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Viruses
Special Issues
Viral Infection and Autoimmune Diseases
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Viral Infection and Autoimmune Diseases

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 16538

Special Issue Editors

Prof. Dr. Hideki Nakamura

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Guest Editor
Division of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan
Interests: epidemiology; infection mechanism; inflammation; autoantibody production
Prof. Dr. Masami Takei

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Guest Editor
Division of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, Itabashi-ku, Tokyo 173-8610, Japan
Interests: epidemiology; infection mechanism; inflammation; autoantibody production

Special Issue Information

Dear Colleagues,

In the development of autoimmune diseases, the effects of microorganisms, such as bacteria and viruses, are assumed as environmental factors. While some rheumatic diseases have a high incidence only in the endemic area of ​​the virus, there are reports showing a link between the universally present virus and autoimmune diseases. The mechanism by which the virus stimulates ligands in the innate immune system to produce type I interferon is being elucidated. However, the detailed induction mechanism of how the virus causes immune disorders in the clinical pathology of autoimmune diseases has not been clarified.

In this Special Issue, we discuss the involvement of viral infections in rheumatic diseases such as rheumatoid arthritis or Sjögren's syndrome, type 1 diabetes, thyroid diseases, and neurological diseases. In addition, we would like to specifically evaluate the inflammation-inducing mechanism, organ damage, and effects on autoantibody production associated with virus infection. We hope that these reviews will help readers understand how viral infections are involved in autoimmune diseases and help in the differential diagnosis and treatment strategies.

Prof. Dr. Hideki Nakamura
Prof. Dr. Masami Takei
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Epstein–Barr virus
  • human T-cell leukemia virus
  • rheumatoid arthritis
  • MTX-lymphoproliferative disease (LPD)
  • Sjögren’s syndrome
  • systemic lupus erythematosus
  • diabetes
  • thyroiditis
  • COVID-19 and anti-phospholipid syndrome

Published Papers (7 papers)

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Editorial

Jump to: Review, Other

2 pages, 172 KiB  
Editorial
Special Issue ‘Viral Infection and Autoimmune Diseases’
by Hideki Nakamura and Masami Takei
Viruses 2022, 14(11), 2491; https://0-doi-org.brum.beds.ac.uk/10.3390/v14112491 - 11 Nov 2022
Viewed by 931
Abstract
Viral infection, which is one of the environmental factors, and human autoimmune diseases are often associated with each other [...] Full article
(This article belongs to the Special Issue Viral Infection and Autoimmune Diseases)

