Changes in the haemagglutinin and the neuraminidase genes prior to the emergence of highly pathogenic H7N1 avian influenza viruses in Italy
Changes in the haemagglutinin and the neuraminidase genes prior to the emergence of highly pathogenic H7N1 avian influenza viruses in Italy
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DOI：
10.1007/s007050170128
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发表时间：
2001-01-01
影响因子：
2.7
通讯作者：
Alexander, DJ
中科院分区：
文献类型：
--
作者：
Banks, J;Speidel, ES;Alexander, DJ
从1999年3月至1999年12月，北方意大利的家禽中发生了由低致病性H7 N1病毒引起的禽流感暴发，当时出现了高致病性禽流感（HPAI）病毒。核苷酸序列测定的HA 1和茎区的神经氨酸酶（NA）的病毒从爆发。高致病性禽流感病毒有一个不寻常的多碱基血凝素（HA）切割位点基序，PEIPKG（SRVR）下的酒吧RGLF。系统发育分析显示，高致病性禽流感病毒来自低致病性病毒，它们与野鸟分离株A/teal/Taiwan/98关系最密切。另外的糖基化位点存在于两个独立谱系的HA的氨基酸位置149处，以及所有HPAI和一些低致病性病毒的位置123处。其他病毒没有额外的糖基化位点。从意大利暴发中检查的所有病毒在NA茎中有22个氨基酸缺失，这在所检查的野生鸟类病毒的N1基因中不存在。我们的结论是，意大利HPAI病毒产生的低致病性菌株，并在NA柄的缺失，随后收购额外的糖基化附近的受体结合位点的HA 1可能是一个适应的H7病毒的一个新的宿主物种，即家禽。
Outbreaks of avian influenza due to an H7N1 virus of low pathogenicity occurred in domestic poultry in northern Italy from March 1999 until December 1999 when a highly pathogenic avian influenza (HPAI) virus emerged. Nucleotide sequences were determined for the HA1 and the stalk region of the neuraminidase (NA) for viruses from the outbreaks. The HPAI viruses have an unusual multibasic haemagglutinin (HA) cleavage site motif, PEIPKG (SRVR) under bar RGLF. Phylogenetic analysis showed that the HPAI viruses arose from low pathogenicity viruses and that they are most closely related to a wild bird isolate, A/teal/Taiwan/98. Additional glycosylation sites were present, at amino acid position 149 of the HA for two separate lineages, and at position 123 for all HPAI and some low pathogenicity viruses. Other viruses had no additional glycosylation sites. All viruses examined from the Italian outbreaks had a 22 amino acid deletion in the NA stalk that is not present in the N1 genes of the wild bird viruses examined. We conclude that the Italian HPAI viruses arose from low pathogenicity strains, and that a deletion in the NA stalk followed by the acquisition of additional glycosylation near the receptor binding site of HA1 may be an adaptation of H7 viruses to a new host species i.e. domestic poultry.