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Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
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Related Experiment Video

Updated: May 23, 2026

Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line
09:14

Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line

Published on: September 28, 2022

Lupus and Epstein-Barr.

Judith A James1, Julie M Robertson

  • 1Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA. jamesj@omrf.ouhsc.edu

Current Opinion in Rheumatology
|April 17, 2012
PubMed
Summary
This summary is machine-generated.

Systemic lupus erythematosus (SLE) patients show immune dysregulation against Epstein-Barr virus (EBV). Evidence suggests EBV may play a role in SLE development and progression.

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Last Updated: May 23, 2026

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An Efficient and Simple Method to Establish NK and T Cell Lines from Patients with Chronic Active Epstein-Barr Virus Infection
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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
12:04

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice

Published on: November 1, 2015

Area of Science:

  • Immunology
  • Virology
  • Rheumatology

Background:

  • Systemic lupus erythematosus (SLE) is a complex autoimmune disease with multifactorial etiology.
  • Genetic and environmental factors are implicated, with a growing focus on viral associations.
  • Epstein-Barr virus (EBV) is a ubiquitous herpesvirus with known immunomodulatory effects.

Purpose of the Study:

  • To review evolving evidence on Epstein-Barr virus (EBV)-specific roles in Systemic lupus erythematosus (SLE).
  • To focus on experimental studies published between 2009 and 2011 regarding EBV and SLE.
  • To explore the interplay between EBV infection and SLE pathogenesis.

Main Methods:

  • Review of experimental studies published 2009-2011.
  • Analysis of immune responses in SLE patients against EBV.
  • Investigation of molecular mimicry between EBV and SLE-associated antigens.
  • Assessment of EBV seroconversion rates, viral loads, and T-cell responses in SLE patients.

Main Results:

  • SLE patients exhibit dysregulated immune responses to EBV, including molecular mimicry.
  • Higher rates of EBV seroconversion and frequent viral reactivation observed in SLE patients.
  • Increased EBV viral loads and impaired EBV-specific CD8 cytotoxic T-cell responses noted in SLE.
  • Irregular cytokine production by immune cells upon EBV stimulation in lupus patients.

Conclusions:

  • Recent findings support a potential role for EBV in the etiology and pathogenesis of SLE.
  • SLE-specific serologic responses, gene expression, and T-cell reactivity to EBV are evident.
  • Molecular mimicry between EBV and SLE components further implicates the virus in lupus.