Abstract
More and more epidemiologic and experimental data support the notion that Ljungan virus (LV), originally isolated from some rodent populations in Sweden, Denmark, and the United States, plays an important role in stillbirth and fetal malformation. Mouse dams infected with LV may result in uterine resorption and perinatal deaths that may cross generations, and their offspring may suffer high rates of malformations including cranial, brain, and limb malformations. In humans, researches founded that LV infection is related to malformation, intrauterine fetal death, and even central nervous system malformation. Although molecularly characterized, little is known about the biophysical nature of LV. Consequently, the role of LV infections in sudden infant death syndrome is still confusing, and the mechanism of how LV infections cause diseases is not clear. More research is clearly necessary to explore the mechanisms of LV infection in human and animal diseases to bring improvement to the clinical outcomes.
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