Abstract
Anaplasma phagocytophilum invades neutrophils to cause the emerging infection, human granulocytic anaplasmosis. Here, we provide a focused review of the A. phagocytophilum invasin-host cell receptor interactions that promote bacterial entry and the degradative and membrane traffic pathways that the organism exploits to route nutrients to the organelle in which it resides. Because its obligatory intracellular nature hinders knock out-complementation approaches, we also discuss the current methods used to study A. phagocytophilum gene function and the potential benefit of applying novel tools that have advanced studies of other obligate intracellular bacterial pathogens.
Original language | English (US) |
---|---|
Pages (from-to) | 1017-1025 |
Number of pages | 9 |
Journal | Microbes and Infection |
Volume | 15 |
Issue number | 14-15 |
DOIs | |
State | Published - Dec 2013 |
Funding
We apologize to our colleagues whose papers we could not cite due to space limitation. This work was supported by funding from NIH/NIAID grant 2R56 AI067283 . Scanning electron microscopy was performed in the VCU Department of Anatomy and Neurobiology Microscopy Facility, supported, in part, with funding from NIH-NINDS Center core grant 5P30NS047463 .
Keywords
- Bacterial invasion
- Ehrlichia
- Nutritional virulence
- Obligate intracellular
- Rab GTPase
- Rickettsia
ASJC Scopus subject areas
- Microbiology
- Immunology
- Infectious Diseases