scispace - formally typeset
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.

Papers
More filters
Journal ArticleDOI

The spectrum of latent tuberculosis: rethinking the biology and intervention strategies

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.
Journal ArticleDOI

A small-molecule nitroimidazopyran drug candidate for the treatment of tuberculosis.

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.
Journal ArticleDOI

A glycolipid of hypervirulent tuberculosis strains that inhibits the innate immune response

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.
Journal ArticleDOI

Host-directed therapy of tuberculosis based on interleukin-1 and type I interferon crosstalk

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.