Commentary - (2025) Volume 9, Issue 5
Received: 01-Sep-2025, Manuscript No. vcrh-26-180168;
Editor assigned: 03-Sep-2025, Pre QC No. P-180168;
Reviewed: 17-Sep-2025, QC No. Q-180168;
Revised: 22-Sep-2025, Manuscript No. R-180168;
Published:
29-Sep-2025
, DOI: 10.37421/2736-657X.2025.9.325
Citation: Tran, Linh. ”Viruses: Triggers Of Autoimmune Disease Development.” Virol Curr Res 09 (2025):325.
Copyright: © 2025 Tran L. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
The intricate interplay between viral infections and the genesis or exacerbation of autoimmune diseases represents a significant area of immunological research. Viruses, through diverse mechanisms, have been implicated as potent initiators or amplifiers of aberrant immune responses that mistakenly target self-antigens. Understanding these complex interactions is crucial for developing effective diagnostic and therapeutic strategies for a wide spectrum of autoimmune conditions. This review aims to consolidate current knowledge on the viral etiologies of autoimmunity, exploring the specific viruses, their proposed mechanisms, and the evidence supporting their roles. This article explores the intricate relationship between viral infections and the subsequent development or exacerbation of autoimmune diseases. It highlights how viral triggers can initiate or amplify autoimmune responses through mechanisms like molecular mimicry, bystander activation, and the disruption of immune tolerance. The review emphasizes specific viruses implicated in various autoimmune conditions, such as Epstein-Barr virus in multiple sclerosis and parvovirus B19 in rheumatoid arthritis, underscoring the critical need for further research into preventative strategies and targeted therapies. [1] Focusing on the role of RNA viruses, this study delves into how their replication processes and genetic material can directly influence immune dysregulation, leading to autoimmunity. It discusses specific RNA viruses like enteroviruses and flaviviruses and their proposed links to conditions such as type 1 diabetes and Guillain-Barré syndrome. The research points out the importance of understanding viral RNA structures and their interaction with host immune cells in triggering autoimmune cascades. [2] This review examines the evidence linking Epstein-Barr virus (EBV) to multiple sclerosis (MS), a prominent autoimmune neurological disorder. It details how EBV infection, particularly in early life, can prime the immune system for a dysregulated response targeting myelin. The authors discuss serological studies, genetic predispositions, and the biological plausibility of EBV's role in MS pathogenesis, emphasizing its persistent nature and reactivation potential. [3] The paper investigates the potential of cytomegalovirus (CMV) as an etiological factor in autoimmune diseases, particularly among immunocompromised individuals and in the context of organ transplantation. It explores how CMV can induce immune responses that cross-react with host tissues, potentially triggering or worsening autoimmune conditions like vasculitis or autoimmune hepatitis. The study highlights the need to consider CMV status in the management of autoimmune patients. [4] This research focuses on enteroviruses as potential triggers for type 1 diabetes (T1D), an autoimmune disease affecting pancreatic beta cells. It examines epidemiological links and proposes mechanisms by which enteroviral infections might initiate or accelerate the autoimmune destruction of insulin-producing cells. The authors discuss viral persistence and immune responses in the pancreatic islets, suggesting a role for enteroviruses in T1D pathogenesis. [5] The article critically reviews the association between human papillomavirus (HPV) and autoimmune diseases, moving beyond its established link to cancer. It explores potential cross-reactivity between HPV antigens and host tissues, as well as the inflammatory responses triggered by chronic HPV infection, which could contribute to autoimmune conditions like rheumatoid arthritis or Sjögren's syndrome. The authors emphasize the need for more robust evidence to confirm these associations. [6] The paper discusses the role of parvovirus B19 in the pathogenesis of rheumatoid arthritis (RA). It examines how the virus can induce immune responses that target joint tissues, potentially leading to chronic inflammation and joint damage characteristic of RA. The study highlights the detection of parvovirus B19 in synovial tissue of RA patients and discusses its potential as an environmental trigger for the disease. [7] The authors explore the impact of flavivirus infections, such as Dengue virus, on immune system modulation and their potential links to autoimmune phenomena. They discuss how flaviviruses can disrupt cytokine production, induce immune tolerance breakdown, and potentially trigger cross-reactive immune responses that contribute to autoimmune diseases. The article emphasizes the complex immunological consequences of flavivirus infections. [8] This paper investigates the potential role of retroviruses, including human endogenous retroviruses (HERVs), in the development of autoimmune diseases. It examines how HERV expression can lead to the production of autoantibodies and inflammatory responses that target host tissues, particularly in conditions like systemic lupus erythematosus (SLE) and rheumatoid arthritis. The study highlights the reactivation of dormant HERVs as a potential contributor to autoimmunity. [9] This comprehensive review discusses the complex relationship between viral infections and the development of autoimmune disorders, focusing on the concept of molecular mimicry. It provides examples of viral epitopes that resemble self-antigens, leading to cross-reactive immune responses that attack the body's own tissues. The authors emphasize the importance of understanding these mimicry mechanisms for developing novel diagnostic and therapeutic approaches to autoimmune diseases. [10]
The complex relationship between viral infections and the pathogenesis of autoimmune diseases is a multifaceted field of study. Viruses can initiate or exacerbate autoimmune conditions through a variety of mechanisms, including molecular mimicry, bystander activation, and the disruption of immune tolerance, as highlighted by current research [1].
