Pathogenicity and immunogenicity of recombinant methyltransferase-defective vesicular stomatitis virus
To prevent the vesicular stomatitis virus (VSV) disease, using a panel of recombinant VSV (E1764A, S1827A, Y1650A, and F1691A) that were defective in mRNA cap methylation as vaccine to inoculate five-week-old BALB/c female mice through oral route with 1×10<sup>6</sup> PFU, the pathogenic...
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Main Authors: | , , , |
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Format: | Article |
Language: | English |
Published: |
Zhejiang University Press
2011-07-01
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Series: | 浙江大学学报. 农业与生命科学版 |
Subjects: | |
Online Access: | https://www.academax.com/doi/10.3785/j.issn.1008-9209.2011.04.001 |
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Summary: | To prevent the vesicular stomatitis virus (VSV) disease, using a panel of recombinant VSV (E1764A, S1827A, Y1650A, and F1691A) that were defective in mRNA cap methylation as vaccine to inoculate five-week-old BALB/c female mice through oral route with 1×10<sup>6</sup> PFU, the pathogenicity and immunogenicity of these viruses were determined. The result showed that recombinant S 1827A, Y1650A, F1691A were attenuated in mice and E1764A was still pathogenic to mice. The immunized mice were challenged with wild type VSV. Mice immunized with S1827A and Y1650A trigged a high level of neutralizing antibody and were protected from virulent challenge. Taken together, the results above demonstrated that methyltransferase (MTase)-defective VSV (S1827A and Y1650A) were not only attenuated in animals, but also exhibited excellent immunogenicity. Therefore, MTase-defective viruses will be good live vaccine candidates against VSV. |
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ISSN: | 1008-9209 2097-5155 |