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Cross‐protection against influenza A virus infection by passively transferred respiratory tract IgA antibodies to different hemagglutinin molecules
Author(s) -
Tamura ShinIchi,
Funato Hirono,
Hirabayashi Yoshihiro,
Suzuki Vujiro,
Nagamine Takashi,
Aizawa Chikara,
Kurata Takeshi
Publication year - 1991
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830210602
Subject(s) - biology , virology , hemagglutinin (influenza) , respiratory tract , virus , antibody , immunoglobulin a , microbiology and biotechnology , influenza a virus , immunization , nasal administration , immunology , orthomyxoviridae , respiratory system , immunoglobulin g , anatomy
Abstract Mice that were intranasally immunized with different influenza A virus hemagglutinins (HA), derived from PR8 (H1N1), A/Yamagata (H1N1) or A/Fukuoka (H3N2) virus, together with cholera toxin B subunit as an adjuvant, were examined for protection against PR8 infection; PR8 HA and A/Yamagata HA immunization conferred complete protection, while A/Fukuoka HA immunization failed to confer protection. In parallel with protection, PR8 HA‐, A/Yamagata HA‐, and A/Fukuoka HA‐immunized mice produced a high, a moderate and a low level of PR8 HA‐reactive IgA in the respiratory tract, respectively. These IgA antibodies were not only higher in content in the nasal secretions, but also more cross‐reactive than IgG. The purified IgA antibodies from respiratory tract washings of PR8 HA‐immunized mice, which contained the HA‐specific IgA corresponding to the amount deteced in the nasal wash, were able to protect mice from PR8 challenge when transferred to the respiratory tract of naive mice. The transfer of IgA from A/Yamagata HA‐immunized mice also afforded cross‐protection against PR8 infection, whereas the IgA from A/Fukuoka HA‐immunized mice failed to provide protection. The ability of transferred IgA to prevent viral infection was dependent on the amount of HA‐reactive IgA remaining in the respiratory tract of the host at the time of infection. These experiments directly demonstrate that IgA antibodies to influenza A virus HA by themselves play a pivotal role in defence not only against homologous virus infection, but also against heterologous drift virus infection at the respiratory mucosa, the portal of entry for the viruses.