Ectromelia virus replication in major target organs of innately resistant and susceptible mice after intravenous infection

The kinetics of ectromelia virus replication in the spleen and liver and of alpha/beta interferon production in the spleen were determined during the first 3 days after intravenous infection with the virulent Moscow strain in resistant C57 BL/6 and susceptible DBA/2 mice. Virus replication in the sp...

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Bibliographic Details
Published in:Archives of virology 1993-01, Vol.129 (1-4), p.65-75
Main Authors: Brownstein, D G, Bhatt, P N, Gras, L
Format: Article
Language:English
Subjects:
Animals
DNA, Viral - biosynthesis
Ectromelia virus
Ectromelia virus - physiology
Ectromelia, Infectious - genetics
Ectromelia, Infectious - immunology
Ectromelia, Infectious - microbiology
Immunity, Innate
Interferons - biosynthesis
Liver - immunology
Liver - microbiology
Male
Mice
Mice, Inbred C57BL
Mice, Inbred DBA
Species Specificity
Spleen - immunology
Spleen - microbiology
Viral Plaque Assay
Virus Replication
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Summary:The kinetics of ectromelia virus replication in the spleen and liver and of alpha/beta interferon production in the spleen were determined during the first 3 days after intravenous infection with the virulent Moscow strain in resistant C57 BL/6 and susceptible DBA/2 mice. Virus replication in the spleen as measured by assays for virus DNA and infectious centers was suppressed in C57BL/6 mice relative to DBA/2 mice within the first 1 or 2 days of infection. Infectious centers increased in DBA/2 mice but not in C57 BL/6 mice. Differences in virus replication between strains were less discrete when spleens were assayed for infectious virus than when they were assayed for infectious centers because infectious centers of most C57 BL/6 mice had more infectious virus than infectious centers of DBA/2 mice. Virus replication in the liver, the major target organ, as measured by virus DNA and infectious virus assays, was suppressed in C57 BL/6 mice relative to DBA/2 mice 3 days after infection but not before that interval. The results indicate that genetic control of ectromelia virus replication begins within the first 1 or 2 days of infection in the spleen but is delayed in the liver and that genetic control is directed at the prevention of virus spread more than at virus replication.
ISSN:0304-8608
1432-8798
DOI:10.1007/BF01316885