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在西柏林分离出的甲型(H3N2)人流感病毒神经氨酸酶的抗原变异

Antigenic variation of neuraminidase of human type A influenza (H3N2) viruses isolated in Berlin (West).

作者信息

Werner J, Schudrowitz C, Köhler H

出版信息

Zentralbl Bakteriol Orig A. 1975 Dec;233(4):440-6.

PMID:56831
Abstract

After the emergence of the A/Hong Kong/1/68 (H3N2) strain of influenza virus antigenic variation of the hemagglutinin and neuraminidase antigens have been demonstrated leading to the identification of the variants A/England/42/72,a/Port Chalmers/1/73 and A/Scotland/840/74. This study describes antigenic changes of neuraminidases in influenza viruses isolated since 1968 in Berlin (West). A collection of 13 isolates of human type A influenza was studied in neuraminidase inhibition tests. The results are in line with data from other laboratories indicating a major change in the neuraminidase antigen as early as December 1969. The strains isolated at that time cross-reacted with an antiserum against the N2-Hong Kong enzyme to less than 50%. During the following years (1970 to 1972) the neuraminidase remained fairly stable. Serological cross-reactions showing 47 to 38% inhibition as compared to the homologous N2-antigen. The neuraminidase of the A/Berlin/3/72 strain revealed a close antigenic relationship to the later appearing A/Port Chalmers 1/73 variant. Two strains isolated in 1975 (January) showed an even further drift away from the then representative A/Port Chalmers/1/73 strain. The fact that the neuraminidase antigens of the Berlin viruses had changed in December 1969 may account for the severe 1969/70 influenza epidemic in Berlin affecting a large proportion of the population. Prevalent anti-neuraminidase antibodies may play a role in restricting a variant carrying a new hemagglutinin to primarily infected individuals by cross-reacting with a closely related enzyme.

摘要

在A/香港/1/68(H3N2)流感病毒株出现后,已证实血凝素和神经氨酸酶抗原发生了抗原变异,从而鉴定出变异株A/英格兰/42/72、A/查尔默斯港/1/73和A/苏格兰/840/74。本研究描述了1968年以来在西柏林分离的流感病毒中神经氨酸酶的抗原变化。对13株人A型流感病毒分离株进行了神经氨酸酶抑制试验研究。结果与其他实验室的数据一致,表明早在1969年12月神经氨酸酶抗原就发生了重大变化。当时分离的毒株与抗N2-香港酶的抗血清交叉反应率低于50%。在随后的几年(1970年至1972年),神经氨酸酶保持相当稳定。血清学交叉反应显示与同源N2抗原相比抑制率为47%至38%。A/柏林/3/72毒株的神经氨酸酶与后来出现的A/查尔默斯港1/73变异株显示出密切的抗原关系。1975年1月分离的两株毒株甚至与当时具有代表性的A/查尔默斯港/1/73毒株有更大的抗原漂移。1969年12月柏林病毒的神经氨酸酶抗原发生变化这一事实,可能是导致1969/70年柏林流感大流行、影响很大一部分人口的原因。普遍存在的抗神经氨酸酶抗体可能通过与密切相关的酶交叉反应,在将携带新血凝素的变异株限制在主要感染个体中发挥作用。

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