期刊
VIROLOGY
卷 361, 期 1, 页码 229-241出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2006.11.012
关键词
West Nile virus; NS4B; Flavivirus replication
类别
资金
- NIAID NIH HHS [U54AI57158, AI065562, U01 AI061193, N01AI25490, N01-AI25490, R21 AI065562, U54 AI057158-04, U01 AI061193-03, AI061193, R21 AI065562-02, U54 AI057158-019001, U54 AI057158, U54 AI57518] Funding Source: Medline
An adaptive mutation (E249G) within West Nile virus (WNV) NS4B gene was consistently recovered from replicon RNAs in C3H/He mouse cells. The E249G is located at the C-terminal tail of NS4B predicted to be on the cytoplasmic side of the endoplasmic reticulum membrane. The E249G substitution reduced replicon RNA synthesis. Compared with the wild-type NS4B, the E249G mutant protein exhibited a similar efficiency in evasion of interferon-beta response. Recombinant E249G virus exhibited smaller plaques, slower growth kinetics, and lower RNA synthesis than the wild-type virus in a host-dependent manner, with the greatest difference in rodent cells (C3H/He and BHK-21) and the least difference in mosquito cells (C3/36). Selection of revertants of E249G virus identified a second site mutation at residue 246, which could compensate for the low replication phenotype in cell culture. These results demonstrate that distinct residues within the C-terminal tail of flavivirus NS4B are critical for viral replication. (c) 2006 Elsevier Inc. All rights reserved.
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