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Future Microbiol. 2016 Jul;11:919-39. doi: 10.2217/fmb-2016-0044. Epub 2016 Jul 15.

Right on Q: genetics begin to unravel Coxiella burnetii host cell interactions.

Author information

1
Coxiella Pathogenesis Section, Laboratory of Bacteriology, Rocky Mountain Laboratories, National Institute of Allergy & Infectious Diseases, National Institutes of Health, 903 South 4th Street, Hamilton, MT 59840, USA.
2
CNRS, FRE3698, CPBS, 1919 Route de Mende, 34293 Montpellier, France.
3
Université de Montpellier, Montpellier, France.
4
Bioinformatics & Computational Biosciences Branch, Rocky Mountain Laboratories, National Institute of Allergy & Infectious Diseases, National Institutes of Health, 903 South 4th Street, Hamilton, MT 59840, USA.

Abstract

Invasion of macrophages and replication within an acidic and degradative phagolysosome-like vacuole are essential for disease pathogenesis by Coxiella burnetii, the bacterial agent of human Q fever. Previous experimental constraints imposed by the obligate intracellular nature of Coxiella limited knowledge of pathogen strategies that promote infection. Fortunately, new genetic tools facilitated by axenic culture now allow allelic exchange and transposon mutagenesis approaches for virulence gene discovery. Phenotypic screens have illuminated the critical importance of Coxiella's type 4B secretion system in host cell subversion and discovered genes encoding translocated effector proteins that manipulate critical infection events. Here, we highlight the cellular microbiology and genetics of Coxiella and how recent technical advances now make Coxiella a model organism to study macrophage parasitism.

KEYWORDS:

Coxiella burnetii; apoptosis; autophagy; effector protein; host cell invasion; macrophages; mutagenesis; phagolysosome; type 4B secretion; vacuole remodeling

PMID:
27418426
PMCID:
PMC5619019
DOI:
10.2217/fmb-2016-0044
[Indexed for MEDLINE]
Free PMC Article

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