Epstein-Barr virus (EBV) is deemed a necessary, yet insufficient factor in the development of multiple sclerosis (MS). In this study, myelin basic protein-specific transgenic T cell receptor mice were infected with murid gammaherpesvirus 68 virus (MHV68), an EBV-like virus that infects mice, resulting in the onset neurological deficits at a significantly higher frequency than influenza or mock-infected mice. MHV68 infected mice exhibited signs including optic neuritis and ataxia which are frequently observed in MS patients but not in experimental autoimmune encephalomyelitis mice. MHV68-infected mice exhibited increased focal immune cell infiltration in the central nervous system. Single cell RNA sequencing identified the emergence of a population of B cells that express genes associated with antigen presentation and costimulation, indicating that gammaherpesvirus infection drives a distinct, pro-inflammatory transcriptional program in B cells that may promote autoreactive T cell responses in MS.
Keyphrases
- epstein barr virus
- multiple sclerosis
- high fat diet induced
- single cell
- diffuse large b cell lymphoma
- mass spectrometry
- end stage renal disease
- ms ms
- white matter
- traumatic brain injury
- wild type
- oxidative stress
- skeletal muscle
- case report
- newly diagnosed
- brain injury
- transcription factor
- amino acid
- small molecule
- protein protein
- heat stress
- patient reported
- disease virus