Latent microbial infections leading  to myelin and axonal damage in  multiple sclerosis: A narrative review

Fatemeh Nezam  Zadeh; Aylin  Esmaeilkhani; Mansour  Sedighi; Nour  Amirmozafari; Mohammad  Rahbar; Saeed  Soleiman-Meigooni; Abed Zahedi  Bialvaei

doi:10.18502/cjn.v23i4.18769

Fatemeh Nezam Zadeh School of Medicine, Tonekabon Branch, Islamic Azad University, Tonekabon, Iran
Aylin Esmaeilkhani Department of Microbiology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
Mansour Sedighi Zoonoses Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran
Nour Amirmozafari Microbial Biotechnology Research Center, Iran University of Medical Sciences, Tehran, Iran
Mohammad Rahbar Iranian Reference Health Laboratory Research Center, Ministry of Health and Medical Education, Tehran, Iran
Saeed Soleiman-Meigooni Infectious Diseases Research Center, Aja University of Medical Sciences, Tehran, Iran
Abed Zahedi Bialvaei Microbial Biotechnology Research Center, Iran University of Medical Sciences, Tehran, Iran

DOI: https://doi.org/10.18502/cjn.v23i4.18769

Keywords: Multiple Sclerosis; Therapeutics; Demyelinating Diseases; Axonal Damage; Latent Infections

Abstract

Background: Multiple sclerosis (MS) is a complex autoimmune disease characterized by chronic inflammation, demyelination, and axonal damage in the central nervous system (CNS). This review specifically aims to investigate the role of latent microbial infections-such as those caused by Epstein-Barr virus (EBV), Chlamydia pneumoniae, and others-in contributing to myelin and axon damage in MS.

Methods: We evaluated recent studies from PubMed, Google Scholar, and Scopus databases that focus on the relationship between latent microbial infections and MS pathogenesis.

Results: In MS, emerging evidence suggests that latent microbial infections play a significant role in triggering and perpetuating the inflammatory processes associated with the disease. The potential mechanisms by which these infections contribute to the pathogenesis of MS, highlighting the interplay between the immune system, microbial agents, and the CNS are evaluated. These include molecular mimicry, where similarities in sequence or structure between viral, bacterial, or self-peptides can activate autoreactive T or B cells through cross activation by pathogen-derived peptides, chronic inflammation triggered by persistent infection, leading to immune-mediated damage, and disruption of the blood-brain barrier, allowing microbial agents or immune cells to infiltrate the CNS.

Conclusion: This review underscores the critical role of latent microbial infections in MS pathogenesis. By elucidating these mechanisms, we provide new insights that could inform the development of innovative therapeutic interventions and preventive strategies for MS.