禽流感病毒NS第263～277位核苷酸缺失降低其抗干扰素能力

2000年以来，多数H5N1亚型禽流感病毒在NS基因的263～277位发牛15个碱基的缺失。为了研究此缺失在流感病毒进化中的生物学意义，构建H5N1亚型流感病毒A／SD／04株的HA、NA、NS的全基因表达载体，以及NS基因263～277位删除的突变载体。通过反向遗传学技术，与编码WSN的其他内部基因（PB2，PB1，PA，NP和M）的表达载体进行组合转染，获得在NS基因的263～277位缺失和不缺失的2个重组H5N1亚型流感病毒（RWSN—m248和RWSN-248）。此两个重组病毒在无干扰素产生的Vero细胞上的繁殖滴度相似，在能产生干扰素的细胞MDCK和COS-1细胞上的繁殖滴度有明显差异。两个重组病毒在鸡胚中的繁殖滴，IVPI，MDT和EID50均无显著差异。说明NS基因的263～277位核苷酸的缺失不影响病毒的整体毒力，但降低了H5N1的抗干扰素能力。

Deletion of Nucleotides of NS Gene from 263 to 277 Decreases the Viral Anti-IFN Ability of H5N1

Since 2000,most of H5N1 subtype influenza A virus had a unique mutation of NS gene with 15base pair deletion from 263 to 277. In order to investigate the bio-characteristics of this mutation,two different NS recombinants,RWSN-248 and RWSN-m248,were generated via plasmid rescue from A/WSN/33(H1N1) and A/SD/04(H5N1). RWSN-248 had a higher viral titer than RWSN-m248 in MDCK and COS-1 cells that have an IFN response,but they had the similar growth ability in Vero cells that lack an IFN response. Both of two recombinants grew well in embryonated chicken eggs and had the similar viral titer and MDT. The results above revealed that the deletion from 263 to 277 sites of NS gene did not influence viral virulence to but decreased viral anti-IFN ability of H5N1.