Review

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12 pages, 960 KiB  
Review
Are Viral Infections Key Inducers of Autoimmune Diseases? Focus on Epstein–Barr Virus
by Masami Takei, Noboru Kitamura, Yosuke Nagasawa, Hiroshi Tsuzuki, Mitsuhiro Iwata, Yasuko Nagatsuka, Hideki Nakamura, Kenichi Imai and Shigeyoshi Fujiwara
Viruses 2022, 14(9), 1900; https://0-doi-org.brum.beds.ac.uk/10.3390/v14091900 - 27 Aug 2022
Cited by 8 | Viewed by 2135
Abstract
It is generally accepted that certain viral infections can trigger the development of autoimmune diseases. However, the exact mechanisms by which these viruses induce autoimmunity are still not understood. In this review, we first describe hypothetical mechanisms by which viruses induce some representative [...] Read more.
It is generally accepted that certain viral infections can trigger the development of autoimmune diseases. However, the exact mechanisms by which these viruses induce autoimmunity are still not understood. In this review, we first describe hypothetical mechanisms by which viruses induce some representative autoimmune diseases. Then, we focus on Epstein–Barr virus (EBV) and discuss its role in the pathogenesis of rheumatoid arthritis (RA). The discussion is mainly based on our own previous findings that (A) EBV DNA and its products EBV-encoded small RNA (EBER) and latent membrane protein 1 (LMP1) are present in the synovial lesions of RA, (B) mRNA expression of the signaling lymphocytic activation molecule-associated protein (SAP)/SH2D1A gene that plays a critical role in cellular immune responses to EBV is reduced in the peripheral T cells of patients with RA, and (C) EBV infection of mice reconstituted with human immune system components (humanized mice) induced erosive arthritis that is pathologically similar to RA. Additionally, environmental factors may contribute to EBV reactivation as follows: Porphyromonas gingivalis peptidylarginine deiminase (PAD), an enzyme required for citrullination, engenders antigens leading to the production of citrullinated peptides both in the gingiva and synovium. Anti-citrullinated peptides autoantibody is an important marker for diagnosis and disease activity of RA. These findings, as well as various results obtained by other researchers, strongly suggest that EBV is directly involved in the pathogenesis of RA, a typical autoimmune disease. Full article
(This article belongs to the Special Issue Viral Infection and Autoimmune Diseases)
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12 pages, 2113 KiB  
Review
Virus Infections Play Crucial Roles in the Pathogenesis of Sjögren’s Syndrome
by Kunihiro Otsuka, Mami Sato, Takaaki Tsunematsu and Naozumi Ishimaru
Viruses 2022, 14(7), 1474; https://0-doi-org.brum.beds.ac.uk/10.3390/v14071474 - 04 Jul 2022
Cited by 6 | Viewed by 2357
Abstract
Sjögren’s syndrome (SS) is an autoimmune disease especially targeting exocrine glands, such as the salivary and lacrimal glands. A radical therapy for SS based on its etiology has not been established because of the complex pathogenesis of the disease. Several studies have demonstrated [...] Read more.
Sjögren’s syndrome (SS) is an autoimmune disease especially targeting exocrine glands, such as the salivary and lacrimal glands. A radical therapy for SS based on its etiology has not been established because of the complex pathogenesis of the disease. Several studies have demonstrated a relationship between virus infection and SS pathogenesis. In particular, infection with the Epstein-Barr (EB) virus among others is a potent factor associated with the onset or development of SS. Specifically, virus infection in the target organs of SS triggers or promotes autoreactive responses involving the process of autoantigen formation, antigen-presenting function, or T-cell response. Our review of recent research highlights the crucial roles of virus infection in the pathogenesis of SS and discusses the critical association between virus infection and the etiology of autoimmunity in SS. Full article
(This article belongs to the Special Issue Viral Infection and Autoimmune Diseases)
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15 pages, 1256 KiB  
Review
