Author
Listed:
- Kariem Ezzat
(Stockholm University
Karolinska Institutet)
- Maria Pernemalm
(Science for Life Laboratory and Karolinska Institutet)
- Sandra Pålsson
(Stockholm University)
- Thomas C. Roberts
(University of Oxford
Sanford Burnham Prebys Medical Discovery Institute, Development, Aging and Regeneration Program)
- Peter Järver
(Stockholm University)
- Aleksandra Dondalska
(Stockholm University)
- Burcu Bestas
(Karolinska Institutet
Discovery Sciences, R&D Biopharmaceuticals, AstraZeneca)
- Michal J. Sobkowiak
(Karolinska University Hospital Huddinge)
- Bettina Levänen
(Karolinska Institutet)
- Magnus Sköld
(Karolinska Institutet
Karolinska University Hospital)
- Elizabeth A. Thompson
(Karolinska Institutet)
- Osama Saher
(Karolinska Institutet
Cairo University)
- Otto K. Kari
(University of Helsinki)
- Tatu Lajunen
(University of Helsinki)
- Eva Sverremark Ekström
(Stockholm University)
- Caroline Nilsson
(Karolinska Institutet and Sachs’ Children and Youth Hospital)
- Yevheniia Ishchenko
(University of Eastern Finland)
- Tarja Malm
(University of Eastern Finland)
- Matthew J. A. Wood
(University of Oxford)
- Ultan F. Power
(Queens’ University Belfast)
- Sergej Masich
(Karolinska Institutet)
- Anders Lindén
(Karolinska Institutet
Karolinska University Hospital)
- Johan K. Sandberg
(Karolinska University Hospital Huddinge)
- Janne Lehtiö
(Science for Life Laboratory and Karolinska Institutet)
- Anna-Lena Spetz
(Stockholm University)
- Samir EL Andaloussi
(Karolinska Institutet
University of Oxford
Evox Therapeutics Limited, Oxford Science Park)
Abstract
Artificial nanoparticles accumulate a protein corona layer in biological fluids, which significantly influences their bioactivity. As nanosized obligate intracellular parasites, viruses share many biophysical properties with artificial nanoparticles in extracellular environments and here we show that respiratory syncytial virus (RSV) and herpes simplex virus type 1 (HSV-1) accumulate a rich and distinctive protein corona in different biological fluids. Moreover, we show that corona pre-coating differentially affects viral infectivity and immune cell activation. In addition, we demonstrate that viruses bind amyloidogenic peptides in their corona and catalyze amyloid formation via surface-assisted heterogeneous nucleation. Importantly, we show that HSV-1 catalyzes the aggregation of the amyloid β-peptide (Aβ42), a major constituent of amyloid plaques in Alzheimer’s disease, in vitro and in animal models. Our results highlight the viral protein corona as an acquired structural layer that is critical for viral–host interactions and illustrate a mechanistic convergence between viral and amyloid pathologies.
Suggested Citation
Kariem Ezzat & Maria Pernemalm & Sandra Pålsson & Thomas C. Roberts & Peter Järver & Aleksandra Dondalska & Burcu Bestas & Michal J. Sobkowiak & Bettina Levänen & Magnus Sköld & Elizabeth A. Thompson , 2019.
"The viral protein corona directs viral pathogenesis and amyloid aggregation,"
Nature Communications, Nature, vol. 10(1), pages 1-16, December.
Handle:
RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-10192-2
DOI: 10.1038/s41467-019-10192-2
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