科研之友
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摘要
The nonvirion (NV) protein of infectious hematopoietic necrosis virus (IHNV) has been previously reported to be essential for efficient growth and pathogenicity of IHNV. However, little is known about the mechanism by which the NV supports the viral growth. In this study, cellular localization of NV and its role in IHNV growth in host cells was investigated. Through transient transfection in RTG-2 cells of NV fused to green fluorescent protein (GFP), a nuclear localization of NV was demonstrated. Deletion analyses showed that the (32)EGDL(35) residues were essential for nuclear localization of NV protein, and fusion of these 4 amino acids to GFP directed its transport to the nucleus. We generated a recombinant IHNV, rIHNV-NV-Delta EGDL in which the (32)EGDL(35) was deleted from the NV. rIHNVs with wild-type NV (rIHNV-NV) or with the NV gene replaced with GFP (rIHNV-Delta NV-GFP) were used as controls. RTG-2 cells infected with rIHNV-Delta NV-GFP and rIHNV-NV-Delta EGDL yielded 12- and 5-fold less infectious virion, respectively, than wild type rIHNV-infected cells at 48 h post-infection (p.i.). While treatment with poly I: C at 24 h p.i. did not inhibit replication of wild-type rIHNVs, replication rates of rIHNV-Delta NV-GFP and rIHNV-NV-Delta EGDL were inhibited by poly I: C. In addition, both rIHNV-Delta NV and rIHNV-NV-Delta EGDL induced higher levels of expressions of both IFN1 and Mx1 than wild-type rIHNV. These data suggest that the IHNV NV may support the growth of IHNV through inhibition of the INF system and the amino acid residues of 32 EGDL 35 responsible for nuclear localization are important for the inhibitory activity of NV.
- 出版日期2011-7-21
