tetano
Editor, Senior Moderator
Antiviral Res. 2018 Sep 1. pii: S0166-3542(18)30314-0. doi: 10.1016/j.antiviral.2018.08.017. [Epub ahead of print]
[h=1]Passively transferred M2e-specific monoclonal antibody reduces influenza A virus transmission in mice.[/h] Kolpe A[SUP]1[/SUP], Schepens B[SUP]1[/SUP], Ye L[SUP]2[/SUP], Staeheli P[SUP]3[/SUP], Saelens X[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza represents a global public health threat. Currently available influenza vaccines are effective against strain-matched influenza A and B viruses but do not protect against novel pandemic viruses. Vaccine candidates that target conserved B or T cell epitopes of influenza viruses could circumvent this shortcoming. The conserved extracellular domain of matrix protein 2 (M2e) of influenza A is an example of such a broadly protective vaccine candidate. Protection by M2e-based vaccine candidates largely depends on M2e-specific IgG antibodies. Here we show that the M2e-specific IgG2a monoclonal antibody 65 (MAb 65) can reduce influenza A/Udorn/72 (H3N2) and A/Hong Kong/68 (H3N2) virus plaque formation. This effect was not observed with other influenza A virus strains tested. We further show that passive transfer of MAb 65 to mice can reduce viral loads in the upper and lower airways, which results in reduced transmission of A/Udorn/72 and A/Hong Kong/68 viruses to cohoused, unimmunized contact mice. Virus restriction by passively transferred Mab 65 was significantly less pronounced in Fcgr1[SUP]-/-[/SUP]Fcgr3[SUP]-/-[/SUP] mutant mice compared with wild type controls, suggesting that in vivo protection provided by MAb 65 depends on Fcγ receptor-mediated antibody effector mechanisms. We conclude that M2e-based antibody immune therapy has the potential to diminish influenza A virus replication in the immunized host as well as in exposed na?ve contacts.
[h=4]KEYWORDS:[/h] Broadly protecting antibody; Influenza A virus; M2 ectodomain; Mouse transmission model
PMID: 30179634 DOI: 10.1016/j.antiviral.2018.08.017
[h=1]Passively transferred M2e-specific monoclonal antibody reduces influenza A virus transmission in mice.[/h] Kolpe A[SUP]1[/SUP], Schepens B[SUP]1[/SUP], Ye L[SUP]2[/SUP], Staeheli P[SUP]3[/SUP], Saelens X[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza represents a global public health threat. Currently available influenza vaccines are effective against strain-matched influenza A and B viruses but do not protect against novel pandemic viruses. Vaccine candidates that target conserved B or T cell epitopes of influenza viruses could circumvent this shortcoming. The conserved extracellular domain of matrix protein 2 (M2e) of influenza A is an example of such a broadly protective vaccine candidate. Protection by M2e-based vaccine candidates largely depends on M2e-specific IgG antibodies. Here we show that the M2e-specific IgG2a monoclonal antibody 65 (MAb 65) can reduce influenza A/Udorn/72 (H3N2) and A/Hong Kong/68 (H3N2) virus plaque formation. This effect was not observed with other influenza A virus strains tested. We further show that passive transfer of MAb 65 to mice can reduce viral loads in the upper and lower airways, which results in reduced transmission of A/Udorn/72 and A/Hong Kong/68 viruses to cohoused, unimmunized contact mice. Virus restriction by passively transferred Mab 65 was significantly less pronounced in Fcgr1[SUP]-/-[/SUP]Fcgr3[SUP]-/-[/SUP] mutant mice compared with wild type controls, suggesting that in vivo protection provided by MAb 65 depends on Fcγ receptor-mediated antibody effector mechanisms. We conclude that M2e-based antibody immune therapy has the potential to diminish influenza A virus replication in the immunized host as well as in exposed na?ve contacts.
[h=4]KEYWORDS:[/h] Broadly protecting antibody; Influenza A virus; M2 ectodomain; Mouse transmission model
PMID: 30179634 DOI: 10.1016/j.antiviral.2018.08.017