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|Title:||Ljungan virus: A commentary on its association with fetal and infant morbidity and mortality in animals and humans|
|Citation:||Birth Defects Research Part A: Clinical and Molecular Teratology, 2010; 88(11):947-952|
|Henry F. Krous and Neil E. Langlois|
|Abstract:||Epidemiologic and experimental data support the notion that Ljungan virus (LV), endemic in some rodent populations in Sweden, Denmark, and the United States, can cause morbidity and mortality in animals and humans. LV infection can cause type I diabetes mellitus, myocarditis, and encephalitis in bank voles and experimental mice, and lemmings. Mouse dams infected with LV experience high rates of stillbirth that may persist across generations, and their fetuses may develop cranial, brain, and limb malformations. In humans, epidemiologic and serologic data suggest that LV infection correlates with intrauterine fetal death, malformations, placental inflammation, myocarditis, encephalitis, and Guillain-Barré syndrome. The proposed role of LV infection in SIDS is unconvincing. Further research is necessary to clarify the role of LV infection in animal and human disease.|
|Rights:||© 2010 Wiley-Liss, Inc.|
|Appears in Collections:||Aurora harvest 5|
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