期刊
JOURNAL OF VIROLOGY
卷 82, 期 21, 页码 10580-10590出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01213-08
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资金
- NIH [R01 AI46954, U01 AI70469, U19 AI62623, T32 AI007647]
- CRIP (Center for Research on Influenza Pathogenesis, NIAID) [HHSN266200700010C]
Type B influenza viruses can cause substantial morbidity and mortality in the population, and vaccination remains by far the best means of protection against infections with these viruses. Here, we report the construction of mutant influenza B viruses for potential use as improved live-virus vaccine candidates. Employing reverse genetics, we altered the NS1 gene, which encodes a type I interferon (IFN) antagonist. The resulting NS1 mutant viruses induced IFN and, as a consequence, were found to be attenuated in vitro and in vivo. The absence of pathogenicity of the NS1 mutants in both BALB/c and C57BL/6 PKR-/- mice was confirmed. We also provide evidence that influenza B virus NS1 mutants induce a self-adjuvanted immune response and confer effective protection against challenge with both homologous and heterologous B virus strains in mice.
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