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James P. Stewart

Researcher at University of Liverpool

Publications -  152
Citations -  5411

James P. Stewart is an academic researcher from University of Liverpool. The author has contributed to research in topics: Virus & Gammaherpesvirinae. The author has an hindex of 40, co-authored 146 publications receiving 4860 citations. Previous affiliations of James P. Stewart include Peterson Institute for International Economics & Northwest A&F University.

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Lung Epithelial Cells Are a Major Site of Murine Gammaherpesvirus Persistence

TL;DR: Results show that mucosal epithelia can act as a nonlymphoid reservoir for gammaherpesvirus persistence, and that there is a two-way movement of virus between lymphoid and nonly mphoid compartments during persistence.
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Natural history of murine gamma-herpesvirus infection.

TL;DR: MHV-68 provides an excellent model to explore methods for controlling gamma-herpesvirus infection through vaccination and chemotherapy and the observations that this virus can downregulate major histocompatibility complex class I expression and also restrict inflammatory cell responses by producing a chemokine-binding protein (M3 gene product).
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The Detection of Epstein-Barr Virus DNA in Lung Tissue from Patients with Idiopathic Pulmonary Fibrosis

TL;DR: Lung tissue obtained surgically from 27 patients with IPF and 28 control subjects was investigated for the presence of EBV by immunohistochemistry and polymerase chain reaction (PCR) analysis, suggesting an association between EBV and IPF.
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Malignant catarrhal fever: a review.

TL;DR: The pathogenesis of MCF and the virus life cycle are poorly understood and, currently, there is no effective disease control, but new and improved methods of disease diagnosis have been developed and promising vaccine strategies are being tested.
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Epstein-Barr virus replication within pulmonary epithelial cells in cryptogenic fibrosing alveolitis.

TL;DR: This is the first report of in vivo EBV replication within epithelial cells of the lower respiratory tract in an immunocompetent human host, and suggests that EBV may be an immune trigger or contribute to lung injury in cryptogenic fibrosing alveolitis, thus offering a potential new avenue of treatment.