1887

Abstract

Summary

Four temperature-sensitive () mutants of the A7 strain of Semliki Forest virus (SFV) have been isolated. All mutants were defective in RNA synthesis at the restrictive temperature (39 °C) compared to the permissive temperature (30 °C). Since the body temperature of mice fluctuates between 37 °C and 39 °C, multiplication was also examined at 37 °C; only the multiplication of 4 was restricted. After intraperitoneal infection of 8-day pregnant mice, the wild-type induced rapid abortion. 4 and 26 had no effect on embryonic development. Litters born to 4-infected mothers developed no postnatal immunity whereas 50% of litters from 26-infected mothers were immune. Unlike the wild-type, 14 induced the same or higher virus titres in placental tissue in most mice than in foetal tissue. 22 and 14 induced a range of development defects, including developmental arrest, mummification, abortion and postnatal death. Most surviving offspring were immune. Although 4 induced no viraemia, 14, 22 and 26 induced a lower titre but longer lasting viraemia than the wild-type. It is concluded that infections of pregnant mice with 14 and 22 in particular are good models for analysis of the mechanism of virus-induced developmental defects.

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/content/journal/jgv/10.1099/0022-1317-68-1-107
1987-01-01
2019-09-23
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http://instance.metastore.ingenta.com/content/journal/jgv/10.1099/0022-1317-68-1-107
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