Long‐Term Patterns of Immune Investment by Wild Deer Mice Infected with Sin Nombre Virus

2010 ◽  
Vol 83 (5) ◽  
pp. 847-857 ◽  
Author(s):  
Erin M. Lehmer ◽  
Jeremy D. Jones ◽  
Mariana G. Bego ◽  
Johanna M. Varner ◽  
Stephen St. Jeor ◽  
...  
Keyword(s):  

1997 ◽  
Vol 78 (2) ◽  
pp. 661-668 ◽  
Author(s):  
C. S. O'Connor ◽  
J. P. Hayes ◽  
S. C. S. Jeor


2021 ◽  
Author(s):  
John L. Orrock ◽  
Brian M. Connolly ◽  
Peter W. Guiden ◽  
Jennifer L. Chandler ◽  
Gebbiena M. Bron ◽  
...  


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Bryan D. Griffin ◽  
Mable Chan ◽  
Nikesh Tailor ◽  
Emelissa J. Mendoza ◽  
Anders Leung ◽  
...  

AbstractWidespread circulation of SARS-CoV-2 in humans raises the theoretical risk of reverse zoonosis events with wildlife, reintroductions of SARS-CoV-2 into permissive nondomesticated animals. Here we report that North American deer mice (Peromyscus maniculatus) are susceptible to SARS-CoV-2 infection following intranasal exposure to a human isolate, resulting in viral replication in the upper and lower respiratory tract with little or no signs of disease. Further, shed infectious virus is detectable in nasal washes, oropharyngeal and rectal swabs, and viral RNA is detectable in feces and occasionally urine. We further show that deer mice are capable of transmitting SARS-CoV-2 to naïve deer mice through direct contact. The extent to which these observations may translate to wild deer mouse populations remains unclear, and the risk of reverse zoonosis and/or the potential for the establishment of Peromyscus rodents as a North American reservoir for SARS-CoV-2 remains unknown.



2007 ◽  
Vol 104 (39) ◽  
pp. 15496-15501 ◽  
Author(s):  
T. Schountz ◽  
J. Prescott ◽  
A. C. Cogswell ◽  
L. Oko ◽  
K. Mirowsky-Garcia ◽  
...  


2000 ◽  
Vol 81 (3) ◽  
pp. 676-682 ◽  
Author(s):  
James R. Biggs ◽  
Kathy D. Bennett ◽  
Mary A. Mullen ◽  
Timothy K. Haarmann ◽  
Mary Salisbury ◽  
...  


Viruses ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 183 ◽  
Author(s):  
Bryce Warner ◽  
Derek Stein ◽  
Bryan Griffin ◽  
Kevin Tierney ◽  
Anders Leung ◽  
...  

In North America, Sin Nombre virus (SNV) is the main cause of hantavirus cardiopulmonary syndrome (HCPS), a severe respiratory disease with a fatality rate of 35–40%. SNV is a zoonotic pathogen carried by deer mice (Peromyscus maniculatus), and few studies have been performed examining its transmission in deer mouse populations. Studying SNV and other hantaviruses can be difficult due to the need to propagate the virus in vivo for subsequent experiments. We show that when compared with standard intramuscular infection, the intraperitoneal infection of deer mice can be as effective in producing SNV stocks with a high viral RNA copy number, and this method of infection provides a more reproducible infection model. Furthermore, the age and sex of the infected deer mice have little effect on viral replication and shedding. We also describe a reliable model of direct experimental SNV transmission. We examined the transmission of SNV between deer mice and found that direct contact between deer mice is the main driver of SNV transmission rather than exposure to contaminated excreta/secreta, which is thought to be the main driver of transmission of the virus to humans. Furthermore, increases in heat shock responses or testosterone levels in SNV-infected deer mice do not increase the replication, shedding, or rate of transmission. Here, we have demonstrated a model for the transmission of SNV between deer mice, the natural rodent reservoir for the virus. The use of this model will have important implications for further examining SNV transmission and in developing strategies for the prevention of SNV infection in deer mouse populations.



2007 ◽  
Vol 43 (1) ◽  
pp. 12-22 ◽  
Author(s):  
Richard J. Douglass ◽  
Charles H. Calisher ◽  
Kent D. Wagoner ◽  
James N. Mills


1999 ◽  
Vol 68 (4) ◽  
pp. 733-740 ◽  
Author(s):  
Andrew G. McAdam ◽  
JohN. S. Millar




2009 ◽  
Vol 276 (1660) ◽  
pp. 1305-1312 ◽  
Author(s):  
Christine A Clay ◽  
Erin M Lehmer ◽  
Andrea Previtali ◽  
Stephen St. Jeor ◽  
M. Denise Dearing

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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