Coxsackievirus B infections in pregnant mice impair fetal growth, likely secondary to maternal pancreatic exocrine insufficiency and reduced maternal health.
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May indicate serotype-specific fetal risks in mice; leaves open human translation and clinical relevance.
Coxsackieviruses B1, B3, B4, and B5 injected into TO outbred mice on the 8th day of pregnancy resulted in increased fetal wastage and growth retardation. Coxsackievirus B2 caused increased fetal wastage, whereas Coxsackievirus B6 exhibited no fetal effects. Pregnant animals injected with viruses causing fetal growth impairment ate more food than controls yet did not increase their body weight as much as control animals. Autopsy and pathological findings of advanced destruction of pancreatic exocrine‐tissue and hepatic‐cell vacuolation suggest that the animals were subject to a dietary defect resulting from pancreatic exocrine insufficiency. Fetal growth impairment in mice due to infection with certain Coxsackieviruses of the B group appears to be largely due to a virus‐induced reduction in the state of maternal health. However, since some of these viruses have been shown to pass transplacentally, further studies are necessary to show whether the viruses may also exert a direct effect on fetal tissues.
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A. B. G. Lansdown (1976) studied this question.
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