Mouse hepatitis virus infection upregulates genes involved in innate immune responses.

Authors

Dhriti Chatterjee, Department of Biological Sciences, Indian Institute of Science Education and Research-Kolkata (IISER-K)
Sankar Addya, Kimmel Cancer Center, Department of Cancer Biology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PennsylvaniaFollow
Reas S Khan, Scheie Eye Institute, FM Kirby Centre for Molecular Ophthalmology, University of Pennsylvania
Lawrence C. Kenyon, Departments of Anatomy, Pathology and Cell Biology, Thomas Jefferson UniversityFollow
Alexander Choe, Departments of Neurology and Microbiology, University of Colorado School of MedicineAurora
Randall J Cohrs, Departments of Neurology and Microbiology, University of Colorado School of MedicineAurora
Kenneth S Shindler, Scheie Eye Institute, FM Kirby Centre for Molecular Ophthalmology, University of PennsylvaniaFollow
Jayasri Das Sarma, Department of Biological Sciences, Indian Institute of Science Education and Research-Kolkata (IISER-K)

Document Type

Article

Publication Date

10-31-2014

Comments

This article has been peer reviewed. It was published in: PloS ONE.

Volume 9, Issue 10, 31 October 2014, Article number e111351.

The published version is available at DOI: 10.1371/journal.pone.0111351

Copyright © 2014 Chatterjee et al

Abstract

Neurotropic recombinant strain of Mouse Hepatitis Virus, RSA59, induces meningo-encephalitis, myelitis and demyelination following intracranial inoculation. RSA59 induced neuropathology is partially caused by activation of CNS resident microglia, as demonstrated by changes in cellular morphology and increased expression of a microglia/macrophage specific calcium ion binding factor, Iba1. Affymetrix Microarray analysis for mRNA expression data reveals expression of inflammatory mediators that are known to be released by activated microglia. Microglia-specific cell surface molecules, including CD11b, CD74, CD52 and CD68, are significantly upregulated in contrast to CD4, CD8 and CD19. Protein analysis of spinal cord extracts taken from mice 6 days post-inoculation, the time of peak inflammation, reveals robust expression of IFN-γ, IL-12 and mKC. Data suggest that activated microglia and inflammatory mediators contribute to a local CNS microenvironment that regulates viral replication and IFN-γ production during the acute phase of infection, which in turn can cause phagolysosome maturation and phagocytosis of the myelin sheath, leading to demyelination.

Recommended Citation

Chatterjee, Dhriti; Addya, Sankar; Khan, Reas S; Kenyon, Lawrence C.; Choe, Alexander; Cohrs, Randall J; Shindler, Kenneth S; and Sarma, Jayasri Das, "Mouse hepatitis virus infection upregulates genes involved in innate immune responses." (2014). Department of Pathology, Anatomy, and Cell Biology Faculty Papers. Paper 154.
https://jdc.jefferson.edu/pacbfp/154

PubMed ID

25360880