Antibodies specific to the HA2 glycopolypeptide of influenza A virus haemagglutinin with fusion-inhibition activity contribute to the protection of mice against lethal infection

• Published in: Journal of general virology 2007-03, Vol.88 (3), p.951-955
• Main Authors: Gocnik, M, Fislova, T, Sladkova, T, Mucha, V, Kostolansky, F, Vareckova, E
• Format: Article
• Language: English
• Subjects: Animals; Antibodies, Monoclonal - immunology; Antibodies, Viral - immunology; Biological and medical sciences; Disease Models, Animal; Fundamental and applied biological sciences. Psychology; Hemagglutinins, Viral - immunology; Humans; Immunization, Passive; Influenza A virus; Influenza A Virus, H3N2 Subtype - immunology; Influenza, Human - immunology; Influenza, Human - prevention & control; Lung - virology; Mice; Mice, Inbred BALB C; Microbiology; Miscellaneous; Virology; Viruses
• ISSN: 0022-1317; 1465-2099
• DOI: 10.1099/vir.0.82563-0

Institute of Virology, Slovak Academy of Sciences, 845 05 Bratislava, Slovak Republic Correspondence E. Vare ková viruevar{at}savba.sk Four monoclonal antibodies (mAbs) recognizing distinct antigenic sites on the HA2 glycopolypeptide of influenza virus A/Dunedin/4/73 (H3N2) have been tested for in vivo protection. When applied intravenously before infection, three of them increased the survival of BALB/c mice infected with 1 LD 50 homologous virus. The protection resulted simultaneously in 2 days earlier clearance of virus from the lungs. These three antibodies inhibited the fusion activity of virus in previous in vitro experiments. One of them, specific to N-terminal aa 1–38 of the HA2 glycopolypeptide, was also tested for protection against the heterologous virus A/Mississippi/1/85 (H3N2). Protection similar to that against the homologous virus was observed. The fourth mAb, without fusion-inhibition activity, did not protect mice. It is concluded that antibodies specific to the antigenically conserved HA2 glycopolypeptide that exhibit fusion-inhibition activity can contribute to the protection of infected mice and mediate more effective recovery from infection.