中文摘要：

积极喉咙拖把在在 6 月和 2009 年 11 月之间的浙江，湖北和广东从发烧病人收集了的 100 H1N1 流感 real-time-PCR 的一个总数，被本地 CDC 实验室提供。在 MDCK 房间文化以后， 57 流行性感冒 A 流行(H1N1 ) 病毒为整个染色体定序被孤立并且提交。39 的一个总数哈序列， 52 个 NA 序列， 36 个 PB2 序列， 31 个 PB1 序列， 40 个 PA 序列， 48 个 NP 序列， 51 个 MP 序列和 36 个 NS 序列被获得，包括 20 个整个染色体序列顺序比较表明他们与已知的流行紧张分享了相同(96%99%) 的高度(A/California/04/2009 (H1N1 ) 。种系发生的分析证明尽管序列高度被保存，他们与仅仅一些不同紧张聚类进组的一个小数字。地点分析揭示了三 HA 受体绑定地点在的在循环 220 点的替换(221228 ) 39 哈序列：A/Hubei/86/2009 PKVRDQEGPKVRDQEA， A/Zhejiang/08/2009 PKVRDQEGPKVRDQER， A/Hubei/75/2009 PKVRDQEGPKVRDQGG， A/Hubei/75/2009 从一个尖锐盒子被孤立，当时另外的二来自有温和症状的病人。另外的关键地点象 NA 蛋白质的 119， 274， 292 和 294 氨基酸那样， 627 PB2 蛋白质被保存。同时，所有 M2 蛋白质序列拥有了 Ser32Asn 变化，建议这些病毒对 adamantanes 抵抗。有从 NCBI 数据库收集的另外的 H1N1 病毒的这些序列的比较提供卓见进 H1N1 传播和发行量模式。

英文摘要：

A total of 100 H1N1 flu real-time-PCR positive throat swabs collected from fever patients in Zhejiang, Hubei and Guangdong between June and November 2009, were provided by local CDC laboratories. After MDCK cell culture, 57 Influenza A Pandemic （H1N1） viruses were isolated and submitted for whole genome sequencing. A total of 39 HA sequences, 52 NA sequences, 36 PB2 sequences, 31 PB1 sequences, 40 PA sequences, 48 NP sequences, 51 MP sequences and 36 NS sequences were obtained, including 20 whole genome sequences. Sequence comparison revealed they shared a high degree of homology （96%-99%） with known epidemic strains （A/Califomia/04/2009（H1N1）. Phylogenetic analysis showed that although the sequences were highly conserved, they clustered into a small number of groups with only a few distinct strains. Site analysis revealed three substitutions at loop 220 （221-228） of the HA receptor binding site in the 39 HA sequences： A/Hubei/86/2009 PKVRDQEG→PKVRDQEA, A/Zhejiang/08/2009 PKVRDQEG→PKVRDQER, A/Hubei/75/2009 PKVRDQEG→PKVRDQGG, the A/Hubei/75/2009 was isolated from an acute case, while the other two were from patients with mild symptoms. Other key sites such as 119, 274, 292 and 294 amino acids of NA protein,627 of PB2 protein were conserved. Meanwhile, all the M2 protein sequences possessed the Ser32Asn mutation, suggesting that these viruses were resistant to adamantanes. Comparison of these sequences with other H1N1 viruses collected from the NCBI database provides insight into H1N1 transmission and circulation patterns.