Effect of HTLV-1 Infection on the Clinical Course of Patients with Rheumatoid Arthritis
by Kunihiko Umekita
Viruses 2022, 14(7), 1460; https://0-doi-org.brum.beds.ac.uk/10.3390/v14071460 - 01 Jul 2022
Cited by 4 | Viewed by 2527
Abstract
Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia/lymphoma (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The effects of HTLV-1 on health are not fully elucidated. Epidemiological studies have shown that the prevalence of HTLV-1 infection is [...] Read more.
Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia/lymphoma (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The effects of HTLV-1 on health are not fully elucidated. Epidemiological studies have shown that the prevalence of HTLV-1 infection is high in patients with rheumatic diseases. The prevalence of comorbidities, such as Sjögren’s syndrome and rheumatoid arthritis (RA), is higher in patients with HAM/TSP than the in general population. Studies have shown the effects of HTLV-1-infection on the clinical course of RA. Major questions on the association between HTLV-1 infection and RA: (1) Is it possible that HTLV-1 infection causes RA? (2) Do patients with RA who are infected with HTLV-1 have different clinical features? (3) Are immunosuppressants associated with an increased prevalence of HAM/TSP or ATL in RA patients with HTLV-1 infection? Is ATL an immunosuppressive therapy-associated lymphoproliferative disorder? No large-scale studies have investigated the incidence of ATL in patients with RA. However, several studies have reported the development of ATL in patients with RA who have HTLV-1 infection. This review aimed to shed light on the association between HTLV-1 infection and RA and summarize the unmet medical needs of RA patients with HTLV-1 infection. Full article
(This article belongs to the Special Issue Viral Infection and Autoimmune Diseases)
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16 pages, 2078 KiB  
Review
Does HTLV-1 Infection Show Phenotypes Found in Sjögren’s Syndrome?
by Hideki Nakamura, Masako Tsukamoto, Yosuke Nagasawa, Noboru Kitamura, Toshimasa Shimizu, Atsushi Kawakami, Kinya Nagata and Masami Takei
Viruses 2022, 14(1), 100; https://0-doi-org.brum.beds.ac.uk/10.3390/v14010100 - 06 Jan 2022
Cited by 8 | Viewed by 2463
Abstract
Viruses are a possible cause for Sjögren’s syndrome (SS) as an environmental factor related to SS onset, which exhibits exocrine gland dysfunction and the emergence of autoantibodies. Although retroviruses may exhibit lymphocytic infiltration into exocrine glands, human T-cell leukemia virus type 1 (HTLV-1) [...] Read more.
Viruses are a possible cause for Sjögren’s syndrome (SS) as an environmental factor related to SS onset, which exhibits exocrine gland dysfunction and the emergence of autoantibodies. Although retroviruses may exhibit lymphocytic infiltration into exocrine glands, human T-cell leukemia virus type 1 (HTLV-1) has been postulated to be a causative agent for SS. Transgenic mice with HTLV-1 genes showed sialadenitis resembling SS, but their phenotypic symptoms differed based on the adopted region of HTLV-1 genes. The dominance of tax gene differed in labial salivary glands (LSGs) of SS patients with HTLV 1-associated myelopathy (HAM) and adult T-cell leukemia. Although HTLV-1 was transmitted to salivary gland epithelial cells (SGECs) by a biofilm-like structure, no viral synapse formation was observed. After infection to SGECs derived from SS patients, adhesion molecules and migration factors were time-dependently released from infected SGECs. The frequency of the appearance of autoantibodies including anti-Ro/SS-A, La/SS-B antibodies in SS patients complicated with HAM is unknown; the observation of less frequent ectopic germinal center formation in HTLV-1-seropositive SS patients was a breakthrough. In addition, HTLV-1 infected cells inhibited B-lymphocyte activating factor or C-X-C motif chemokine 13 through direct contact with established follicular dendritic cell-like cells. These findings show that HTLV-1 is directly involved in the pathogenesis of SS. Full article
(This article belongs to the Special Issue Viral Infection and Autoimmune Diseases)
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Other

