TY - JOUR
T1 - Maporal viral infection in the Syrian golden hamster
T2 - A model of hantavirus pulmonary syndrome
AU - Milazzo, Mary Louise
AU - Eyzaguirre, Eduardo J.
AU - Molina, Claudia P.
AU - Fulhorst, Charles F.
N1 - Funding Information:
Received 24 April 2002; revised 15 July 2002; electronically published 29 October 2002. Financial support: National Institutes of Health (grant AI-41435). Reprints or correspondence: Mary Louise Milazzo, Dept. of Pathology, Route 0609, 301 University Blvd., University of Texas Medical Branch, Galveston, TX 77555-0609 ([email protected]).
PY - 2002/11/15
Y1 - 2002/11/15
N2 - Hantavirus pulmonary syndrome (HPS) is a severe and often fatal rodent-borne zoonosis. Maporal (MAP) virus is a newly discovered hantavirus that originally was isolated from an arboreal rice rat captured in central Venezuela. The results of this study indicate that MAP virus in the Syrian golden hamster (Mesocricetus auratus) can cause a disease that is clinically and pathologically remarkably similar to HPS. The similarities include the time course of clinical disease, presence of virus-specific IgG at the onset of clinical disease, subacute pneumonitis, rapid onset of diffuse alveolar edema in the absence of necrosis, hepatic-portal triaditis, mononuclear-cellular infiltrate in lung and liver, widespread distribution of hantaviral antigen in endothelial cells of the microvasculature of lung and other tissues, and variable lethality. These similarities suggest that the MAP virus-hamster system is a useful model for studies of the pathogenesis of HPS and for the evaluation of potential therapeutic agents.
AB - Hantavirus pulmonary syndrome (HPS) is a severe and often fatal rodent-borne zoonosis. Maporal (MAP) virus is a newly discovered hantavirus that originally was isolated from an arboreal rice rat captured in central Venezuela. The results of this study indicate that MAP virus in the Syrian golden hamster (Mesocricetus auratus) can cause a disease that is clinically and pathologically remarkably similar to HPS. The similarities include the time course of clinical disease, presence of virus-specific IgG at the onset of clinical disease, subacute pneumonitis, rapid onset of diffuse alveolar edema in the absence of necrosis, hepatic-portal triaditis, mononuclear-cellular infiltrate in lung and liver, widespread distribution of hantaviral antigen in endothelial cells of the microvasculature of lung and other tissues, and variable lethality. These similarities suggest that the MAP virus-hamster system is a useful model for studies of the pathogenesis of HPS and for the evaluation of potential therapeutic agents.
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U2 - 10.1086/344735
DO - 10.1086/344735
M3 - Article
C2 - 12404153
AN - SCOPUS:0037111065
SN - 0022-1899
VL - 186
SP - 1390
EP - 1395
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 10
ER -