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Chronic Obstructive Pulmonary Disease

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Updated: Feb 16, 2026

Measuring Progressive Neurological Disability in a Mouse Model of Multiple Sclerosis

Measuring Progressive Neurological Disability in a Mouse Model of Multiple Sclerosis

Published on: November 14, 2016

Viruses in chronic progressive neurologic disease.

Emily C Leibovitch¹, Steven Jacobson¹

¹Viral Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.

Multiple Sclerosis (Houndmills, Basingstoke, England)

|January 9, 2018

Summary

Human herpesvirus 6 (HHV-6) infection accelerated experimental neuroinflammatory disease, suggesting a potential role for this virus in multiple sclerosis (MS) pathogenesis. Further research and antiviral trials are crucial for confirmation.

Keywords:

Human herpesvirus 6 (HHV-6)central nervous system inflammation herpesviruses multiple sclerosis viral triggers

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Lipidomics and Transcriptomics in Neurological Diseases

Lipidomics and Transcriptomics in Neurological Diseases

Published on: March 18, 2022

Area of Science:

Neuroimmunology
Virology
Experimental Neurology

Background:

Viruses, particularly Epstein-Barr virus (EBV) and human herpesvirus 6 (HHV-6), are suspected triggers for multiple sclerosis (MS) and other neuroinflammatory diseases.
The ubiquitous nature of these viruses and their acquisition decades before disease onset complicate direct causal links.
Experimental models are essential for understanding viral contributions to MS pathogenesis.

Purpose of the Study:

To investigate the role of human herpesvirus 6 (HHV-6) in the development and progression of experimental neuroinflammatory disease.
To utilize a nonhuman primate model to study virus-induced neuroinflammation relevant to MS.

Main Methods:

Infection of marmosets with human herpesvirus 6 (HHV-6).
Induction of an experimental neuroinflammatory disease mimicking aspects of multiple sclerosis (MS).
Comparison of disease progression between HHV-6 inoculated and control marmosets.

Main Results:

Marmosets inoculated with HHV-6 exhibited significantly accelerated experimental neuroinflammatory disease compared to control subjects.
This finding supports a potential role for HHV-6 in exacerbating neuroinflammatory conditions.

Conclusions:

Human herpesvirus 6 (HHV-6) infection can accelerate the onset and progression of experimental neuroinflammatory disease in a nonhuman primate model.
These results underscore the need for further investigation into viral mechanisms in MS.
Clinical trials with antiviral agents represent the definitive approach to confirm a causal link between HHV-6 and MS.