期刊
JOURNAL OF INFECTIOUS DISEASES
卷 209, 期 2, 页码 270-274出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jit424
关键词
Mycobacterium tuberculosis; tuberculosis; influenza; Interferon; type I IFN; co-infection
资金
- Medical Research Council, United Kingdom [U117565642, U117597139]
- European Research Council [ERC-2011-AdG 294682-TB-PATH]
- National Institute of Allergy and Infectious Diseases, National Institutes of Health
- MRC [MC_U117597139, MC_U117565642] Funding Source: UKRI
- Medical Research Council [MC_U117597139, MC_U117565642] Funding Source: researchfish
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.
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