• Humans
• Inflammatory Bowel Diseases/complications
• Skin Diseases/etiology
• Skin Diseases/therapy

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.

• Crohn’s Disease
• Efficacy
• Herpes Zoster
• Inflammatory Bowel Disease
• Recombinant Zoster Vaccine
• Shingrix
• Ulcerative Colitis

• Chronic Disease
• Herpes Zoster/epidemiology
• Herpes Zoster/prevention & control
• Herpes Zoster Vaccine/therapeutic use
• Humans
• Inflammatory Bowel Diseases/drug therapy
• Retrospective Studies
• Vaccination

• T32 DK007740 NIDDK NIH HHS

Over the past decades, the treatment of inflammatory bowel diseases (IBD) has become more targeted, anticipating the use of immune-modifying therapies at an earlier stage. This top-down approach has been correlated with favorable short and long-term outcomes, but it has also brought with it concerns regarding potential infectious complications. This large IBD population treated with immune-modifying therapies, especially if combined, has an increased risk of severe infections, including opportunistic infections that are sustained by viral, bacterial, parasitic, and fungal agents. Viral infections have emerged as a focal safety concern in patients with IBD, representing a challenge for the clinician: they are often difficult to diagnose and are associated with significant morbidity and mortality. The first step is to improve effective preventive strategies, such as applying vaccination protocols, adopt adequate prophylaxis and educate patients about potential risk factors. Since viral infections in immunosuppressed patients may present atypical signs and symptoms, the challenges for the gastroenterologist are to suspect, recognize and diagnose such complications. Appropriate treatment of common viral infections allows us to minimize their impact on disease outcomes and patients’ lives. This practical review supports this standard of care to improve knowledge in this subject area.

• Inflammatory bowel diseases
• Viral infections
• Opportunistic infections
• Standard of care
• Crohn’s disease
• Ulcerative colitis

• Colitis
• Humans
• Immunocompromised Host
• Inflammatory Bowel Diseases/epidemiology
• Inflammatory Bowel Diseases/therapy
• Opportunistic Infections/diagnosis
• Opportunistic Infections/epidemiology
• Opportunistic Infections/prevention & control
• Virus Diseases/epidemiology