[Molecular basis of Brucella persistence].
This review focuses on Brucella persistence. Data on Brucella--macrophage interaction and the role of molecular-genetic systems including homologues of Mos operon Rhizobium, a type IV secretion system, a flagellum apparatus and a "quorum sensing"--virulence factors using signal or effector molecules are updated. Brucella enters macrophages through lipid raft microdomains, avoids its bactericidal attacks, phagolysosome fusion, expressing a set of virulence genes and inhibits TNF-alpha secretion and apoptosis for persistence in macroorganisms. Comparative whole-genome microarray analyses reveal genomic islands, limited genome diversity in Brucella species and also alterations and deletions of genes responsible for virulence.
Kulakov
Iu K
IuK
Zheludkov
M M
MM
D000818:Animals; D017209:Apoptosis; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D002002:Brucella / Q000254:growth & development / Q000502:physiology*; D002006:Brucellosis / Q000276:immunology / Q000382:microbiology*; D005407:Flagella / Q000502:physiology; D006801:Humans; D008264:Macrophages / Q000382:microbiology; D021962:Membrane Microdomains / Q000382:microbiology; D009876:Operon; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000378:metabolism; D014774:Virulence / Q000235:genetics
D001426:Bacterial Proteins; D014409:Tumor Necrosis Factor-alpha