Influenza A virus-infected hosts boost an invasive type of Streptococcus pyogenes infection in mice.

Abstract

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.

• Authors: Shigefumi Okamoto, Shigetada Kawabata, Ichiro Nakagawa, Yoshinobu Okuno, Toshiyuki Goto, Kouichi Sano, Shigeyuki Hamada
• Journal: Journal of virology (J Virol) Vol. 77 Issue 7 Pg. 4104-12 (Apr 2003) ISSN: 0022-538X [Print] United States
• PMID: 12634369 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antibodies, Monoclonal
• Antibodies, Viral
• Hemagglutinins, Viral
• Interleukin-6
• Tumor Necrosis Factor-alpha

Topics

• Animals
• Antibodies, Monoclonal (pharmacology)
• Antibodies, Viral (pharmacology)
• Cell Line
• Fasciitis, Necrotizing (etiology, pathology)
• Female
• Hemagglutinins, Viral (metabolism)
• Humans
• Influenza A virus (pathogenicity)
• Influenza, Human (complications, pathology)
• Interleukin-6 (metabolism)
• Mice
• Mice, Inbred BALB C
• Microscopy, Electron
• Streptococcal Infections (etiology, microbiology, pathology, virology)
• Streptococcus pyogenes (pathogenicity)
• Superinfection (etiology, microbiology, pathology, virology)
• Tumor Necrosis Factor-alpha (metabolism)
• Virulence