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  • Title: Surveillance of influenza in Houston, Texas, USA: gradual transition from A/Victoria/75 (H3N2) to A/Texas/77 (H3N2) predominance and antigenic characterization of "intermediate" strains.
    Author: Velazco JG, Couch RB, Six HR, Glezen WP.
    Journal: Bull World Health Organ; 1983; 61(2):345-52. PubMed ID: 6190585.
    Abstract:
    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.
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