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Ifit2 Protect Mice from Murine-β-Coronavirus Induced Neuroinflammatory Demyelination | OMICS International| Abstract
ISSN: 2332-0877

Journal of Infectious Diseases & Therapy
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  • Short Communication   
  • J Infect Dis Ther,

Ifit2 Protect Mice from Murine-?-Coronavirus Induced Neuroinflammatory Demyelination

Madhav Sharma and Jayasri Das Sarma*
Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, West Bengal, India
*Corresponding Author : Jayasri Das Sarma, Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, West Bengal, India, Email: dassarmaj@iiserkol.ac.in

Received Date: Sep 25, 2023 / Published Date: Oct 27, 2023

Abstract

Ifit2, an interferon-induced protein with tetratricopeptide repeats 2, is critical in restricting neurotropic murine β- coronavirus RSA59 infection. While the protective role of Ifit2 is established for acute viral encephalitis, less is known about its influence on demyelination during the chronic phase of RSA59 infection. This commentary highlights key aspects of the study by Sharma et al., which demonstrated that Ifit2 deficiency causes extensive RSA59 viral spread in the spinal cord associated with impaired T-cell infiltration. Infected Ifit2-/- mice showed reduced T-cell activation in the cervical lymph nodes and preserved blood-brain-barrier integrity. Also, RSA59- infected Ifit2-/- mice showed severe demyelination and persistent viral load in the chronic phase of the disease. Thus, Ifit2 provides antiviral functions by promoting acute Neuroinflammation, aiding virus control, and limiting severe demyelination.

Keywords: Interferon; Neuro inflammatory; Corona virus

Citation: Sarma M, Sharma JD (2023) Ifit2 Protect Mice from Murine-β-Coronavirus Induced Neuroinflammatory Demyelination. J infect Dis Ther S5:001

Copyright: © 2023 Sharma M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permitsunrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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