The vRNAs of influenza A viruses contain 12 and 13 nucleotide-long sequences at their 3′ and 5′ termini respectively that are highly conserved and constitute the vRNA promoter. These sequences and the next three segment-specific nucleotides show inverted partial complementarity and are followed by several unpaired nucleotides of poorly characterized function at the 3′ end. We have performed systematic point-mutations at the segment-specific nucleotides 15–18 of the 3′-end of a NS-like vRNA segment. All NS-like vRNAs containing mutations at position 15, and some at positions 16–18 showed reduced transcription/replication efficiency in a transfection/infection system. In addition, the replication of recombinant viruses containing mutations at position 15 was impaired both in single and multi-cycle experiments. This reduction was the consequence of a decreased expression of the NS segment. The data indicate that NS1 plays a role in the transcription/replication of its own segment, which elicits a global defect on virus replication.

甲型流感病毒的vRNA在其3'和5'末端分别包含12和13个核苷酸长的序列，这些序列高度保守并构成vRNA启动子。这些序列和接下来的三个片段特异性核苷酸显示出反向的部分互补性，并在3'端跟随几个功能不佳的未配对核苷酸。我们在NS样vRNA片段3'末端的片段特异性核苷酸15-18处进行了系统的点突变。在转染/感染系统中，所有在15位含有突变的NS类vRNA以及在16-18位具有某些突变的vRNA均显示出降低的转录/复制效率。另外，在单周期和多周期实验中，在位置15处含有突变的重组病毒的复制均受到损害。这种减少是NS节段表达减少的结果。数据表明NS1在其自身片段的转录/复制中起作用，这引发了病毒复制的整体缺陷。