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- W2090956815 abstract "Most infectious microorganisms have devised molecular mechanisms that allow them to strategically evade host immunity, thus permitting colonization and replication at privileged sites. For a number of intracellular pathogens, immune evasion comprises remodeling the membrane-bound vacuole formed during uptake into host cells in a manner that affects fusion of the phagosome with lysosomes 1 Meresse S. et al. Controlling the maturation of pathogen-containing vacuoles: a matter of life and death. Nat. Cell Biol. 1999; 1: E183-E188 Crossref PubMed Scopus (294) Google Scholar , 2 Sinai A.P. Joiner K.A. Safe haven: the cell biology of nonfusogenic pathogen vacuoles. Annu. Rev. Microbiol. 1997; 51: 415-462 Crossref PubMed Scopus (198) Google Scholar . It has been postulated that, for the majority of pathogens, this tactic has the added advantage of creating a niche permissive for intracellular growth. However, it has been difficult to determine whether the bacterial factors required for phagosome trafficking are absolutely essential for intracellular growth, because evasion of phagosome–lysosome fusion is necessary for the survival of most microbial pathogens within host cells. Recent studies demonstrating that the dot and icm genes are required for evasion of phagosome–lysosome fusion by the facultative intracellular pathogen Legionella pneumophila have provided a foundation from which to ask whether these factors are also required for intracellular replication 3 Wiater L.A. et al. Early events in phagosome establishment are required for intracellular survival of Legionella pneumophila. Infect. Immun. 1998; 66: 4450-4460 Crossref PubMed Google Scholar , 4 Roy C.R. et al. Legionella pneumophila DotA protein is required for early phagosome trafficking decisions that occur within minutes of bacterial uptake. Mol. Microbiol. 1998; 28: 663-674 Crossref PubMed Scopus (290) Google Scholar ." @default.
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- W2090956815 date "2000-02-01" @default.
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- W2090956815 title "Exploitation of macrophages as a replication niche by Legionella pneumophila: Response" @default.
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- W2090956815 doi "https://doi.org/10.1016/s0966-842x(99)01673-x" @default.
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