C
Clifton E. Barry
Researcher at National Institutes of Health
Publications - 323
Citations - 41928
Clifton E. Barry is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Mycobacterium tuberculosis & Tuberculosis. The author has an hindex of 95, co-authored 314 publications receiving 38051 citations. Previous affiliations of Clifton E. Barry include Stellenbosch University & University of Cape Town.
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Journal ArticleDOI
Deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence
Stewart T. Cole,Roland Brosch,Julian Parkhill,Thierry Garnier,Carol Churcher,David Harris,Stephen V. Gordon,Karin Eiglmeier,S. Gas,Clifton E. Barry,Fredj Tekaia,K. Badcock,D. Basham,D. Brown,Tracey Chillingworth,R. Connor,Robert L. Davies,K. Devlin,Theresa Feltwell,S. Gentles,N. Hamlin,S. Holroyd,T. Hornsby,Kay Jagels,Anders Krogh,J. McLean,Sharon Moule,Lee Murphy,K. Oliver,J. Osborne,Michael A. Quail,Marie-Adèle Rajandream,Jane Rogers,S. Rutter,K. Seeger,Jason Skelton,Rob Squares,S. Squares,John Sulston,K. Taylor,Sally Whitehead,Bart Barrell +41 more
TL;DR: The complete genome sequence of the best-characterized strain of Mycobacterium tuberculosis, H37Rv, has been determined and analysed in order to improve the understanding of the biology of this slow-growing pathogen and to help the conception of new prophylactic and therapeutic interventions.
Journal ArticleDOI
The spectrum of latent tuberculosis: rethinking the biology and intervention strategies
Clifton E. Barry,Helena I. Boshoff,Véronique Dartois,Thomas Dick,Sabine Ehrt,JoAnne L. Flynn,Dirk Schnappinger,Robert J. Wilkinson,Robert J. Wilkinson,Robert J. Wilkinson,Douglas B. Young,Douglas B. Young +11 more
TL;DR: The biology of latent tuberculosis is discussed as part of a broad range of responses that occur following infection with Mycobacterium tuberculosis, which result in the formation of physiologically distinct granulomatous lesions that provide microenvironments with differential ability to support or suppress the persistence of viable bacteria.
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A small-molecule nitroimidazopyran drug candidate for the treatment of tuberculosis.
C. Kendall Stover,Paul Warrener,Donald R. VanDevanter,David R. Sherman,Taraq M. Arain,Michael H. Langhorne,Scott Anderson,J. Andrew Towell,Ying Yuan,David N. McMurray,Barry N. Kreiswirth,Clifton E. Barry,William R. Baker +12 more
TL;DR: It is concluded that nitroimidazopyrans offer the practical qualities of a small molecule with the potential for the treatment of tuberculosis and bactericidal activity against both replicating and static M. tuberculosis.
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A glycolipid of hypervirulent tuberculosis strains that inhibits the innate immune response
Michael B. Reed,Pilar Domenech,Claudia Manca,Hua Su,Amy K. Barczak,Barry N. Kreiswirth,Gilla Kaplan,Clifton E. Barry +7 more
TL;DR: The identification and functional relevance of a highly biologically active lipid species—a polyketide synthase-derived phenolic glycolipid (PGL) produced by a subset of M. tuberculosis isolates belonging to the W-Beijing family that show ‘hyperlethality’ in murine disease models are described.
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Host-directed therapy of tuberculosis based on interleukin-1 and type I interferon crosstalk
Katrin D. Mayer-Barber,Bruno B. Andrade,Sandra D. Oland,Eduardo P. Amaral,Eduardo P. Amaral,Daniel L. Barber,Jacqueline Gonzales,Steven C. Derrick,Ruiru Shi,Nathella Pavan Kumar,Wang Wei,Xing Yuan,Guolong Zhang,Ying Cai,Subash Babu,Subash Babu,Marta Catalfamo,Andres M. Salazar,Laura E. Via,Clifton E. Barry,Alan Sher +20 more
TL;DR: It is demonstrated that interleukin-1 (IL-1) confers host resistance through the induction of eicosanoids that limit excessive type I interferon (IFN) production and foster bacterial containment and it is established that host-directed immunotherapy with clinically approved drugs that augment prostaglandin E2 levels in these settings prevented acute mortality of Mtb-infected mice.