Author

A.-K. Reuschl

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· 7

Signature Assays, Organisms & Methods

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Approach:experimental assay· 7 Research Focus:host-pathogen & immune response· 6 Organism:human· 5 Assay:bulk RNA-seq· 2 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Assay:proteomics· 2 Organism:virus· 2

Frequent Co-Authors

C. Jolly· 7 shared G. J. Towers· 6 shared L. G. Thorne· 5 shared D. Mesner· 3 shared M. Noursadeghi· 3 shared M. V. X. Whelan· 3 shared A. Garcia-Sastre· 2 shared J. Fabius· 2 shared

Activity by Year

2020-2022 · peak 4/yr

Co-Author Collaboration Network

10 top collaborators · 41 mutual co-author links

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7 shared papersMicrobiology

C. Jolly

Mutual co-authors in cluster

Author profile →

7 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

Evolution of enhanced innate immune evasion by the SARS-CoV-2 B.1.1.7 UK variant

L. G. Thorne, M. Bouhaddou, A.-K. Reuschl, L. Zuliani-Alvarez, B. J. Polacco, A. Pelin, J. Batra, M. V. X. Whelan, M. Ummadi, A. Roic, J. Turner, K. Obernier, H. Braberg, M. Soucheray, A. L. Richards, , N. J. Krogan

This study identifies that the B.1.1.7 SARS-CoV-2 variant enhances innate immune evasion through increased Orf9b and Orf6 expression and activity.

bioRxiv · Jun 6, 2021 · PreprintMicrobiology

Characterisation of B.1.1.7 and Pangolin coronavirus spike provides insights on the evolutionary trajectory of SARS-CoV-2

S. J. Dicken, M. J. Murray, L. G. Thorne, A.-K. Reuschl, C. Forrest, M. Ganeshalingham, L. Muir, M. D. Kalemera, M. Palor, L. E. McCoy, C. Jolly, G. J. Towers, M. Reeves, J. Grove

This study characterizes the B.1.1.7 and Pangolin coronavirus spike proteins, revealing how NTD mutations enhance viral entry and provide insights into SARS-CoV-2 evolution.

bioRxiv · Mar 22, 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

Host-directed therapies against early-lineage SARS-CoV-2 retain efficacy against B.1.1.7 variant

A.-K. Reuschl, L. Thorne, L. Zuliani Alvarez, M. Bouhaddou, K. Obernier, J. Hiatt, M. Soucheray, J. Turner, J. Fabius, G. T. Nguyen, D. Swaney, R. Rosales, K. M. White, P. Aviles, I. T. Kirby, , N. J. Krogan

This study evaluates the efficacy of host-directed therapies against the B.1.1.7 SARS-CoV-2 variant and finds similar antiviral activity compared to early-lineage SARS-CoV-2.

bioRxiv · Jan 24, 2021 · PreprintMicrobiology

SARS-CoV-2 sensing by RIG-I and MDA5 links epithelial infection to macrophage inflammation

L. G. Thorne, A.-K. Reuschl, L. Zuliani-Alvarez, M. V. X. Whelan, M. Noursadeghi, C. Jolly, G. J. Towers

This study shows SARS-CoV-2 activates RNA sensors in lung epithelial cells, driving macrophage inflammation, which can be mitigated by inhibiting RNA sensing or downstream signaling.

bioRxiv · Dec 23, 2020Microbiology