Reviews

Review articles

Posted on May 21, 2026  •  4 minutes  • 787 words
Table of contents

BEHIND-MS Review articles

  • Triggering multiple sclerosis: infection with Epstein-Barr virus activates multiple pre-existing autoreactive B and T cells

Münz, C. Triggering multiple sclerosis: infection with Epstein-Barr virus activates multiple pre-existing autoreactive B and T cells , Signal Transduction and Targeted Therapy (2026)

This Research Highlight highlights three recent publications which show that the Epstein-Barr virus (EBV) activates pre-existing autoreactive T cells by altering the immunopeptidome and inducing molecular mimicry, while also preventing the elimination of autoreactive B cells. These multiple autoimmune responses against the central nervous system (CNS) triggered by EBV might then synergistically precipitate multiple sclerosis (MS) within years after encountering this virus.

  • Neuroinflammation as a result of non-neurotropicherpesvirus infection

Münz, C. Neuroinflammation as a result of non-neurotropicherpesvirus infection , Immunology & Cell Biology (2026)

This review discusses mechanisms by which EBV might cause neuroinflammatory B-cell migration to the central nervous system (CNS), as observed during primary CNS lymphomas and MS. It also summarizes mechanisms of molecular mimicry and autoreactive B-cell expansion by EBV and explores approaches to target EBV-mediated neuroinflammation for therapeutic interventions in people with MS. The recently provided information on EBV’s association with MS gives exciting insights into the initiation of this autoimmune disease. Successful therapeutic interventions on the basis of this knowledge might provide evidence that EBV contributes also to the clinical phase of this autoimmune disease.

  • Latent, Lytic, and Linked to Multiple Sclerosis—How EBV Drives Autoimmunity

Münz, C. et al. Latent, Lytic, and Linked to Multiple Sclerosis—How EBV Drives Autoimmunity European Journal of Immunology (2026)

This review discusses how insufficient immune control might allow for sizeable populations of a certain type of immune cell (T-bet+CXCR3+ B cells) to infiltrate the central nervous system (CNS), attract other lymphocytes, efficiently stimulate T cells in the CNS, and differentiate into antibody-producing plasma cells, thereby contributing to inflammation and autoantibody production in a subset of MS patients. This CNS-infiltrating B-cell population could be targeted by EBV-specific treatments to complement existing MS therapies.

  • Recent advances in animal models of lymphomagenesis caused by human γ-herpesviruses

Münz, C. Recent advances in animal models of lymphomagenesis caused by human γ-herpesviruses , Current Opinion in Virology (2025)

The two human γ-herpesviruses Epstein Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV) cause around 2–3% of all cancers in man. Their exclusive tropism for humans and associated lack of small animal models has impeded the dissection of individual viral gene contributions to tumor formation and of protection by distinct immune responses that are observed in virus carriers. Mice with reconstituted human immune systems (humanized mice) now offer the possibility to study these questions and to develop adoptive antibody and T cell transfers against EBV- and KSHV-associated pathologies. Based on such protective immune responses, vaccine candidates can then be developed to prophylactically and therapeutically induce immune control, similar to the one that avoids virus-associated pathologies in the vast majority of infected individuals.

  • Epstein–Barr virus pathogenesis and emerging control strategies

Münz, C. Epstein–Barr virus pathogenesis and emerging control strategies Nat Rev Microbiol (2025).

Sixty years after its discovery as the first human tumour virus, Epstein–Barr virus (EBV)-specific therapies and vaccines have entered clinical trials. These might not only be applicable for EBV-associated malignancies, where the virus was originally discovered, but also to immunopathologies, including the autoimmune disease multiple sclerosis, which might be triggered in susceptible individuals by primary EBV infection. This Review discusses the surprisingly large spectrum of diseases that EBV seems to cause, as well as which of these might be treated by the therapeutic approaches that are currently being developed or are already clinically applied. New pharmacological inhibitors, antibody therapies, adoptive T cell therapies and active vaccinations are beginning to offer possibilities to target the various EBV infection programmes that are associated with different diseases. These novel developments might allow us to specifically target EBV rather than its host cells in virus-associated pathologies.

  • Altered EBV specific immune control in multiple sclerosis

Münz, C., Altered EBV specific immune control in multiple sclerosis Journal of Neuroimmunology (2024).

This review discusses the epidemiological evidence that EBV infection starts the pathogenic process that leads to multiple sclerosis (MS). It also outlines possible mechanisms by which EBV might trigger and sustain the underlying disease process.

  • EBV-specific T-cell immunity: relevance for multiple sclerosis

Behrens M, Comabella M, Lünemann JD. EBV-specific T-cell immunity: relevance for multiple sclerosis Front Immunol. (2024)

While the infection with Epstein-Barr virus infection has been shown to be a consistent risk factor for the development of multiple sclerosis in recent years, the biological basis of this association remains incompletely understood. This review presents the most up to date research in the field, specifically regarding the role of T and B cells, and provides future avenues for further research elucidating the role of EBV in MS.