Elleman C J, Barclay W S
School of Animal and Microbial Sciences, University of Reading, Whiteknights, Reading RG6 6AJ, UK.
Virology. 2004 Mar 30;321(1):144-53. doi: 10.1016/j.virol.2003.12.009.
We show that most isolates of influenza A induce filamentous changes in infected cells in contrast to A/WSN/33 and A/PR8/34 strains which have undergone extensive laboratory passage and are mouse-adapted. Using reverse genetics, we created recombinant viruses in the naturally filamentous genetic background of A/Victoria/3/75 and established that this property is regulated by the M1 protein sequence, but that the phenotype is complex and several residues are involved. The filamentous phenotype was lost when the amino acid at position 41 was switched from A to V, at the same time, this recombinant virus also became insensitive to the antibody 14C2. On the other hand, the filamentous phenotype could be fully transferred to a virus containing RNA segment 7 of the A/WSN/33 virus by a combination of three mutations in both the amino and carboxy regions of the M1 protein. This observation suggests that an interaction among these regions of M1 may occur during assembly.
我们发现，与经过广泛实验室传代并适应小鼠的A/WSN/33和A/PR8/34毒株不同，大多数甲型流感病毒分离株会在感染细胞中诱导丝状变化。利用反向遗传学技术，我们在A/维多利亚/3/75自然丝状遗传背景下创建了重组病毒，并确定该特性受M1蛋白序列调控，但表型复杂且涉及多个残基。当第41位氨基酸从A切换为V时，丝状表型消失，同时，这种重组病毒也对抗体14C2不敏感。另一方面，通过在M1蛋白的氨基和羧基区域进行三个突变的组合，丝状表型可以完全转移到含有A/WSN/33病毒RNA片段7的病毒中。这一观察结果表明，M1这些区域之间的相互作用可能在组装过程中发生。