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10 pages, 274 KiB  
Brief Report
Epidemiology of the Epstein–Barr Virus in Autoimmune Inflammatory Rheumatic Diseases in Northern Brazil
by Samires Avelino de Souza França, Julimar Benedita Gomes de Oliveira Viana, Hilda Carla Azevedo Góes, Ricardo Roberto de Souza Fonseca, Rogério Valois Laurentino, Igor Brasil Costa, Aldemir Branco Oliveira-Filho and Luiz Fernando Almeida Machado
Viruses 2022, 14(4), 694; https://0-doi-org.brum.beds.ac.uk/10.3390/v14040694 - 27 Mar 2022
Cited by 9 | Viewed by 2271
Abstract
The present study aimed to describe the seroprevalence infection, Epstein-Barr virus (EBV) genotypes, relate the infection’s profile with the epidemiological and corticotherapy data of patients with Autoimmune inflammatory rheumatic diseases (AIRD). A cross-sectional study was carried out with 139 individuals, 92 with systemic [...] Read more.
The present study aimed to describe the seroprevalence infection, Epstein-Barr virus (EBV) genotypes, relate the infection’s profile with the epidemiological and corticotherapy data of patients with Autoimmune inflammatory rheumatic diseases (AIRD). A cross-sectional study was carried out with 139 individuals, 92 with systemic lupus erythematosus (SLE), 27 with rheumatoid arthritis (RA) and 20 with other autoimmune diseases, who were undergoing clinical follow-up in Brazil. Serological tests for the detection of EBV anti-VCA IgM and IgG antibodies, as well as the amplification of a segment of the EBV EBNA-3c gene by conventional PCR were performed to identify the infection and the viral subtype. The Epstein–Barr nuclear antigen 3 (EBNA3C) gene participates of maintenance of viral latency and infected B-lymphocytes immortalization by unclear signaling cascades. The association of active/latent EBV infection with EBV infection profile was assessed by Fisher’s exact test and multiple logistic regression. The seroprevalence of EBV anti-VCA IgG was 100%, while that of anti-VCA IgM was 1.43% (2/139). Active-phase infection was confirmed by the presence of EBV DNA in 40.29% of the population evaluated (56/139), with 45.65% (42/92) in SLE, 25.92% (7/27) in the RA and in 35% (7/20) in other autoimmune diseases. It was observed that individuals with SLE had a higher prevalence of active/lytic EBV infection and that oral corticosteroid therapy at a dose lower than 20 mg/day increased the risk of EBV activity by up to 11 times. Only the presence of EBV-1 was identified. Thus, EBV lytic infection was higher in individuals with SLE when compared to other autoimmune diseases with rheumatologic involvement and the lytic activity of the virus precedes corticosteroid-induced immunosuppression. Full article
(This article belongs to the Special Issue Viral Infection and Autoimmune Diseases)
13 pages, 3045 KiB  
Systematic Review
New Evidence of Significant Association between EBV Presence and Lymphoproliferative Disorders Susceptibility in Patients with Rheumatoid Arthritis: A Systematic Review with Meta-Analysis
by Ana Banko, Danijela Miljanovic, Ivana Lazarevic, Ivica Jeremic, Aleksa Despotovic, Milka Grk and Andja Cirkovic
Viruses 2022, 14(1), 115; https://0-doi-org.brum.beds.ac.uk/10.3390/v14010115 - 10 Jan 2022
Cited by 9 | Viewed by 2963
Abstract
Development of lymphoproliferative disorders (LPDs) is one of the well-known life-threatening complications in rheumatoid arthritis (RA) patients. However, there is a lack of definitive conclusions regarding the role of Epstein-Barr virus (EBV) activity in RA initiation and progression, especially in promoting LPDs. A [...] Read more.
Development of lymphoproliferative disorders (LPDs) is one of the well-known life-threatening complications in rheumatoid arthritis (RA) patients. However, there is a lack of definitive conclusions regarding the role of Epstein-Barr virus (EBV) activity in RA initiation and progression, especially in promoting LPDs. A systematic review and meta-analysis of studies that reported an EBV positive result in RA-LPD patients and controls were conducted. Studies published before 27 July 2021 were identified through PubMed, Web of Science, and SCOPUS. A total of 79 articles were included in the systematic review. The prevalence of EBV positive result among RA-LPD patients was 54% (OR = 1.54, 95% CI = 1.45–1.64). There was a statistically significant association between EBV presence and LPD susceptibility in RA patients in comparison with all controls (OR = 1.88, 95% CI = 1.29–2.73) and in comparison with LPD patients only (OR = 1.92, 95% CI = 1.15–3.19). This association was not shown in comparison with patients with autoimmune diseases other than RA who developed LPD (OR = 0.79, 95% CI = 0.30–2.09). This meta-analysis confirmed a high prevalence of EBV in the RA-LPD population. Furthermore, it provides evidence for the association between EBV presence and LPD susceptibility in RA patients, but not in those with other autoimmune diseases who developed LPD. Full article
(This article belongs to the Special Issue Viral Infection and Autoimmune Diseases)
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