https://cmr.asm.org/content/23/2/274
SUMMARY
Summary: The genus Legionella
contains more than 50 species, of which at least 24 have been
associated with human infection. The best-characterized member of the
genus, Legionella pneumophila, is the major causative agent of Legionnaires' disease, a severe form of acute pneumonia. L. pneumophila
is an intracellular pathogen, and as part of its pathogenesis, the
bacteria avoid phagolysosome fusion and replicate within alveolar
macrophages and epithelial cells in a vacuole that exhibits many
characteristics of the endoplasmic reticulum (ER). The formation of the
unusual L. pneumophila vacuole is a feature of its interaction
with the host, yet the mechanisms by which the bacteria avoid classical
endosome fusion and recruit markers of the ER are incompletely
understood. Here we review the factors that contribute to the ability of
L. pneumophila to infect and replicate in human cells and amoebae with an emphasis on proteins that are secreted by the bacteria into the Legionella
vacuole and/or the host cell. Many of these factors undermine
eukaryotic trafficking and signaling pathways by acting as functional
and, in some cases, structural mimics of eukaryotic proteins. We discuss
the consequences of this mimicry for the biology of the infected cell
and also for immune responses to L. pneumophila infection.
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