tetano
Editor, Senior Moderator
Virology. 2017 Sep 6;511:214-221. doi: 10.1016/j.virol.2017.08.016. [Epub ahead of print]
[h=1]An influenza A virus (H7N9) anti-neuraminidase monoclonal antibody protects mice from morbidity without interfering with the development of protective immunity to subsequent homologous challenge.[/h] Wilson JR[SUP]1[/SUP], Belser JA[SUP]2[/SUP], DaSilva J[SUP]3[/SUP], Guo Z[SUP]2[/SUP], Sun X[SUP]2[/SUP], Gansebom S[SUP]1[/SUP], Bai Y[SUP]2[/SUP], Stark TJ[SUP]2[/SUP], Chang J[SUP]2[/SUP], Carney P[SUP]2[/SUP], Levine MZ[SUP]2[/SUP], Barnes J[SUP]2[/SUP], Stevens J[SUP]2[/SUP], Maines TR[SUP]2[/SUP], Tumpey TM[SUP]2[/SUP], York IA[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The emergence of A(H7N9) virus strains with resistance to neuraminidase (NA) inhibitors highlights a critical need to discover new countermeasures for treatment of A(H7N9) virus-infected patients. We previously described an anti-NA mAb (3c10-3) that has prophylactic and therapeutic efficacy in mice lethally challenged with A(H7N9) virus when delivered intraperitoneally (i.p.). Here we show that intrananasal (i.n.) administration of 3c10-3 protects 100% of mice from mortality when treated 24h post-challenge and further characterize the protective efficacy of 3c10-3 using a nonlethal A(H7N9) challenge model. Administration of 3c10-3 i.p. 24h prior to challenge resulted in a significant decrease in viral lung titers and deep sequencing analysis indicated that treatment did not consistently select for viral variants in NA. Furthermore, prophylactic administration of 3c10-3 did not inhibit the development of protective immunity to subsequent homologous virus re-challenge. Taken together, 3c10-3 highlights the potential use of anti-NA mAb to mitigate influenza virus infection.
Published by Elsevier Inc.
[h=4]KEYWORDS:[/h] A(H7N9); Antiviral; Avian influenza; Immunotherapeutic; Influenza; Monoclonal antibody; Neuraminidase; Passive transfer
PMID: 28888111 DOI: 10.1016/j.virol.2017.08.016
[h=1]An influenza A virus (H7N9) anti-neuraminidase monoclonal antibody protects mice from morbidity without interfering with the development of protective immunity to subsequent homologous challenge.[/h] Wilson JR[SUP]1[/SUP], Belser JA[SUP]2[/SUP], DaSilva J[SUP]3[/SUP], Guo Z[SUP]2[/SUP], Sun X[SUP]2[/SUP], Gansebom S[SUP]1[/SUP], Bai Y[SUP]2[/SUP], Stark TJ[SUP]2[/SUP], Chang J[SUP]2[/SUP], Carney P[SUP]2[/SUP], Levine MZ[SUP]2[/SUP], Barnes J[SUP]2[/SUP], Stevens J[SUP]2[/SUP], Maines TR[SUP]2[/SUP], Tumpey TM[SUP]2[/SUP], York IA[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The emergence of A(H7N9) virus strains with resistance to neuraminidase (NA) inhibitors highlights a critical need to discover new countermeasures for treatment of A(H7N9) virus-infected patients. We previously described an anti-NA mAb (3c10-3) that has prophylactic and therapeutic efficacy in mice lethally challenged with A(H7N9) virus when delivered intraperitoneally (i.p.). Here we show that intrananasal (i.n.) administration of 3c10-3 protects 100% of mice from mortality when treated 24h post-challenge and further characterize the protective efficacy of 3c10-3 using a nonlethal A(H7N9) challenge model. Administration of 3c10-3 i.p. 24h prior to challenge resulted in a significant decrease in viral lung titers and deep sequencing analysis indicated that treatment did not consistently select for viral variants in NA. Furthermore, prophylactic administration of 3c10-3 did not inhibit the development of protective immunity to subsequent homologous virus re-challenge. Taken together, 3c10-3 highlights the potential use of anti-NA mAb to mitigate influenza virus infection.
Published by Elsevier Inc.
[h=4]KEYWORDS:[/h] A(H7N9); Antiviral; Avian influenza; Immunotherapeutic; Influenza; Monoclonal antibody; Neuraminidase; Passive transfer
PMID: 28888111 DOI: 10.1016/j.virol.2017.08.016