Influenza A Virus Impairs Control of Mycobacterium tuberculosis Coinfection Through a Type I Interferon Receptor–Dependent Pathway

PS Redford, KD Mayer-Barber… - The Journal of …, 2014 - academic.oup.com
PS Redford, KD Mayer-Barber, FW McNab, E Stavropoulos, A Wack, A Sher, A O'Garra
The Journal of infectious diseases, 2014academic.oup.com
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 …
Abstract
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.
Oxford University Press