Journal
JOURNAL OF VIROLOGY
Volume 83, Issue 21, Pages 11330-11340Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00763-09
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Funding
- CIVIA
- NIH-NIAID [U19 AI62623, RO1AI47140, R56AI077719-01A1, R56A1077719-01A1]
- Northeast Biodefense Center [U54AI57158]
- DoD [W81XWH-07]
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Lymphocytic choriomeningitis virus (LCVM) nucleoprotein (NP) counteracts the host type I interferon (IFN) response by inhibiting activation of the IFN regulatory factor 3 (IRF3). In this study, we have mapped the regions and specific amino acid residues within NP involved in its anti-IFN activity. We identified a region spanning residues 382 to 386 as playing a critical role in the IFN-counteracting activity of NP. Alanine substitutions at several positions within this region resulted in NP mutants that lacked the IFN-counteracting activity but retained their functions in virus RNA synthesis and assembly of infectious particles. We used reverse genetics to rescue a recombinant LCMV strain carrying mutation D382A in its NP [ rLCMV/NP*(D382A)]. Compared to wild-type (WT) LCMV, rLCMV/NP*(D382A) exhibited a higher level of attenuation in IFN-competent than IFN-deficient cells. In addition, A549 cells infected with rLCMV/NP*(D382A), but not with WT LCMV, produced IFN and failed to rescue replication of the IFN-sensitive Newcastle disease virus.
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