Right on Q: Genetics begin to Unravel Coxiella Burnetii host cell Interactions
Author(s) -
C. L. Larson,
Eric Martínez,
Paul A. Beare,
Brendan M. Jeffrey,
Robert A. Heinzen,
Matteo Bonazzi
Publication year - 2016
Publication title -
future microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.797
H-Index - 82
eISSN - 1746-0921
pISSN - 1746-0913
DOI - 10.2217/fmb-2016-0044
Subject(s) - coxiella burnetii , biology , q fever , obligate , effector , transposon mutagenesis , virulence , phagolysosome , genetics , intracellular parasite , microbiology and biotechnology , pathogen , gene , transposable element , bacteria , genome , phagosome , ecology
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.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom