4.7 Article

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

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

  1. Medical Research Council, United Kingdom [U117565642, U117597139]
  2. European Research Council [ERC-2011-AdG 294682-TB-PATH]
  3. National Institute of Allergy and Infectious Diseases, National Institutes of Health
  4. MRC [MC_U117597139, MC_U117565642] Funding Source: UKRI
  5. Medical Research Council [MC_U117597139, MC_U117565642] Funding Source: researchfish

向作者/读者索取更多资源

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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