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Raymond J. Pickles

Researcher at University of North Carolina at Chapel Hill

Publications -  101
Citations -  10453

Raymond J. Pickles is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Virus & Respiratory epithelium. The author has an hindex of 50, co-authored 94 publications receiving 9293 citations. Previous affiliations of Raymond J. Pickles include National Center for Toxicological Research.

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The NLRP3 Inflammasome Mediates in vivo Innate Immunity to Influenza A Virus through Recognition of Viral RNA

TL;DR: Mechanistically, NLRP3 inflammasome activation by the influenza virus was dependent on lysosomal maturation and reactive oxygen species (ROS), and inhibition of ROS induction eliminated IL-1beta production in animals during influenza infection.
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The coxsackievirus and adenovirus receptor is a transmembrane component of the tight junction.

TL;DR: Results indicate that CAR is a component of the tight junction and of the functional barrier to paracellular solute movement and thatquestration of CAR in tight junctions may limit virus infection across epithelial surfaces.
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Respiratory Syncytial Virus Infection of Human Airway Epithelial Cells Is Polarized, Specific to Ciliated Cells, and without Obvious Cytopathology

TL;DR: Investigation of human primary airway epithelial cell cultures revealed that lumenal columnar cells, specifically ciliated epithelial cells, were targeted by RSV and that cultures became susceptible to infection as they differentiated into a ciliated phenotype, suggesting that RSV infection in the absence of an immune response can be tolerated for >3 months.
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Inefficient gene transfer by adenovirus vector to cystic fibrosis airway epithelia of mice and humans

TL;DR: It is found that even repeated high doses can only partially correct the CF defect in Cl− transport in vivo and do not correct the Na+ transport defect at all, and indicates that more efficient adenoviral gene-transfer vectors and/or refinement of dosing strategies are needed for therapy of CF lung disease.
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SARS-like WIV1-CoV poised for human emergence

TL;DR: An approach that combines existing metagenomics data with reverse genetics to engineer reagents to evaluate emergence and pathogenic potential of circulating zoonotic viruses indicates that the WIV1-coronavirus (CoV) cluster has the ability to directly infect and may undergo limited transmission in human populations.