Understanding these viral triggers is paramount for developing targeted interventions and preventative strategies. The introduction of such a comprehensive review is essential for setting the stage for a deeper exploration of this critical area of immunology. This foundational understanding allows for a more nuanced appreciation of the subsequent detailed discussions on specific viral agents and their associated autoimmune sequelae. Viral infections represent a significant etiological factor in the development and progression of autoimmune diseases. The intricate mechanisms by which viruses interact with the host immune system can lead to a breakdown of self-tolerance, resulting in chronic inflammation and tissue damage characteristic of autoimmunity. This review synthesizes current knowledge on this topic, providing a critical overview of the viral triggers and their associated pathogenetic pathways. This foundational understanding is crucial for the development of novel therapeutic approaches. [1] RNA viruses, in particular, have emerged as key players in the induction of autoimmune conditions. Their unique replication strategies and genetic material can directly influence immune dysregulation, leading to aberrant self-recognition. The study delves into specific RNA viruses and their proposed links to various autoimmune disorders, underscoring the importance of understanding their interaction with host immune cells in initiating autoimmune cascades. [2] Epstein-Barr virus (EBV) has been strongly implicated in the pathogenesis of multiple sclerosis (MS), a chronic autoimmune neurological disorder. The review meticulously examines the evidence linking EBV infection to MS, detailing how early-life exposure can prime the immune system for a dysregulated response targeting myelin. The persistence and reactivation potential of EBV are key factors contributing to its role in MS pathogenesis. [3] Cytomegalovirus (CMV) is another viral agent that warrants consideration in the context of autoimmune diseases, especially in immunocompromised individuals and transplant recipients. CMV can induce immune responses that cross-react with host tissues, potentially triggering or worsening conditions like vasculitis and autoimmune hepatitis, necessitating attention to CMV status in managing autoimmune patients. [4] Enteroviruses are proposed to be significant triggers for type 1 diabetes (T1D), an autoimmune disease characterized by the destruction of insulin-producing pancreatic beta cells. Research in this area explores the epidemiological links and proposed mechanisms by which enteroviral infections might initiate or accelerate this autoimmune process, highlighting the role of viral persistence in the pancreatic islets. [5] The association between human papillomavirus (HPV) and autoimmune diseases, beyond its known role in cancer, is an area of growing interest. The review explores potential cross-reactivity between HPV antigens and host tissues, as well as inflammatory responses triggered by chronic HPV infection, which may contribute to conditions like rheumatoid arthritis and Sjögren's syndrome, although further robust evidence is needed. [6] Parvovirus B19 has been investigated for its role in the pathogenesis of rheumatoid arthritis (RA). The virus can induce immune responses targeting joint tissues, potentially leading to the chronic inflammation and joint damage characteristic of RA. The presence of parvovirus B19 in synovial tissue of RA patients suggests its potential as an environmental trigger for the disease. [7] Flavivirus infections, such as Dengue virus, can profoundly modulate the immune system and are increasingly linked to autoimmune phenomena. These viruses can disrupt cytokine profiles, induce immune tolerance breakdown, and trigger cross-reactive immune responses that contribute to autoimmune diseases, presenting a complex pathophysiological nexus. [8] Retroviruses, including human endogenous retroviruses (HERVs), are also implicated in the development of autoimmune diseases. Their expression can lead to the production of autoantibodies and inflammatory responses that target host tissues, particularly in conditions like systemic lupus erythematosus (SLE) and rheumatoid arthritis, with the reactivation of dormant HERVs being a key area of investigation. [9] Molecular mimicry serves as a cornerstone mechanism linking viral infections to autoimmunity. This comprehensive review elucidates how viral epitopes that resemble self-antigens can elicit cross-reactive immune responses, leading to the immune system attacking the body's own tissues. Understanding these mimicry mechanisms is vital for developing novel diagnostic and therapeutic strategies for autoimmune diseases. [10]
Viruses are increasingly recognized as significant contributors to the development and exacerbation of autoimmune diseases. Various viruses, including Epstein-Barr virus (EBV), enteroviruses, parvovirus B19, cytomegalovirus (CMV), human papillomavirus (HPV), flaviviruses, and retroviruses, have been linked to conditions such as multiple sclerosis, type 1 diabetes, rheumatoid arthritis, vasculitis, Sjögren's syndrome, and systemic lupus erythematosus. These viruses can trigger autoimmune responses through mechanisms like molecular mimicry, where viral proteins resemble host antigens, leading to cross-reactive immune attacks. Other mechanisms include bystander activation, where inflammation induced by viral infection activates self-reactive immune cells, and the disruption of immune tolerance, compromising the body's ability to distinguish self from non-self. The persistence and reactivation of certain viruses, such as EBV, further contribute to chronic autoimmune processes. Understanding these complex viral-host interactions is crucial for identifying preventative strategies and developing targeted therapies for autoimmune disorders.
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Virology: Current Research received 187 citations as per Google Scholar report
