Key result
Recombinant pSIgA, but not IgG, significantly inhibited the production of progeny virus particles and reduced plaque formation in vitro across multiple Influenza A virus subtypes.
Why the study?
The mechanisms by which influenza A virus hemagglutinin-specific pSIgA antibodies exert cross-protective immunity against multiple influenza A subtypes were not fully understood.
Polymeric secretory IgA (pSIgA) exerts broad cross-protective antiviral activity against multiple influenza A virus subtypes by inhibiting progeny virus production and plaque formation, unlike IgG.
pSIgA may inform broad anti-influenza strategies; leaves open translation from in vitro data to clinical use.
Mucosal immunity represented by pSIgA plays important roles in protection from IAV infection. Furthermore, IAV HA-specific pSIgA antibodies are thought to contribute to cross-protective immunity against multiple IAV subtypes. However, the mechanisms by which pSIgA exerts such versatile antiviral activity are not fully understood. In this study, we generated broadly cross-reactive recombinant IgG and pSIgA having the same antigen-recognition site and compared their antiviral activities in vitro . These recombinant antibodies did not show “classical” neutralizing activity, whereas pSIgA, but not IgG, significantly inhibited the production of progeny virus particles from infected cells. Plaque formation was also significantly reduced by pSIgA, but not IgG. These effects were seen in infection with IAVs of several different HA subtypes. Based on our findings, we propose an antibody-mediated host defense mechanism by which mucosal immunity may contribute to broad cross-protection from IAVs of multiple HA subtypes, including viruses with pandemic potential.
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Okuya et al. (2020) studied Influenza A Virus (IAV) infection. Recombinant pSIgA vs. Recombinant IgG was evaluated on Inhibition of progeny virus particle production and plaque formation in vitro. Recombinant pSIgA, but not IgG, significantly inhibited the production of progeny virus particles and reduced plaque formation in vitro across multiple Influenza A virus subtypes.
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