tetano
Editor, Senior Moderator
J Infect Dis. 2017 Dec 27;217(1):3-11. doi: 10.1093/infdis/jix546.
[h=1]Primary Human Influenza B Virus Infection Induces Cross-Lineage Hemagglutinin Stalk-Specific Antibodies Mediating Antibody-Dependent Cellular Cytoxicity.[/h] de Vries RD[SUP]1[/SUP], Nieuwkoop NJ[SUP]1[/SUP], van der Klis FRM[SUP]2[/SUP], Koopmans MPG[SUP]1[/SUP], Krammer F[SUP]3[/SUP], Rimmelzwaan GF[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A virus (IAV) and influenza B virus (IBV) cause substantial morbidity and mortality during annual epidemics. Two distinct lineages of IBV are distinguished, based on variation in hemagglutinin (HA): B/Victoria/2/87-like (B/Vic) and B/Yamagata/16/88-like (B/Yam). Here, we show that, in humans, primary IBV infection with either lineage induces HA-specific antibody-dependent cellular cytotoxicity (ADCC)-mediating antibodies. IBV infection induced antibodies specific to the HA head and stalk, but only HA stalk-specific antibodies mediated ADCC efficiently and displayed cross-reactivity with IBV of both lineages. This corresponds to recent findings that 2 points of contact between the effector and target cell (ie, HA and sialic acid, respectively, and the fragment crystallizable [Fc] domain and Fcγ receptor IIIα, respectively) are required for efficient ADCC activity and that antibodies specific for the receptor-binding site located in the head domain of HA therefore fail to mediate ADCC. Potentially, ADCC-mediating antibodies directed to the HA stalk of IBV contribute to cross-protective immunity to IBV of both lineages.
[h=4]KEYWORDS:[/h] Influenza B virus; antibodies; antibody-dependent cellular cytotoxicity; hemagglutinin; natural killer cells
PMID: 29294018 DOI: 10.1093/infdis/jix546
[h=1]Primary Human Influenza B Virus Infection Induces Cross-Lineage Hemagglutinin Stalk-Specific Antibodies Mediating Antibody-Dependent Cellular Cytoxicity.[/h] de Vries RD[SUP]1[/SUP], Nieuwkoop NJ[SUP]1[/SUP], van der Klis FRM[SUP]2[/SUP], Koopmans MPG[SUP]1[/SUP], Krammer F[SUP]3[/SUP], Rimmelzwaan GF[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A virus (IAV) and influenza B virus (IBV) cause substantial morbidity and mortality during annual epidemics. Two distinct lineages of IBV are distinguished, based on variation in hemagglutinin (HA): B/Victoria/2/87-like (B/Vic) and B/Yamagata/16/88-like (B/Yam). Here, we show that, in humans, primary IBV infection with either lineage induces HA-specific antibody-dependent cellular cytotoxicity (ADCC)-mediating antibodies. IBV infection induced antibodies specific to the HA head and stalk, but only HA stalk-specific antibodies mediated ADCC efficiently and displayed cross-reactivity with IBV of both lineages. This corresponds to recent findings that 2 points of contact between the effector and target cell (ie, HA and sialic acid, respectively, and the fragment crystallizable [Fc] domain and Fcγ receptor IIIα, respectively) are required for efficient ADCC activity and that antibodies specific for the receptor-binding site located in the head domain of HA therefore fail to mediate ADCC. Potentially, ADCC-mediating antibodies directed to the HA stalk of IBV contribute to cross-protective immunity to IBV of both lineages.
[h=4]KEYWORDS:[/h] Influenza B virus; antibodies; antibody-dependent cellular cytotoxicity; hemagglutinin; natural killer cells
PMID: 29294018 DOI: 10.1093/infdis/jix546