Velazco J G, Couch R B, Six H R, Glezen W P
Bull World Health Organ. 1983;61(2):345-52.
Influenza epidemics in Houston, Texas, USA, during the winters of 1975-76, 1976-77, and 1977-78 were attributed to A/Victoria/3/75 (H3N2), B/Hong Kong/5/72, and A/Texas/1/77 (H3N2)-like viruses, respectively. Both A/Victoria and A/Texas viruses were detected towards the end of the 1976-77 epidemic and throughout the 1977-78 epidemic. To determine if there had been a gradual transition in the predominant strain, 267 viral isolates from the 1975-76 epidemic were tested for A/Texas virus. Eight specimens (3%) that appeared to contain A/Texas antigens were cloned and retested with specific antisera prepared in guinea-pigs and ferrets. One virus was identical to A/Texas/1/77 virus, two reacted like A/Victoria/3/75 and five reacted equally well with antisera prepared against A/Victoria/3/75 and A/Texas/1/77 viruses (bridging strains). The six viral isolates containing A/Texas antigens were obtained at different times during the epidemic, from all parts of the city, from males and females aged between 1 and 20 years.Characterization of type A influenza virus isolates obtained during the 1976-77 and 1977-78 epidemics revealed a progressive increase in the frequency of viruses containing A/Texas antigens, from 2.2% in 1975-76 to 32% in 1976-77 to 70% in 1977-78. Thus, both type A (H3N2) variants were present in the Houston community in 3 successive years.An antigenic analysis of the bridging viruses was performed by competition radio-immunoprecipitation assays and by reactivity with a set of monoclonal antibodies prepared against A/Texas/1/77 virus. These assays confirmed the identity of the A/Texas isolate with the prototype virus and indicated that the bridging strains shared antigenic determinants with both A/Vic/75 and A/Tex/77 viruses, but were more closely related to A/Victoria/3/75 virus.It seems clear that new variants of a subtype of type A influenza may not immediately displace the existing variant and that seeding in a community and transition from predominance of one variant to another may be a gradual process.
美国得克萨斯州休斯敦在1975 - 76年、1976 - 77年和1977 - 78年冬季发生的流感疫情分别归因于A/维多利亚/3/75（H3N2）、B/香港/5/72和A/得克萨斯/1/77（H3N2）样病毒。在1976 - 77年疫情接近尾声时以及整个1977 - 78年疫情期间均检测到了A/维多利亚和A/得克萨斯病毒。为确定优势毒株是否发生了逐渐转变，对1975 - 76年疫情中的267株病毒分离株进行了A/得克萨斯病毒检测。8份似乎含有A/得克萨斯抗原的标本（3%）被克隆，并用豚鼠和雪貂制备的特异性抗血清重新检测。一株病毒与A/得克萨斯/1/77病毒相同，两株的反应类似于A/维多利亚/3/75，5株与针对A/维多利亚/3/75和A/得克萨斯/1/77病毒制备的抗血清反应同样良好（桥接毒株）。这6株含有A/得克萨斯抗原的病毒分离株是在疫情期间的不同时间从全市各地、年龄在1至20岁的男性和女性中获得的。对1976 - 77年和1977 - 78年疫情期间获得的甲型流感病毒分离株的特征分析显示，含有A/得克萨斯抗原的病毒频率逐渐增加，从1975 - 76年的2.2%增至1976 - 77年的32%，再到1977 - 78年的70%。因此，两种甲型（H3N2）变异株连续3年在休斯敦社区中同时存在。通过竞争放射免疫沉淀试验以及与一组针对A/得克萨斯/1/77病毒制备的单克隆抗体的反应性，对桥接病毒进行了抗原分析。这些试验证实了A/得克萨斯分离株与原型病毒的一致性，并表明桥接毒株与A/维克/75和A/得克/77病毒均具有共同抗原决定簇，但与A/维多利亚/3/75病毒关系更密切。显然，甲型流感病毒一个亚型的新变异株可能不会立即取代现有的变异株，在社区中的传播以及从一种变异株占优势向另一种变异株占优势的转变可能是一个渐进的过程。
