Reservoir For Sin Nombre Virus Research Articles

Novel Focus of Sin Nombre Virus in Peromyscus eremicus Mice, Death Valley National Park, California, USA.

The deer mouse (Peromyscus maniculatus) is the primary reservoir for Sin Nombre virus (SNV) in the western United States. Rodent surveillance for hantavirus in Death Valley National Park, California, USA, revealed cactus mice (P. eremicus) as a possible focal reservoir for SNV in this location. We identified SNV antibodies in 40% of cactus mice sampled.

Transcriptome markers of viral persistence in naturally-infected andes virus (bunyaviridae) seropositive long-tailed pygmy rice rats.

Long-tailed pygmy rice rats (Oligoryzomys longicaudatus) are principal reservoir hosts of Andes virus (ANDV) (Bunyaviridae), which causes most hantavirus cardiopulmonary syndrome cases in the Americas. To develop tools for the study of the ANDV-host interactions, we used RNA-Seq to generate a de novo transcriptome assembly. Splenic RNA from five rice rats captured in Chile, three of which were ANDV-infected, was used to generate an assembly of 66,173 annotated transcripts, including noncoding RNAs. Phylogenetic analysis of selected predicted proteins showed similarities to those of the North American deer mouse (Peromyscus maniculatus), the principal reservoir of Sin Nombre virus (SNV). One of the infected rice rats had about 50-fold more viral burden than the others, suggesting acute infection, whereas the remaining two had levels consistent with persistence. Differential expression analysis revealed distinct signatures among the infected rodents. The differences could be due to 1) variations in viral load, 2) dimorphic or reproductive differences in splenic homing of immune cells, or 3) factors of unknown etiology. In the two persistently infected rice rats, suppression of the JAK-STAT pathway at Stat5b and Ccnot1, elevation of Casp1, RIG-I pathway factors Ppp1cc and Mff, and increased FC receptor-like transcripts occurred. Caspase-1 and Stat5b activation pathways have been shown to stimulate T helper follicular cell (TFH) development in other species. These data are also consistent with reports suggestive of TFH stimulation in deer mice experimentally infected with hantaviruses. In the remaining acutely infected rice rat, the apoptotic pathway marker Cox6a1 was elevated, and putative anti-viral factors Abcb1a, Fam46c, Spp1, Rxra, Rxrb, Trmp2 and Trim58 were modulated. Transcripts for preproenkephalin (Prenk) were reduced, which may be predictive of an increased T cell activation threshold. Taken together, this transcriptome dataset will permit rigorous examination of rice rat-ANDV interactions and may lead to better understanding of virus ecology.

Development of an ELISA to detect Sin Nombre virus-specific IgM from deer mice ( Peromyscus maniculatus)

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 μ-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.

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.

Diffusion and home range parameters for rodents: Peromyscus maniculatus in New Mexico

We analyze data from a long-term field project in New Mexico, consisting of repeated sessions of mark-recaptures of Peromyscus maniculatus (Rodentia: Muridae), the host and reservoir of Sin Nombre virus (Bunyaviridae: Hantavirus). The displacements of the recaptured animals provide a means to study their movement from a statistical point of view. We extract two parameters from the data with the help of a simple model: the diffusion constant of the rodents, and the size of their home range. The short time behavior shows the motion to be approximately diffusive and the diffusion constant to be 470 ± 50 m 2/day. The long time behavior provides an estimation of the diameter of the rodent home ranges, with an average value of 100 ± 25 m. As in previous investigations directed at Zygodontomys brevicauda observations in Panama, we use a box model for home range estimation. We also use a harmonic model in the present investigation to study the sensitivity of the conclusions to the model used and find that both models lead to similar estimates.

Research Article: Genomic organization of deer mouse (Peromyscus maniculatus) tumor necrosis factor

Abstract Tumor necrosis factor (TNF) is a mediator of inflammation during immune responses and is produced by activated macrophages and T cells. It is synthesized as a membrane-bound homotrimer that is released from activated cells. Its functions are to inhibit viral replication, cause capillary leakage, induce cell apoptosis, and to recruit other immune cells to the infected area. Many humans infected with Sin Nombre (SN) virus develop an inflammatory pulmonary immunopathology caused by abundant production of TNF. In contrast, infected deer mice, the natural reservoir of SN virus, exhibit no pathology or inflammation in the lungs. Because of this, it is unlikely that deer mice produce appreciable amounts of TNF in response to SN virus infection. To begin to address this issue, we have cloned and sequenced the Tnf gene of deer mice. We obtained all but the final 9 nucleotides of Tnf and have determined that it is highly conserved with orthologous sequences.

