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Isolation and Preliminary Characterization of Semliki Forest Virus Mutants With Altered Pathogenicity for Mouse Embryos

Department of Microbiology, Moyne Institute, Trinity College, Dublin 2, Ireland

Four temperature-sensitive (ts) 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 ts4 was restricted. After intraperitoneal infection of 8-day pregnant mice, the wild-type induced rapid abortion. Ts4 and ts26 had no effect on embryonic development. Litters born to ts4-infected mothers developed no postnatal immunity whereas 50% of litters from ts26-infected mothers were immune. Unlike the wild-type, ts14 induced the same or higher virus titres in placental tissue in most mice than in foetal tissue. Ts22 and ts14 induced a range of development defects, including developmental arrest, mummification, abortion and postnatal death. Most surviving offspring were immune. Although ts4 induced no viraemia, ts14, ts22 and ts26 induced a lower titre but longer lasting viraemia than the wild-type. It is concluded that infections of pregnant mice with ts14 and ts22 in particular are good models for analysis of the mechanism of virus-induced developmental defects.

Received 21 July 1986; accepted 24 September 1986.

This article has been cited by other articles:

				G. J. Atkins, B. J. Sheahan, and P. Liljeström The molecular pathogenesis of Semliki Forest virus: a model virus made useful? J. Gen. Virol., September 1, 1999; 80(9): 2287 - 2297. [Full Text]