scholarly journals An optimized enzyme-linked lectin assay to measure influenza A virus neuraminidase inhibition antibody titers in human sera

2014 ◽  
Vol 210 ◽  
pp. 7-14 ◽  
Author(s):  
Laura Couzens ◽  
Jin Gao ◽  
Kim Westgeest ◽  
Matthew Sandbulte ◽  
Vladimir Lugovtsev ◽  
...  
1977 ◽  
Vol 5 (3) ◽  
pp. 353-360
Author(s):  
Khosrow Farrohi ◽  
Fakhrissadat K. Farrohi ◽  
Gary R. Noble ◽  
Harold S. Kaye ◽  
Alan P. Kendal

Antibodies to the H3 hemagglutinin of influenza A virus could be specifically measured by single radial hemolysis (SRH) when test antigens were recombinant viruses containing the relevant H3 hemagglutinin antigen and irrelevant Neq1 neuraminidase of A/equine/Prague/1/56 virus. Antibodies to influenza B virus could also be measured by the SRH technique. Antibody rises to influenza A or B virus measured by SRH agreed with results of hemagglutination inhibition (HI) tests for about 80% of the sera tested, including sera from volunteers receiving killed influenza vaccine and sera from patients naturally infected with influenza. Correlation between antibody titers measured by SRH and HI was also good. Antibodies to the N2 neuraminidase of influenza A virus could be specifically measured by SRH when test antigens were recombinant viruses containing the relevant N2 neuraminidase antigen and irrelevant Heq1 hemagglutinin of A/equine/Prague/1/56 virus. The SRH test for neuraminidase antibodies was more strain specific than was the SRH test for hemagglutinin antibodies. Probably for this reason, agreement between neuraminidase antibody determinations in human sera by the SRH test and by the neuraminidase inhibition test was poorer than agreement between the SRH test for hemagglutinin antibodies and the HI test.


Author(s):  
Michael Hinojosa ◽  
Samuel S Shepard ◽  
Jessie R Chung ◽  
Jennifer P King ◽  
Huong Q McLean ◽  
...  

Abstract Background Preexisting antibodies to influenza, shaped by early infection and subsequent exposures, may impact responses to influenza vaccination. Methods We enrolled 72 children (aged 7–17 years) in 2015–2016; all received inactivated influenza vaccines. Forty-one were also vaccinated in 2014–2015, with 12 becoming infected with A(H3N2) in 2014–2015. Thirty-one children did not have documented influenza exposures in the prior 5 seasons. Sera were collected pre- and postvaccination in both seasons. We constructed antibody landscapes using hemagglutination inhibition antibody titers against 16 A(H3N2) viruses representative of major antigenic clusters that circulated between 1968 and 2015. Results The breadth of the antibody landscapes increased with age. Vaccine-induced antibody responses correlated with boosting of titers to previously encountered antigens. Postvaccination titers were the highest against vaccine antigens rather than the historic A(H3N2) viruses previously encountered. Prevaccination titers to the vaccine were the strongest predictors of postvaccination titers. Responses to vaccine antigens did not differ by likely priming virus. Influenza A(H3N2)-infected children in 2014–2015 had narrower antibody landscapes than those uninfected, but prior season infection status had little effect on antibody landscapes following 2015–2016 vaccination. Conclusions A(H3N2) antibody landscapes in children were largely determined by age-related immune priming, rather than recent vaccination or infection.


1965 ◽  
Vol 63 (4) ◽  
pp. 479-490 ◽  
Author(s):  
G. C. Schild ◽  
C. H. Stuart-Harris

Determinations were made of the age distribution of antibody to swine virus and representatives of the various families of human influenza A virus in 1961–62 collections of human sera and paired sera from forty individuals taken in 1952 and 1963:(a) The existence of cohorts of the population, each with a dominant antibody type related to strains of virus first encountered in childhood, was confirmed.(b) The basic epidemiological pattern was similar to that previously detected in 1954. However, it seemed that antibody to swine virus had been reinforced but not antibody to A and A1 strains.(c) Neutralizing and HI antibodies to A/Equine/Miami/63 virus were detected only in the sera of older people (65 years or over) collected in 1964. No antibodies were found to A/Equine/Prague/56 or two duck viruses.(d) Relatively constant levels of antibody to A, A1 and A 2 viruses were present in sera from aged persons but antibody to swine virus diminished with age. This could be attributed to a lack of swine antibody in the older females.


2018 ◽  
Vol 97 ◽  
pp. 385-394 ◽  
Author(s):  
Jing Jin ◽  
Shuo Chen ◽  
Dechuan Wang ◽  
Yuanjin Chen ◽  
Yuxu Wang ◽  
...  

1955 ◽  
Vol 101 (6) ◽  
pp. 627-638 ◽  
Author(s):  
Paul Gerber ◽  
Clayton G. Loosli ◽  
Dorothy Hamre

Antigenically different strains of mouse-adapted PR8 influenza A virus have been produced by 17 serial passages of the virus in the lungs of mice immunized with the homologous agent. Comparative serological tests show that the variant strains share antigenic components with the parent strain but the dominant antigen is different. By means of antibody absorption it was shown that the "new" antigenic component of the variant was already present in minor amounts up to the eighth passage and thereafter gained prominence with continued passage in vaccinated mice. Groups of mice vaccinated with either the PR8-S or T21 virus and having comparable antibody titers showed no growth of virus in the lungs following aid-borne challenge with homologous strains. On the other hand, following heterologous air-borne challenge no deaths occurred, but virus grew in the lungs of both groups of vaccinated mice. Almost unrestricted virus multiplication took place in the lungs of mice vaccinated with the parent strain and challenged with the PR8-T21 virus which resulted in extensive consolidation. Less virus grew in the lungs of the mice vaccinated with the variant strains and challenged with the PR8-S virus. In these animals only microscopic evidence of changes due to virus growth in the lungs was observed. The successful serial passage of PR8 influenza A virus in immunized animals was dependent on the initial selection of mice with uniformly low H.I. antibody titers as determined on tail blood, and the intranasal instillation of sufficient virus to favor the survival of those virus particles least related to the antibodies present. The epidemiological implications of these observations are discussed briefly.


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