Molecular mimicry as a mechanism of viral immune evasion and autoimmunity

Cole Maguire, Chumeng Wang, Akshara Ramasamy, Cara Fonken, Brinkley Morse, Nathan Lopez, Dennis Wylie and Esther Melamed ()
Additional contact information
Cole Maguire: Department of Neurology, Dell Medical School, The University of Texas at Austin
Chumeng Wang: Department of Neurology, Dell Medical School, The University of Texas at Austin
Akshara Ramasamy: Department of Neurology, Dell Medical School, The University of Texas at Austin
Cara Fonken: Department of Neurology, Dell Medical School, The University of Texas at Austin
Brinkley Morse: Department of Neurology, Dell Medical School, The University of Texas at Austin
Nathan Lopez: Department of Neurology, Dell Medical School, The University of Texas at Austin
Dennis Wylie: Center for Biomedical Research Support, The University of Texas at Austin
Esther Melamed: Department of Neurology, Dell Medical School, The University of Texas at Austin

Nature Communications, 2024, vol. 15, issue 1, 1-14

Abstract: Abstract Mimicry of host protein structures, or ‘molecular mimicry’, is a common mechanism employed by viruses to evade the host’s immune system. Short linear amino acid (AA) molecular mimics can elicit cross-reactive antibodies and T cells from the host, but the prevalence of such mimics throughout the human virome has not been fully explored. Here we evaluate 134 human-infecting viruses and find significant usage of linear mimicry across the virome, particularly those in the Herpesviridae and Poxviridae families. Furthermore, host proteins related to cellular replication and inflammation, autosomes, the X chromosome, and thymic cells are enriched as viral mimicry targets. Finally, we find that short linear mimicry from Epstein-Barr virus (EBV) is higher in auto-antibodies found in patients with multiple sclerosis than previously appreciated. Our results thus hint that human-infecting viruses leverage mimicry in the course of their infection, and that such mimicry may contribute to autoimmunity, thereby prompting potential targets for therapies.

Date: 2024
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-024-53658-8 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-53658-8

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-024-53658-8

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().