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Anaplasma phagocytophilum and Ehrlichia chaffeensis: subversive manipulators of host cells
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Journal Article
Anaplasma phagocytophilum and Ehrlichia chaffeensis: subversive manipulators of host cells
2010
Overview
Key Points
Anaplasma
spp. and
Ehrlichia
spp. cause several emerging human infectious diseases. They are obligate intracellular bacteria that reside in cells of haematopoietic origin in mammals and also in tick cells. This Review focuses on recent
A. phagocytophilum
and
E. chaffeensis
studies related to their pathogenesis, observed primarily from the bacterial perspective.
A. phagocytophilum
and
E. chaffeensis
lack genes for the biosynthesis of the lipopolysaccharide and peptidoglycan that activate host leukocytes. Instead, they acquire host cholesterol from the low-density-lipoprotein uptake pathway.
Caveolae-mediated endocytosis directs
A. phagocytophilum
and
E. chaffeensis
to an intracellular compartment, or inclusion, that does not acquire components of NADPH oxidase nor show similarity to late endosomes or lysosomes.
E. chaffeensis
inclusions retain early-endosome characteristics, whereas
A. phagocytophilum
inclusions acquire early-autophagosome characteristics.
A. phagocytophilum
and
E. chaffeensis
both have small genomes (approximately 1.2–1.5 Mb) with a low coding capacity for proteins involved in central intermediary metabolism and amino acid synthesis. However, both retained genes for aerobic respiration and for the biosynthesis of all of the necessary nucleotides and most vitamins and cofactors.
In
A. phagocytophilum
there is an expansion of the OMP1–P44 superfamily encoding outer-membrane proteins that are unique to the family Anaplasmataceae. Some of these proteins have been shown to be porins.
In cell culture
A. phagocytophilum
and
E. chaffeensis
undergo developmental stages known as dense-cored cells and reticulate cells. The ApxR and EcxR transcription factors are unique to the family Anaplasmataceae, and three two-component systems are involved in regulating the intracellular development of the species in this family.
Expression of the type IV secretion system is developmentally regulated, and two secreted effectors have been shown to regulate protein tyrosine kinases and cellular apoptosis.
Anaplasma phagocytophilum
and
Ehrlichia chaffeensis
cause the emerging zoonoses human granulocytic anaplasmosis and human monocytic ehrlichiosis, respectively, which are among the most prevalent life-threatening tick-borne zoonoses in the United States. Yasuko Rikihisa reviews the adaptations of these obligate intracellular bacteria that allow them to subvert and manipulate host cells.
Anaplasma
spp. and
Ehrlichia
spp. cause several emerging human infectious diseases.
Anaplasma phagocytophilum
and
Ehrlichia chaffeensis
are transmitted between mammals by blood-sucking ticks and replicate inside mammalian white blood cells and tick salivary-gland and midgut cells. Adaptation to a life in eukaryotic cells and transmission between hosts has been assisted by the deletion of many genes that are present in the genomes of free-living bacteria (including genes required for the biosynthesis of lipopolysaccharide and peptidoglycan), by the acquisition of a cholesterol uptake pathway and by the expansion of the repertoire of genes encoding the outer-membrane porins and type IV secretion system. Here, I review the specialized properties and other adaptations of these intracellular bacteria.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Anaplasma phagocytophilum - genetics
/ Anaplasma phagocytophilum - growth & development
/ Anaplasma phagocytophilum - pathogenicity
/ Anaplasma phagocytophilum - physiology
/ Anemia
/ Animals
/ Bacteria
/ Bacterial Proteins - genetics
/ Bacterial Proteins - physiology
/ Biomedical and Life Sciences
/ Disease
/ Ehrlichia chaffeensis - genetics
/ Ehrlichia chaffeensis - growth & development
/ Ehrlichia chaffeensis - pathogenicity
/ Ehrlichia chaffeensis - physiology
/ Humans
/ Mammals
/ Virology
/ Zoonoses
