Severe pandemic 2009 H1N1 influenza disease due to pathogenic immune complexes

Nat Med. 2011 Feb;17(2):195-9. doi: 10.1038/nm.2262. Epub 2010 Dec 5.

Abstract

Pandemic influenza viruses often cause severe disease in middle-aged adults without preexisting comorbidities. The mechanism of illness associated with severe disease in this age group is not well understood. Here we find preexisting serum antibodies that cross-react with, but do not protect against, 2009 H1N1 influenza virus in middle-aged adults. Nonprotective antibody is associated with immune complex-mediated disease after infection. We detected high titers of serum antibody of low avidity for H1-2009 antigen, and low-avidity pulmonary immune complexes against the same protein, in severely ill individuals. Moreover, C4d deposition--a marker of complement activation mediated by immune complexes--was present in lung sections of fatal cases. Archived lung sections from middle-aged adults with confirmed fatal influenza 1957 H2N2 infection revealed a similar mechanism of illness. These observations provide a previously unknown biological mechanism for the unusual age distribution of severe cases during influenza pandemics.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Adolescent
  • Adult
  • Age Factors
  • Antibodies, Viral / immunology
  • Antigen-Antibody Complex / immunology*
  • Antigens, Viral / immunology
  • Complement C3 / analysis
  • Cross Reactions / immunology
  • Cytokines / blood
  • Humans
  • Influenza A Virus, H1N1 Subtype / immunology*
  • Influenza, Human / blood
  • Influenza, Human / immunology*
  • Influenza, Human / pathology
  • Influenza, Human / virology
  • Interferon-alpha / blood
  • Interferon-beta / blood
  • Lung / immunology
  • Lung / pathology
  • Lung / virology
  • Middle Aged
  • Young Adult

Substances

  • Antibodies, Viral
  • Antigen-Antibody Complex
  • Antigens, Viral
  • Complement C3
  • Cytokines
  • Interferon-alpha
  • Interferon-beta