Related Experiment Videos

What is after cytokine-blocking therapy, a novel therapeutic target--synovial Epstein-Barr virus for rheumatoid

Shigemasa Sawada1, Masami Takei, Hirotake Inomata

  • 1Department of Rheumatology and Hematology, Nihon University Nerima Hikarigaoka Hospital, 2-11-1 Hikarigaoka Nerima-ku, Tokyo, Japan. sswd98@med.nihon-u.ac.jp <sswd98@med.nihon-u.ac.jp>

Autoimmunity Reviews
|February 10, 2007
PubMed

Insights

Epstein-Barr virus (EBV) may drive increased inflammatory cytokines in rheumatoid arthritis (RA). Targeting EBV with antiviral agents offers a potential new therapy for RA, avoiding side effects of current treatments.

Area of Science:

  • Rheumatology
  • Immunology
  • Virology

Background:

  • Current cytokine-blocking therapies for rheumatoid arthritis (RA) show promise but cause severe side effects and are costly.
  • The underlying cause of elevated inflammatory cytokines in RA patients remains incompletely understood.
  • Accumulating evidence suggests a link between Epstein-Barr virus (EBV) and RA pathogenesis.

Purpose of the Study:

  • To explore the role of Epstein-Barr virus (EBV) in the elevated inflammatory cytokine levels observed in rheumatoid arthritis (RA).
  • To review the potential of antiviral agents as a novel therapeutic strategy for RA patients.

Main Methods:

  • Review of existing circumstantial and direct evidence implicating Epstein-Barr virus (EBV) in RA synovial cells.
  • Analysis of recent scientific literature on antiviral agents and their potential application in RA treatment.

Main Results:

  • Significant evidence supports the presence of Epstein-Barr virus (EBV) within the synovial cells of rheumatoid arthritis (RA) patients.
  • Elevated levels of inflammatory cytokines in RA are potentially linked to EBV infection.

Conclusions:

  • Epstein-Barr virus (EBV) is a potential driver of inflammation in rheumatoid arthritis (RA).
  • Antiviral therapies targeting EBV represent a promising novel approach for RA treatment, potentially overcoming limitations of current therapies.

Related Concept Videos

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel Disease...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Respiratory Syncytial Virus Disease01:29

Respiratory Syncytial Virus Disease

Human respiratory syncytial virus (RSV) is a widespread pathogen that primarily targets infants and young children but also poses a serious health risk to elderly and immunocompromised individuals. Belonging to the Pneumoviridae family, RSV is a negative-sense, single-stranded RNA virus within the Pneumovirus genus. Its global health burden is significant, with millions of cases annually resulting in hospitalizations and mortality, particularly in resource-limited settings. Although most...
Rheumatic Heart Disease III: Medical Management01:21

Rheumatic Heart Disease III: Medical Management

Rheumatic heart disease (RHD) management can be divided into two main strategies: prevention and long-term management.Primary PreventionPrimary prevention focuses on timely diagnosis and management of group A streptococcal pharyngitis to prevent acute rheumatic fever. The most widely used antibiotic for treating this condition is intramuscular benzathine penicillin G.Acute Rheumatic Fever TreatmentThe primary treatment goal for a patient diagnosed with acute rheumatic fever is to suppress the...