Author

D. Mesner

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Microbiology· 4

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Research Focus:host-pathogen & immune response· 3 Organism:human· 3 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

C. Jolly· 4 shared A.-K. Reuschl· 3 shared G. J. Towers· 2 shared L. G. Thorne· 2 shared T. Haider· 2 shared A. H. Patel· 1 shared A. Sigal· 1 shared C. Herrera· 1 shared

Activity by Year

2021-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 30 mutual co-author links

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4 shared papersMicrobiology

C. Jolly

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

Evolution of enhanced innate immune suppression by SARS-CoV-2 Omicron subvariants

A.-K. Reuschl, L. G. Thorne, M. X. V. Whelan, R. Ragazzini, W. Furnon, V. M. Cowton, G. de Lorenzo, D. Mesner, J. E. Turner, G. Dowgier, N. Bogoda, P. Bonfanti, M. Palmarini, A. H. Patel, C. Jolly, G. J. Towers

This study shows that later Omicron subvariants of SARS-CoV-2, such as BA.4 and BA.5, have evolved enhanced innate immune suppression compared to earlier subvariants like BA.1 and BA.2.

bioRxiv · Jul 12, 2022Microbiology

SARS-CoV-2 Spike evolution influences GBP and IFITM sensitivity

D. Mesner, A.-K. Reuschl, M. V. X. Whelan, T. Bronzovich, T. Haider, L. G. Thorne, G. J. Towers, C. Jolly

This study shows that SARS-CoV-2 variants differ in their sensitivity to GBP and IFITM restriction factors, with Omicron uniquely restricted by these factors due to changes in its spike protein.

bioRxiv · Mar 7, 2022 · PreprintMicrobiology

The envelope cytoplasmic tail regulates HIV-1 assembly and spread

X. Snetkov, T. Haider, D. Mesner, N. Groves, S. Van Engeleburg, C. Jolly

This study identifies a conserved tryptophan residue in the HIV-1 envelope cytoplasmic tail critical for viral replication, spread, and assembly.

bioRxiv · Feb 8, 2021 · PreprintMicrobiology

HIV-1 Vpr drives a tissue residency-like phenotype during selective infection of resting memory T cells

A.-K. Reuschl, M. Shivkumar, D. Mesner, L. J. Pallett, J. A. Guerra-Assuncao, R. Madansein, K. J. Dullabh, A. Sigal, J. P. Thornhill, C. Herrera, S. Fidler, M. Noursadeghi, M. Maini, C. Jolly

This study shows HIV-1 infects resting memory T cells without prior activation, inducing a tissue-resident memory-like phenotype driven by Vpr.

bioRxiv · Jan 25, 2021Microbiology