Satellite imagery characterizes local animal reservoir populations of Sin Nombre virus in the southwestern United States.

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 Niño Southern Oscillation (ENSO), captures of P. maniculatus increased only in high-risk areas. During 1998, few sites had infected mice, but by 1999, 1820 of the high-risk sites contained infected mice and the crude prevalence was 30.8%. Only 118 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.

Serologic evidence of hantavirus infection in sigmodontine rodents in Mexico.

Antibodies to hantaviruses in two species of sigmodontine rodents (Peromyscus maniculatus and Reithrodontomys sumichrasti) collected in central Mexico are reported. Peromyscus maniculatus, a common species throughout much of Mexico, is the reservoir of Sin Nombre virus (SNV), the etiologic agent of the great majority of cases of hantavirus pulmonary syndrome (HPS) in North America. Although the identity of the virus detected in P. maniculatus in Mexico could not be determined by these serologic results, our findings suggest that SNV may occur throughout the range of P. maniculatus in North America. If true, the failure to identify HPS in Mexico is not due to the absence of pathogenic hantaviruses in Mexico.

Hantavirus infection in the Four Corners region of USA in 1998

The deer mouse (Peromyscus maniculatus) is the reservoir for Sin Nombre virus, the cause of hantavirus pulmonary syndrome (HPS) in the USA. The 1997–98 El Nino southern oscillation (ENSO) was followed by increased rainfall and increases in Peromyscus spp population densities in the Four Corners region of the southwestern USA where the states of New Mexico, Colorado, Arizona, and Utah share a common intersection. 1

Small mammal survival and trapability in mark-recapture monitoring programs for hantavirus.

Following the 1993 hantavirus pulmonary syndrome (HPS) epidemic in the south-western United States, mammalogists and epidemiologists instituted long-term studies to monitor population density and prevalence of infection in rodents which constitute the reservoir for Sin Nombre virus (SNV). In this study, field techniques used in sampling small mammals for SNV infection were evaluated to determine if trapping and handling protocols were having significant effects on future trapability or mortality of animals. We compared rodent mark-recapture control plots, on which all rodents were simply measured, marked, and released on site, with experimental plots on which all animals were anesthetized with methoxyflurane, sampled for blood and saliva, measured, marked, and released. Blood samples were obtained from anesthetized animals on the experimental plots via a retro-orbital sinus puncture using a heparinized capillary tube. Dacron tipped oral swabs were used to collect buccal cells and saliva from the rodent's oral cavity. Field data were collected monthly from August 1994 to August 1996 at two sites in New Mexico (USA). Analyses were based on 3,661 captures of 1,513 individuals representing 21 species from three rodent families (Rodentia: Muridae, Heteromyidae, Sciuridae) and two species of rabbits (Lagomorpha: Leporidae). Overall, for most murid rodents (including five Peromyscus spp., Neotoma albigula, and Onychomys leucogaster) and one rabbit species (Sylvilagus floridanus), the handling/bleeding procedures had no significant effects on recapture rates or mortality. In contrast, several species of heteromyids (Dipodomys ordii and Perognathus flavus), one murid (Reithrodontomys megalotis) and one leporid (S. auduboni) suffered higher mortality rates, and heteromyid kangaroo rats (D. ordii and D. merriami) exhibited lower trapability as a result of the anesthesia and sampling procedures. In view of the overall non-significant influence of the sampling procedures on murid rodents, the anesthesia and blood/saliva sampling protocols described herein appear to be appropriate for hantavirus research, and may serve as a model for environmental monitoring of other zoonotic agents and their reservoirs.

A newly recognized virus associated with a fatal case of hantavirus pulmonary syndrome in Louisiana

Genetic analysis of virus detected in autopsy tissues of a fatal hantavirus pulmonary syndrome-like case in Louisiana revealed the presence of a previously unrecognized hantavirus. Nucleotide sequence analysis of PCR fragments of the complete S and M segments of the virus amplified from RNA extracted from the tissues showed the virus to be novel, differing from the closest related hantavirus, Sin Nombre virus, by approximately 30%. Both genome segments were unique, and there was no evidence of genetic reassortment with previously characterized hantaviruses. The primary rodent reservoir of Sin Nombre virus, the deer mouse Peromyscus maniculatus, is absent from Louisiana. Thus, the virus detected in Louisiana, referred to here as Bayou virus, must possess a different rodent reservoir.