Influenza A virus impairs control of Mycobacterium tuberculosis coinfection through a type I interferon receptor-dependent pathway

J Infect Dis. 2014 Jan 15;209(2):270-4. doi: 10.1093/infdis/jit424. Epub 2013 Aug 9.


Influenza followed by severe acute bacterial pneumonia is a major cause of mortality worldwide. Several mechanisms account for this enhanced susceptibility, including increased production of type I interferon (IFN). In individuals infected with Mycobacterium tuberculosis, the influence of acute viral infections on tuberculosis progression is unclear. We show that prior exposure of mice to influenza A virus, followed by M. tuberculosis infection, leads to enhanced mycobacterial growth and decreased survival. Following M. tuberculosis/influenza virus coinfection, mycobacterial growth is enhanced by a type I IFN signaling pathway. Our findings highlight the detrimental influence influenza virus infection can have before or during M. tuberculosis infection.

Keywords: Interferon; Mycobacterium tuberculosis; co-infection; influenza; tuberculosis; type I IFN.

Publication types

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

MeSH terms

  • Animals
  • Coinfection / immunology*
  • Disease Models, Animal
  • Female
  • Influenza A virus / immunology*
  • Mice
  • Mice, Inbred C57BL
  • Mycobacterium tuberculosis / immunology*
  • Orthomyxoviridae Infections / complications
  • Orthomyxoviridae Infections / immunology*
  • Receptor, Interferon alpha-beta / immunology*
  • Signal Transduction
  • Survival Analysis
  • Tuberculosis / complications
  • Tuberculosis / immunology*


  • Receptor, Interferon alpha-beta