期刊
VIROLOGY
卷 336, 期 2, 页码 318-326出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2005.03.028
关键词
influenza B virus; mouse; adaptation; animal model; matrix protein; virulence; reverse genetics
类别
资金
- NCI NIH HHS [R25 CA023944, CA-21765, P30 CA021765] Funding Source: Medline
- NIAID NIH HHS [R01 AI066349-01, R01 AI066349] Funding Source: Medline
Serial passage of an initially avirulent influenza B virus, B/Memphis/12/97, resulted in the selection of a variant which was lethal in mice. Virulence correlated with improved growth in vivo and prolonged replication. Sequencing of the complete coding regions of the parent and mouse-adapted viruses revealed 8 amino acid differences. Sequencing and characterization of intermediate passages suggested that one change in the C-terminal domain of the M1 protein, an asparagine to a serine at position 22 1, was responsible for acquisition of virulence and lethality. Site-directed mutagenesis of the M segment of a different virus, B/Yamanashi/166/98, to change this amino acid residue confirmed its importance by conferring improved growth and virulence in mice. This observation suggests a role for the C domain of the M I protein in growth and virulence in a mammalian host. (c) 2005 Elsevier Inc. All rights reserved.
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