Antibody status to influenza A/Singapore/1/57(H2N2) in Finland during a period of outbreaks caused by H3N2 and H1N1 subtype viruses

Abstract

The incidence of haemagglutination inhibition (HI) antibody (titre greater than or equal to 12) to influenza A/Singapore/1/57(H2N2) in sera collected from a Finnish population in the summer of 1981 was 58%. Subjects born after 1968 were essentially seronegative, and a comparable low HI antibody status was also recorded among the elderly, the lowest being in people born during the period 1901-10. A small increase in antibody titre to the H2N2 virus was observed in the different age groups after infections with the H3N2, but not the H1N1, subtype influenza A viruses. The heterotypic response, which could be due to HI or NA antibodies, was restricted almost exclusively to subjects already exhibiting this antibody in acute phase sera. Moreover, the anamnestic boosting was not as strong as that described in earlier studies from samples collected at the beginning of the present era of H3N2 viruses. At population level, the HI antibody status to H2N2 was about the same at the beginning and end of the follow-up period which covered eight epidemic seasons. The results are discussed with respect to the doctrine of 'original antigenic sin' and to the threat of re-emergence of the H2N2 viruses.

B Cell Responses during Secondary Dengue Virus Infection Are Dominated by Highly Cross-Reactive, Memory-Derived Plasmablasts

“…The low levels of binding to DENV2 detected validated our hypothesis that these plasmablasts resulted from the reactivation of MBCs from a past DENV1 exposure, rather than as part of a naive response to the current DENV2 infection. OAS has been well described for antibody responses to repeated influenza virus exposures (47)(48)(49)(50), and a few reports have demonstrated this phenomenon in the secondary dengue virus B cell response, as well (29,51,52). Our data strongly suggest that OAS may play a role in the secondary dengue virus immune response and result in decreased binding affinity and neutralization potency against the infecting serotype.…”

Humans and Ferrets with Prior H1N1 Influenza Virus Infections Do Not Exhibit Evidence of Original Antigenic Sin after Infection or Vaccination with the 2009 Pandemic H1N1 Influenza Virus

“…We did not consider Յ4-fold antibody titer rises to be significant. However, some investigators interpret even a 2-fold rise in the titer of antibody against the first virus of a sequential infection to be evidence of OAS (50). Furthermore, some studies reported the occurrence of OAS without observing a boost in the response to the first virus in some instances (51) or without evidence of a diminished response to the second virus (50) in sequential infections.…”

Assessment of transmission, pathogenesis and adaptation of H2 subtype influenza viruses in ferrets

“…H2N2 viruses established a stable presence in humans for 11 years and caused approximately 2 million deaths worldwide before they disappeared from human circulation following the emergence of the 1968 pandemic H3N2 virus (Simonsen et al, 1998). The reintroduction of the H2 subtype into the human population would pose a significant global health threat in a population where the majority of humans now lack anti-H2 hemagglutinin (HA) serologic immunity (Pyhala 1985; Webster 1997; Nabel et al, 2011). Avian influenza virus surveillance provides evidence for the continuing circulation of H2 viruses in wild migratory birds and poultry in live bird markets (Schafer et al, 1993; Piaggio et al, 2012; Chen et al, 2010).…”