info:eu-repo/semantics/article
Single domain antibodies targeting neuraminidase protect against an H5N1 influenza virus challenge
Fecha
2014-05Registro en:
Cardoso, Francisco Miguel; Ibañez, Lorena Itatí; Van Den Hoecke, Silvie; De Baets, Sarah; Smet, Anouk; et al.; Single domain antibodies targeting neuraminidase protect against an H5N1 influenza virus challenge; American Society for Microbiology; Journal of Virology; 88; 15; 5-2014; 8278-8296
0022-538X
Autor
Cardoso, Francisco Miguel
Ibañez, Lorena Itatí
Van Den Hoecke, Silvie
De Baets, Sarah
Smet, Anouk
Roose, Kenny
Schepens, Bert
Descamps, Francis J.
Fiers, Walter
Muyldermans, Serge
Depicker, Ann
Saelens, Xavier
Resumen
Influenza virus neuraminidase (NA) is an interesting target of small-molecule antiviral drugs. We isolated a set of H5N1 NAspecific single-domain antibodies (N1-VHHm) and evaluated their in vitro and in vivo antiviral potential. Two of them inhibited the NA activity and in vitro replication of clade 1 and 2 H5N1 viruses. We then generated bivalent derivatives of N1-VHHm by two methods. First, we made N1-VHHb by genetically joining two N1-VHHm moieties with a flexible linker. Second, bivalent N1-VHH-Fc proteins were obtained by genetic fusion of the N1-VHHm moiety with the crystallizable region of mouse IgG2a (Fc). The in vitro antiviral potency against H5N1 of both bivalent N1-VHHb formats was 30- to 240-fold higher than that of their monovalent counterparts, with 50% inhibitory concentrations in the low nanomolar range. Moreover, single-dose prophylactic treatment with bivalent N1-VHHb or N1-VHH-Fc protected BALB/c mice against a lethal challenge with H5N1 virus, including an oseltamivir-resistant H5N1 variant. Surprisingly, an N1-VHH-Fc fusion without in vitro NA-inhibitory or antiviral activity also protected mice against an H5N1 challenge. Virus escape selection experiments indicated that one amino acid residue close to the catalytic site is required for N1-VHHm binding. We conclude that single-domain antibodies directed against influenza virus NA protect against H5N1 virus infection, and when engineered with a conventional Fc domain, they can do so in the absence of detectable NA-inhibitory activity.