Analyses of Gene Flow Among Populations of Deer Mice (Peromyscus Maniculatus) at Sites Near Hantavirus Pulmonary Syndrome Case-Patient Residences

Abstract

Gene flow and potential for Sin Nombre virus (SNV) trafficking of the deer mouse (Peromyscus maniculatus) was studied in Delta and Mesa counties of western Colorado (USA). The study areas included Grand Mesa and surrounding grazing and agricultural areas. This area has several natural potential barriers to rodent gene flow, including rivers, cliffs, and mountains. Ten study sites were utilized in a spatially nested design ranging from 0.65-81 km apart; four of these sites were at or near human hantavirus pulmonary syndrome (HPS) case-patient residences. One HPS case occurred on the north side of Grand Mesa in 1993; the other three (two confirmed, one presumptive) occurred on the south side of Grand Mesa between 1999-2000. Blood and tissue samples were collected from each of 221 deer mice captured from 1999-2000. Blood samples were tested for IgG antibody to SNV. At least one deer mouse had antibody to SNV at nine of 10 sites. Genomic DNA was isolated from tissue samples and alleles at six microsatellite loci were amplified by polymerase chain reaction (PCR). Polymorphisms were resolved on denaturing polyacrylamide gels and visualized by silver staining. Traditional population genetic analyses of this study indicated moderate population subdivision among the populations surveyed, slight evidence of isolation by distance, and that the Gunnison River system may hinder gene flow in this area. Application of assignment tests indicated that approximately 73-85% of mice were assigned to their population of capture. Many of the misclassifications occurred among sites less than 1 km apart; however, some long-distance misclassifications were noted. Additionally, some misclassifications were noted among study sites on different sides of the Gunnison River system, indicating that the riparian corridor of this system may facilitate some gene flow. Overall, these data indicate that SNV trafficking is more likely at the local level, but some long-distance trafficking may be possible, especially where select habitat variables favor long-distance movements.

How Host Population Dynamics Translate into Time-Lagged Prevalence: An Investigation of Sin Nombre Virus in Deer Mice

“…Spatial effects are likely to be important in several ways. First, movement of infected animals is common (Root et al, 2003), with one study showing that mobile animals typically have higher prevalence (Escutenaire et al, 2000). Second, the disease may persist in spatial refugia during periods of low population and prevalence , and recolonize from those regions during periods of population increase, leading to longer lags (Abramson and Kenkre, 2002).…”

Landscape Genetics of Raccoons (Procyon lotor) Associated with Ridges and Valleys of Pennsylvania: Implications for Oral Rabies Vaccination Programs

“…Population genetics has recently been used successfully to assess various associations involving the transmission and/or trafficking of select etiologic agents causing wildlife and human (i.e., zoonotic) diseases (e.g., Root et al 2003, Blanchong et al 2007). In addition, these techniques have proven useful for addressing various population aspects of multifaceted invasive species issues (Hampton et al 2004).…”

Genetic Relatedness of Deer Mice (Peromyscus maniculatus) Infected with Sin Nombre Virus

“…Amplification was done in a PTC-100 thermal cycler (Primer pairs with the PMs prefix; MJ Research, Inc., Watertown, MA) or a DNA Engine DYAD™ (Primer pairs with the Pml prefix; MJ Research, Inc.) using one of each of the ten primer pairs listed above. PCR conditions and primer sequences are listed elsewhere (Chirhart et al 2000;Root et al 2003). Slight modifications of the remaining protocols listed in Root et al (2003) employed in this study include the use of DNeasy ® Tissue Kits (QIAGEN Inc., Valencia, CA) for genomic DNA extractions and employing slight modifications of the polyacrylamide gel electrophoresis protocols (% acrylamide and run times) outlined in Sambrook et al (1989).…”

“…PCR conditions and primer sequences are listed elsewhere (Chirhart et al 2000;Root et al 2003). Slight modifications of the remaining protocols listed in Root et al (2003) employed in this study include the use of DNeasy ® Tissue Kits (QIAGEN Inc., Valencia, CA) for genomic DNA extractions and employing slight modifications of the polyacrylamide gel electrophoresis protocols (% acrylamide and run times) outlined in Sambrook et al (1989). Each sample was coded prior to being genotyped so that its respective SNV infection status was unidentified.…”

“…These markers included primer pairs of Pml01, Pml02, Pml04, Pml06, Pml10, Pml12 (Chirhart et al 2000) and PMs19, PMs21, PMs26, and PMs29 (Root et al 2003). Enzymelinked immunosorbent assays (ELISA) for IgG antibody to SNV were performed by the method of Feldmann et al (1993).…”