Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Impact of Epstein-Barr Virus Nuclear Antigen 1 on Neuroinflammation in PARK2 Knockout Mice with Mitochondrial Dysfunction

Davide Cossu
* ORCID logo ,
Yuji Tomizawa
,
Sachiko Noda
,
Eiichi Momotani
ORCID logo ,
Tamami Sakanishi
,
Hanna Okada
,
Kazumasa Yokoyama
ORCID logo ,
Leonardo A. Sechi
ORCID logo ,
Nobutaka Hattori
ORCID logo
Version 1 : Received: 24 August 2024 / Approved: 24 August 2024 / Online: 26 August 2024 (06:58:15 CEST)

A peer-reviewed article of this Preprint also exists.

Cossu, D.; Tomizawa, Y.; Noda, S.; Momotani, E.; Sakanishi, T.; Okada, H.; Yokoyama, K.; Sechi, L.A.; Hattori, N. Impact of Epstein–Barr Virus Nuclear Antigen 1 on Neuroinflammation in PARK2 Knockout Mice. Int. J. Mol. Sci. 2024, 25, 10697. Cossu, D.; Tomizawa, Y.; Noda, S.; Momotani, E.; Sakanishi, T.; Okada, H.; Yokoyama, K.; Sechi, L.A.; Hattori, N. Impact of Epstein–Barr Virus Nuclear Antigen 1 on Neuroinflammation in PARK2 Knockout Mice. Int. J. Mol. Sci. 2024, 25, 10697.

Abstract

This study aimed to explore the intricate relationship between mitochondrial dysfunction, infections, and neuroinflammation, focusing specifically on the impact of pathogenic epitopes of Epstein-Barr Virus (EBV) nuclear antigen 1 (EBNA1) in a mouse model of mitochondrial dysfunctions. The investigation included female middle-aged PARK2-/- and C57BL/6J wild-type mice immunized with EBNA1386-405 or with active experimental autoimmune encephalomyelitis (EAE) induction by myelin oligodendrocyte glycoprotein (MOG)35-55 peptide. PARK2-/- mice developed more severe EAE than wild-type mice. Following immunization with EBNA1386-405, only PARK2-/- exhibited symptoms resembling EAE. During the acute phase, PARK2-/- mice immunized with either MOG35-55 or EBNA1386-405 exhibited similar infiltration of T cells and macrophages in the spinal cord and decreased GFAP expression in the brain. However, EBNA1386-405 -immunized PARK2-/- mice showed significantly increased frequencies of CD8a+ T cells and CD11c+ B cells, and distinct cytokine profiles in the periphery compared to wild-type controls. These findings highlight the role of EBV in exacerbating inflammation, particularly in the context of mitochondrial deficiencies.

Keywords

Epstein-Barr Virus; PARK2 Knockout Mice: Mitochondrial Dysfunction 

Subject

Medicine and Pharmacology, Neuroscience and Neurology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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