and its underlying mechanisms remain difficult to assess using experiments or wildlife surveys. High‐throughput sequencing technologies give the opportunity to investigate the genetic bases of tolerance, and the variability of its mechanisms in natural populations. In particular, population genomics may provide preliminary insights into the genes shaping tolerance and potentially influencing epidemiological dynamics. Here, we addressed these questions in the bank vole Myodes glareolus, the specific asymptomatic reservoir host of Puumala hantavirus (PUUV), which causes nephropathia epidemica (NE) in humans. Despite the continuous spatial distribution of M. glareolus in Sweden, NE is endemic to the northern part of the country. Northern bank vole populations in Sweden might exhibit tolerance strategies as a result of coadaptation with PUUV. This may favor the circulation and maintenance of PUUV and lead to high spatial risk of NE in northern Sweden. We performed a genome‐scan study to detect signatures of selection potentially correlated with spatial variations in tolerance to PUUV. We analyzed six bank vole populations from Sweden, sampled from northern NE‐endemic to southern NE‐free areas. We combined candidate gene analyses (Tlr4, Tlr7, and Mx2 genes) and high‐throughput sequencing of restriction site‐associated DNA (RAD) markers. Outlier loci showed high levels of genetic differentiation and significant associations with environmental data including variations in the regional number of NE human cases. Among the 108 outliers that matched to mouse protein‐coding genes, 14 corresponded to immune‐related genes. The main biological pathways found to be significantly enriched corresponded to immune processes and responses to hantavirus, including the regulation of cytokine productions, TLR cascades, and IL‐7, VEGF, and JAK–STAT signaling. In the future, genome‐scan replicates and functional experimentations should enable to assess the role of these biological pathways in M. glareolus tolerance to PUUV.

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Dynamics of Puumala hantavirus infection in naturally infected bank voles (Clethrinomys glareolus)

Cited by 135 publications

References 32 publications

Impact of Puumala Virus Infection on Maturation and Survival in Bank Voles: A Capture-Mark-Recapture Analysis

Impact of Puumala Virus Infection on Maturation and Survival in Bank Voles: A Capture-Mark-Recapture Analysis

Seasonal Variation in Sin Nombre Virus Infections in Deer Mice: Preliminary Results

Preliminary insights into the genetics of bank vole tolerance to Puumala hantavirus in Sweden

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