Influenza A virus-infected hosts boost an invasive type of Streptococcus pyogenes infection in mice.
The apparent worldwide resurgence of invasive Streptococcus pyogenes infection in the last two decades remains unexplained. At present, animal models in which toxic shock-like syndrome or necrotizing fasciitis is induced after S. pyogenes infection are not well developed. We demonstrate here that infection with a nonlethal dose of influenza A virus 2 days before intranasal infection with a nonlethal dose of S. pyogenes strains led to a death rate of more than 90% in mice, 10% of which showed necrotizing fasciitis. Infection of lung alveolar epithelial cells by the influenza A virus resulted in viral hemagglutinin expression on the cell surface and promoted internalization of S. pyogenes. However, treatment with monoclonal antibodies to hemagglutinin markedly decreased this internalization. Our results indicate that prior infection with influenza A virus induces a lethal synergism, resulting in the induction of invasive S. pyogenes infection in mice.
Okamoto
Shigefumi
S
Department of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, Suita-Osaka, Japan.
Kawabata
Shigetada
S
Nakagawa
Ichiro
I
Okuno
Yoshinobu
Y
Goto
Toshiyuki
T
Sano
Kouichi
K
Hamada
Shigeyuki
S
D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D000914:Antibodies, Viral / Q000494:pharmacology; D002460:Cell Line; D019115:Fasciitis, Necrotizing / Q000209:etiology / Q000473:pathology; D005260:Female; D006389:Hemagglutinins, Viral / Q000378:metabolism; D006801:Humans; D009980:Influenza A virus / Q000472:pathogenicity*; D007251:Influenza, Human / Q000150:complications* / Q000473:pathology; D015850:Interleukin-6 / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D008854:Microscopy, Electron; D013290:Streptococcal Infections / Q000209:etiology* / Q000382:microbiology / Q000473:pathology / Q000821:virology; D013297:Streptococcus pyogenes / Q000472:pathogenicity*; D015163:Superinfection / Q000209:etiology* / Q000382:microbiology / Q000473:pathology / Q000821:virology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014774:Virulence
D000911:Antibodies, Monoclonal; D000914:Antibodies, Viral; D006389:Hemagglutinins, Viral; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha