Nakajima S, Nobusawa E, Nakajima K
Department of Microbiology, National Institute of Public Health, Shirokanedai, Minato-ku, Tokyo 108-8638, Japan.
Virology. 2000 Aug 15;274(1):220-31. doi: 10.1006/viro.2000.0453.
Eight convalescent human sera obtained from patients aged 3 to 14 years old, who were infected with influenza A(H3N2) virus during the 1990/1991 influenza season, were characterized by a binding assay with chimeric hemagglutinin (HA) proteins between influenza virus A/Aichi/2/68 and A/Kamata/14/91(H3N2) strains. These sera did not recognize the HA protein of the A/Aichi/2/68 strain but recognized that of the A/Kamata/14/91 strain. The binding assay revealed that these sera recognized only the HA1 domain of A/Kamata/14/91 HA protein. A further assay of the binding of these sera to the chimeric proteins of the HA1 domain revealed that three sera (A-1, A-2, and A-3) from very young patients bound only to region 150-170 (site B1) and one serum (Y-1) bound to regions 96-150 (site A) and 96-170 (sites A and B1). These four sera showed reduced hemagglutination inhibition (HI) activity with the 203v2 strain, a monoclonal variant of the A/Kamata/14/91 strain with two amino acid changes in the HA protein at antigenic sites A and B1. The other four sera (Y-2, G-1, G-2, and A-4) bound to regions 1-96 (site C/E), 96-150 (site A), 96-170 (sites A and B1), and 170-200 (site B2), two of which further bound to region 240-306 (site C); these sera were all fully reactive with the 203v2 strain. All eight sera showed reduced HI reactivity to a drift strain A/Aichi/4/93. Amino acid changes of the A/Aichi/4/93 strain from the A/Kamata/14/91 strain were located at antigenic sites A, B1, B2, and C. We propose a possible model for the emergence of a drift strain A/Aichi/4/93 from an A/Kamata/14/91-like strain by sequential changes during reinfections of individuals starting from A-1-like, next to Y-1-like, and then to Y-2-like populations.
从1990/1991流感季节感染甲型（H3N2）流感病毒的3至14岁患者中获得了8份恢复期人血清，通过与甲型流感病毒A/爱知/2/68和A/镰田/14/91（H3N2）毒株之间的嵌合血凝素（HA）蛋白进行结合试验对其进行了特性分析。这些血清不识别A/爱知/2/68毒株的HA蛋白，但识别A/镰田/14/91毒株的HA蛋白。结合试验表明，这些血清仅识别A/镰田/14/91 HA蛋白的HA1结构域。对这些血清与HA1结构域的嵌合蛋白结合的进一步分析表明，来自非常年幼患者的3份血清（A-1、A-2和A-3）仅与第150 - 170区域（位点B1）结合，1份血清（Y-1）与第96 - 150区域（位点A）和第96 - 170区域（位点A和B1）结合。这4份血清对203v2毒株（A/镰田/14/91毒株的单克隆变异株，其HA蛋白在抗原位点A和B1有两个氨基酸变化）的血凝抑制（HI）活性降低。其他4份血清（Y-2、G-1、G-2和A-4）与第1 - 96区域（位点C/E）、第96 - 150区域（位点A）、第96 - 170区域（位点A和B1）以及第170 - 200区域（位点B2）结合，其中两份还与第240 - 306区域（位点C）结合；这些血清与203v2毒株均具有完全反应性。所有8份血清对漂移毒株A/爱知/4/93的HI反应性均降低。A/爱知/4/93毒株相对于A/镰田/14/91毒株的氨基酸变化位于抗原位点A、B1、B2和C。我们提出了一个可能的模型，用于解释从A/镰田/14/91样毒株出现漂移毒株A/爱知/4/93的过程，即在个体再次感染期间，从类似A-1的群体开始，接着是类似Y-1的群体，然后是类似Y-2的群体依次发生变化。
