COXIELLA BURNETII PATHOGENICITY MOLECULAR BASIS

Coxiella burnetii is an obligate intracellular gram-negative bacterial pathogen, an ethiological agent of Q-fever, a zoonotic disease, elapsing as an acute (mostly atypical pneumonia) or a chronic (mostly endocarditis) form. The host range is represented by wide range of mammal, avian and arthropod...

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Autor principal:	Yu. A. Panferova
Formato:	article
Lenguaje:	RU
Publicado:	Sankt-Peterburg : NIIÈM imeni Pastera 2016
Materias:	coxiella burnetii q-fever molecular pathogenesis virulence transport system secreted effectors Infectious and parasitic diseases RC109-216
Acceso en línea:	https://doaj.org/article/4299e5a6dd144cc583b64841ad8443e2
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spelling	oai:doaj.org-article:4299e5a6dd144cc583b64841ad8443e22021-11-22T07:09:47ZCOXIELLA BURNETII PATHOGENICITY MOLECULAR BASIS2220-76192313-739810.15789/2220-7619-2016-1-7-24https://doaj.org/article/4299e5a6dd144cc583b64841ad8443e22016-06-01T00:00:00Zhttps://www.iimmun.ru/iimm/article/view/381https://doaj.org/toc/2220-7619https://doaj.org/toc/2313-7398Coxiella burnetii is an obligate intracellular gram-negative bacterial pathogen, an ethiological agent of Q-fever, a zoonotic disease, elapsing as an acute (mostly atypical pneumonia) or a chronic (mostly endocarditis) form. The host range is represented by wide range of mammal, avian and arthropod species, but the main source of human infection are farm animals. The main route of infection is aerosolic. In case of contact with organism pathogen binds with phagocytal monocytic-macrophagal cell line. C. burnetii promotes maturation of specific phagolysosome-like compartment in host cell, called coxiella-containing vacuole, within this vacuole pathogen becames metabolically activated and actively replicates. Coxiella persists as metabolically inactive spore-like form in environment. Internalisation of C. burnetii occurs using actin-mediated phagocytosis and zipper mechanism. After internalization of bacteria maturation of phagolysosome-like compartment and large coxiella-containing vacuole formation occure, and vacuole can occupy nearly the whole cytoplasm of the host cell. Survivance of infected cells is important for chronic infection with C. burnetii. C. burnetii elongate the viability of host cell by two ways: it actively inhibits apoptotic signal cascades and induce pro-survival factors. Exceptthat C. burnetii involves autophagic pathway during coxiella-containing vacuole formation, and induction of autophagy promotes pathogen replication. During infection C. burnetii translocates effector substrates from bacterial cytosole to euca ryotic host cell cytosole using type IV secretion system, where effectors modulate host cell proteins. Overall approximately 130 secreted effectors of type IV transport system, but function of most of them remains unknown to date. Specific sec reted proteins for variety of strains and isolates were identified, confirmed that certain pathotypes of C. burnetii can exist. Identification and characterization of novel virulence factors it is now possible through axenic media for C. burnetii cultivation and development of site-specific mutagenesis and other genetic technics, which is important for research of C. burnetii molecular pathogenesis.Yu. A. PanferovaSankt-Peterburg : NIIÈM imeni Pasteraarticlecoxiella burnetiiq-fevermolecular pathogenesisvirulencetransport systemsecreted effectorsInfectious and parasitic diseasesRC109-216RUInfekciâ i Immunitet, Vol 6, Iss 1, Pp 7-24 (2016)
institution	DOAJ
collection	DOAJ
language	RU
topic	coxiella burnetii q-fever molecular pathogenesis virulence transport system secreted effectors Infectious and parasitic diseases RC109-216
spellingShingle	coxiella burnetii q-fever molecular pathogenesis virulence transport system secreted effectors Infectious and parasitic diseases RC109-216 Yu. A. Panferova COXIELLA BURNETII PATHOGENICITY MOLECULAR BASIS
description	Coxiella burnetii is an obligate intracellular gram-negative bacterial pathogen, an ethiological agent of Q-fever, a zoonotic disease, elapsing as an acute (mostly atypical pneumonia) or a chronic (mostly endocarditis) form. The host range is represented by wide range of mammal, avian and arthropod species, but the main source of human infection are farm animals. The main route of infection is aerosolic. In case of contact with organism pathogen binds with phagocytal monocytic-macrophagal cell line. C. burnetii promotes maturation of specific phagolysosome-like compartment in host cell, called coxiella-containing vacuole, within this vacuole pathogen becames metabolically activated and actively replicates. Coxiella persists as metabolically inactive spore-like form in environment. Internalisation of C. burnetii occurs using actin-mediated phagocytosis and zipper mechanism. After internalization of bacteria maturation of phagolysosome-like compartment and large coxiella-containing vacuole formation occure, and vacuole can occupy nearly the whole cytoplasm of the host cell. Survivance of infected cells is important for chronic infection with C. burnetii. C. burnetii elongate the viability of host cell by two ways: it actively inhibits apoptotic signal cascades and induce pro-survival factors. Exceptthat C. burnetii involves autophagic pathway during coxiella-containing vacuole formation, and induction of autophagy promotes pathogen replication. During infection C. burnetii translocates effector substrates from bacterial cytosole to euca ryotic host cell cytosole using type IV secretion system, where effectors modulate host cell proteins. Overall approximately 130 secreted effectors of type IV transport system, but function of most of them remains unknown to date. Specific sec reted proteins for variety of strains and isolates were identified, confirmed that certain pathotypes of C. burnetii can exist. Identification and characterization of novel virulence factors it is now possible through axenic media for C. burnetii cultivation and development of site-specific mutagenesis and other genetic technics, which is important for research of C. burnetii molecular pathogenesis.
format	article
author	Yu. A. Panferova
author_facet	Yu. A. Panferova
author_sort	Yu. A. Panferova
title	COXIELLA BURNETII PATHOGENICITY MOLECULAR BASIS
title_short	COXIELLA BURNETII PATHOGENICITY MOLECULAR BASIS
title_full	COXIELLA BURNETII PATHOGENICITY MOLECULAR BASIS
title_fullStr	COXIELLA BURNETII PATHOGENICITY MOLECULAR BASIS
title_full_unstemmed	COXIELLA BURNETII PATHOGENICITY MOLECULAR BASIS
title_sort	coxiella burnetii pathogenicity molecular basis
publisher	Sankt-Peterburg : NIIÈM imeni Pastera
publishDate	2016
url	https://doaj.org/article/4299e5a6dd144cc583b64841ad8443e2
work_keys_str_mv	AT yuapanferova coxiellaburnetiipathogenicitymolecularbasis
_version_	1718418036076052480

COXIELLA BURNETII PATHOGENICITY MOLECULAR BASIS

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