期刊
JOURNAL OF VIROLOGY
卷 88, 期 8, 页码 4600-4604出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.03158-13
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资金
- National Natural Science Foundation of China [31302102, 31270046]
- National Basic Research Program (973 program) [2011CB504702]
- Chang Jiang Scholars Program
- Chinese Universities Scientific Fund [2014XJ007, 2011JS013]
- Biotechnology and Biological Sciences Research Council (UK) China Partnering Award
- BBSRC [BB/I024704/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/I024704/1] Funding Source: researchfish
We examined the molecular basis of virulence of pandemic H1N1/09 influenza viruses by reverse genetics based on two H1N1/09 virus isolates (A/California/04/2009 [CA04] and A/swine/Shandong/731/2009 [SD731]) with contrasting pathogenicities in mice. We found that four amino acid mutations (P224S in the PA protein [PA-P224S], PB2-T588I, NA-V106I, and NS1-I123V) contributed to the lethal phenotype of SD731. In particular, the PA-P224S mutation when combined with PA-A70V in CA04 drastically reduced the virus's 50% mouse lethal dose (LD50), by almost 1,000-fold.
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