Influenza A virus impairs control of Mycobacterium tuberculosis coinfection through a type I interferon receptor-dependent pathway.
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.
Division of Immunoregulation, Medical Research Council National Institute for Medical Research, The Ridgeway, Mill Hill, London.
Paul S
PS
Redford
Katrin D
KD
Mayer-Barber
Finlay W
FW
McNab
Evangelos
E
Stavropoulos
Andreas
A
Wack
Alan
A
Sher
Anne
A
O'Garra
D000818:Animals; D060085:Coinfection / Q000276:immunology*; D004195:Disease Models, Animal; D005260:Female; D009980:Influenza A virus / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009169:Mycobacterium tuberculosis / Q000276:immunology*; D009976:Orthomyxoviridae Infections / Q000150:complications / Q000276:immunology*; D053633:Receptor, Interferon alpha-beta / Q000276:immunology*; D015398:Signal Transduction; D016019:Survival Analysis; D014376:Tuberculosis / Q000150:complications / Q000276:immunology*
D053633:Receptor, Interferon alpha-beta
Interferon; Mycobacterium tuberculosis; co-infection; influenza; tuberculosis; type I IFN