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Biomedical subjects

R G Webster

Publications and source records attributed to R G Webster.

At least 451 records · Page 25Linked to original sources
PubMed1969

Immunological interrelationships of Hong Kong, Asian and equi-2 influenza viruses in man.

Sera from an elderly population drawn prior to the 1968 Hong Kong influenza epidemic were found to have a high prevalence of Hong Kong antibody, indicating the circulation of a Hong Kong-like virus before 1900. This report compares an elderly (birth dates before 1892) and a young adult population with regard to serum antibody response to Hong Kong variant vaccine, avidity of Hong Kong antibody, and antibody absorption with Asian, A/Equi-2, and Hong Kong viruses.The demonstration of doubly-absorbable Hong Kong and A/Equi-2 antibodies in sera where both are present and of doubly-absorbable Hong Kong and Asian antibodies in young adult sera after Hong Kong variant vaccine lends new support to the view that there is an immunological relationship between these viruses.The difference in the response of the two age-groups to Hong Kong variant vaccine-specifically the anamnestic boosting of Hong Kong antibody together with the lack of Asian antibody rise in the elderly population in contrast to the striking Asian antibody response in the young adult population-leads to the conclusion that a Hong Kong-like virus may have been the original antigenic sin in the elderly population with initial Asian exposure in 1957. The excellent avidity of Hong Kong antibody in pre- and post-vaccine sera from the elderly suggests a close similarity if not identity of the haemagglutinins of the Hong Kong-like virus that circulated in human populations prior to 1900 and of the 1968 Hong Kong virus.

Adult↗
PubMed1968

Antiviral activity of antiserum specific for an influenza virus neuraminidase.

Antiserum specific for influenza A(2) neuraminidase was produced by immunization of rabbits with the purified enzyme which had been isolated by electrophoresis from the proteins of a detergent-disrupted A(0)A(2) influenza virus recombinant [X-7 (F1)]. This recombinant contained hemagglutinin of the A(0) subtype and A(2) neuraminidase. Antiserum to the isolated A(2) neuraminidase did not react in any of four serological tests with A(0) or A(2) subtype viruses that lacked the A(2) enzyme. In contrast, the antiserum inhibited the neuraminidase activity only of wild-type and recombinant viruses containing the A(2) enzyme, regardless of the nature of their hemagglutinin proteins. The antiserum caused hemagglutination-inhibition of some, but not all, viruses bearing the A(2) enzyme, and it reduced the plaque size or plaque number of all viruses tested that contained A(2) neuraminidase. In the chick embryo and in cell culture, low dilutions of antiserum reduced the yield of virus. True neutralization of virus in the chick embryo did not occur. We conclude that an antiserum specific for A(2) neuraminidase influenced the yield and release of virus from influenza virus-infected cells.

Animals↗
PubMed1966

Disquisitions of Original Antigenic Sin. I. Evidence in man.

When primary immunity is boosted not by the homologous but by a crossreacting vaccine, the newly formed antibodies react better with the primary antigen than with the antigen actually eliciting the response. This phenomenon bears the name of Original Antigenic Sin (1). It is shown that the number of antibody molecules produced against the original and the vaccinating antigen is the same; that each of these molecules is capable of reacting with both antigens; that the activity of an antiserum can be completely absorbed with either antigen; that both residual and adsorbed-dissociated fractions of antibody exhibit the same relative affinities towards the two antigens as did the native serum; that, unlike standard primary and secondary responses, the population of antibody molecules characterizing the Original Antigenic Sin is homogeneous; that each molecule has a lower equilibrium constant (i.e. higher avidity) against the original antigen than against the antigen stimulating the present response; and that all equilibrium constants are typical of secondary antibody. It is concluded that the Original Antigenic Sin is a partial anamnestic response, a related antigen stimulating that sector only of the originally primed cells which is destined to produce cross-reacting antibody. A hypothesis is developed according to which the basic difference between primary and secondary reactivity rests on the presence of a trapping mechanism that allows anamnestic production of antibody against lower doses of the homologous antigen. Such a mechanism is capable of cross-trapping related antigens, thus preventing a standard primary response and allowing manifestations of Original Antigenic Sin.

Antibody Formation↗
PubMed1966

Disquisitions on Original Antigenic Sin. II. Proof in lower creatures.

Experiments in rabbits were designed to test the two unproven assumptions of the hypothesis proposed in the companion paper (1): that Original Antigenic Sin is fundamentally a restricted anamnestic response, and that there exists a trapping mechanism capable of deflecting antigen from one kind of cell and guiding it to another. It is shown that whole-body X-irradiation, sufficient to abolish primary but not secondary production of antibodies, leaves all manifestations of the Original Antigenic Sin untouched. This proves the first assumption. Primary immune animals challenged with very large doses of a related antigen produce an immediate response of cross-reactive antibodies, followed by a standard primary response to the challenging antigen. When boosted with an appropriate mixture of both antigens, the response is of standard secondary type to the homologous antigen, followed by a standard primary response to the crossreacting antigen. When animals are primarily vaccinated with a mixture of two related antigens, small booster doses of either will stimulate a standard secondary response only. When such animals are given very large booster doses of either antigen, the response is a compound of a homologous secondary and of an Original Antigenic Sin-type against the related antigen. Each of these findings demonstrates a corollary of the second assumption. The results are discussed in terms of the limitations they impose on theories concerned with the production of antibodies.

Animals↗