scispace - formally typeset
P

Paul Digard

Researcher at University of Edinburgh

Publications -  153
Citations -  15134

Paul Digard is an academic researcher from University of Edinburgh. The author has contributed to research in topics: Influenza A virus & Virus. The author has an hindex of 53, co-authored 138 publications receiving 13670 citations. Previous affiliations of Paul Digard include University of Warwick & Harvard University.

Papers
More filters
Journal ArticleDOI

The P323L substitution in the SARS-CoV-2 polymerase (NSP12) confers a selective advantage during infection

Hannah Goldswain, +393 more
- 13 Mar 2023 - 
TL;DR: In this article , the authors investigated the role of P323L/D614G substitutions in the emergence of SARS-CoV-2 variants in the COVID-19 pandemic.
Journal ArticleDOI

Heterogeneity of Early Host Response to Infection with Four Low-Pathogenic H7 Viruses with a Different Evolutionary History in the Field.

TL;DR: In this paper, transcriptomic sequencing of tracheal tissue from chickens infected with four distinct LP H7 viruses, characterized by a different history of pathogenicity evolution in the field, was implemented.
Journal ArticleDOI

Comparison of the efficacy of a commercial inactivated influenza A/H1N1/pdm09 virus (pH1N1) vaccine and two experimental M2e-based vaccines against pH1N1 challenge in the growing pig model

TL;DR: A commercial Inact/pH1N1 specific vaccine effectively protected pigs against homologous challenge as evidenced by reduced clinical signs, virus shedding in nasal secretions and oral fluids and reduced macroscopic and microscopic lesions whereas intranasal vaccination with experimental M2e epitope-based subunit vaccines did not.
Posted ContentDOI

Comprehensive characterisation of molecular host-pathogen interactions in influenza A virus-infected human macrophages

TL;DR: Host gene expression reveals that human macrophages exposed to IAV exhibit sustained production of key inflammatory mediators and failure to induce expression of feedback inhibitors of inflammation, demonstrating that cap-snatching has a strong preference for, and aversion to, different groups of host transcripts.