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. 2002 Aug;76(15):7587-94.
doi: 10.1128/jvi.76.15.7587-7594.2002.

Shedding and Intracage Transmission of Sin Nombre Hantavirus in the Deer Mouse (Peromyscus Maniculatus) Model

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Free PMC article

Shedding and Intracage Transmission of Sin Nombre Hantavirus in the Deer Mouse (Peromyscus Maniculatus) Model

Jason Botten et al. J Virol. .
Free PMC article

Abstract

The mechanism(s) by which Sin Nombre (SN) hantavirus is maintained in deer mouse populations is unclear. Field studies indicate that transmission occurs primarily if not exclusively via a horizontal mechanism. Using an experimental deer mouse infection model in an outdoor laboratory, we tested whether infected rodents shed SN virus in urine, feces, and saliva, whether infected mice transmit infection to naïve cage mates, and whether infected dams are able to vertically transmit virus or antibody to offspring. Using pooled samples of urine, feces, and saliva collected from mice infected 8 to 120 days postinoculation (p.i.), we found that a subset of saliva samples, collected between 15 and 90 days p.i., contained viral RNA. Parallel studies conducted on wild-caught, naturally infected deer mice showed a similar pattern of intermittent positivity, also only in saliva samples. Attempts to isolate virus through inoculation of cells or naïve deer mice with the secreta or excreta of infected mice were uniformly negative. Of 54 attempts to transmit infection by cohousing infected deer mice with seronegative cage mates, we observed only a single case of transmission, which occurred between 29 and 42 days p.i. Dams passively transferred antibodies to neonatal pups via milk, and those antibodies persisted for at least 2 months after weaning, but none transmitted infection to their pups. Compared to other hantavirus models, SN virus is shed less efficiently and transmits inefficiently among cage mates. Transmission of SN virus among reservoir rodents may require factors that are not required for other hantaviruses.

Figures

FIG. 1.
FIG. 1.
Viral RNA spiking experiments. Viral supernatants of SN77734-infected cultures that contained known numbers of copies of SN virus S-segment RNA were added into either PBS or pooled samples of urine, feces, and saliva before extraction of viral RNA. These RNAs were then used in nested RT-PCRs. NC, negative control; PC, positive control.
FIG. 2.
FIG. 2.
Kinetics of SN virus replication after primary isolation in Vero E6 cells from a positive control tissue (day 13 p.i. lung) homogenate. (A) Nested RT-PCR specific for viral S-segment RNA carried out on supernatant RNAs; (B) copies of negative-strand S-segment RNA per microliter of supernatant as determined by TaqMan quantitative RT-PCR.
FIG. 3.
FIG. 3.
(A) Timeline (in days) for manipulations performed on litters born to infected dams. I, dams inoculated; B, pups born; W, weaning; Bl, phlebotomy performed; S, sacrifice. (B) Sera from pups (litters 1 and 2) born to infected dams were examined at a dilution of 1:200 for reactivity to the SN virus N antigen by SIA (central band). In addition to the viral band, high-intensity (3+) and low-intensity (1+) bands of deer mouse serum were loaded, as described previously (5). Although each lot of SIA strips was independently tested for reactivity to the viral N antigen with a standard positive control serum, a wider degree of lot-to-lot variation was allowed for the conjugate reactivity bands (3+ and 1+). For that reason, some variation in the intensities of those control bands was observed in this study. PC, positive control; pw, postweaning. All sera tested were reactive at the 1:125 dilution.

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