ISSN: 2167-7719

Air & Water Borne Diseases
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  • Review Article   
  • Air Water Borne Dis 12: 189., Vol 12(3)
  • DOI: 10.4172/2167-7719.1000189

Pathogenesis of Chronic Chikungunya Arthritis: Uncovering the Shared Features with Rheumatoid Arthritis

Robert T Schoen*
Department of Microbiology, Institute of Medical Sciences, USA
*Corresponding Author: Robert T Schoen, Department of Microbiology, Institute of Medical Sciences, USA, Email: Schoenrobert667@gmail.com

Received: 02-Jun-2023 / Manuscript No. awbd-23-102195 / Editor assigned: 05-Jun-2023 / PreQC No. awbd-23-102195 / Reviewed: 19-Jun-2023 / QC No. awbd-23-102195 / Revised: 23-Jun-2023 / Manuscript No. awbd-23-102195 / Published Date: 30-Jun-2023 DOI: 10.4172/2167-7719.1000189

Abstract

Chronic chikungunya arthritis and rheumatoid arthritis (RA) are two distinct conditions characterized by chronic joint inflammation and damage. This article aims to explore the shared features in the pathogenesis of chronic chikungunya arthritis and RA, shedding light on the underlying mechanisms that contribute to the development and progression of these conditions. Both chronic chikungunya arthritis and RA involve immunological dysregulation, with aberrant immune responses leading to persistent joint inflammation. The release of pro-inflammatory cytokines and the presence of autoantibodies contribute to the perpetuation of the inflammatory cascade in both conditions. Synovial inflammation, characterized by hyperplasia, infiltration of immune cells, and increased vascularity, is a common feature observed in affected joints of patients with chronic chikungunya arthritis and RA.

Joint destruction is a shared outcome in both conditions, driven by the chronic inflammatory milieu. Cartilage degradation, bone erosions, and an imbalance between the production and degradation of extracellular matrix components contribute to progressive joint damage in chronic chikungunya arthritis and RA. Genetic susceptibility, including specific human leukocyte antigen associations, plays a role in the development of both conditions, influencing immune dysregulation and joint pathology Autoimmunity may also be a contributing factor in the pathogenesis of chronic chikungunya arthritis and RA. The presence of autoantibodies, such as rheumatoid factor and anti-citrullinated protein antibodies, suggests an autoimmune component in chronic chikungunya arthritis, similar to RA. Molecular mimicry may trigger an immune response against self-structures, leading to the production of autoantibodies.

Understanding the shared features between chronic chikungunya arthritis and RA provides insights into the underlying mechanisms and pathways involved in these conditions. This knowledge may contribute to the development of targeted therapeutic strategies and interventions aimed at reducing joint inflammation and preventing joint damage in both chronic chikungunya arthritis and RA. Further research is warranted to unravel the complexities of these conditions and identify novel therapeutic targets for effective management.

Keywords

Chikungunya virus; Chronic chikungunya arthritis; Mesenchyme stem cells; Pathogenesis

Introduction

Chikungunya virus (CHIKV) infection has gained global attention in recent years due to its ability to cause chronic arthritis [1]. While acute chikungunya infection is characterized by fever, rash, and joint pain, a significant proportion of patients develop persistent joint symptoms, leading to a condition known as chronic chikungunya arthritis. Interestingly, the pathogenesis of chronic chikungunya arthritis shares several features with rheumatoid arthritis (RA), a chronic autoimmune disorder affecting the joints. This article aims to explore the shared features between these two conditions, shedding light on the underlying mechanisms that contribute to the development and progression of chronic chikungunya arthritis [2].

Immunological dysregulation

Both chronic chikungunya arthritis and RA are associated with aberrant immune responses. In chronic chikungunya arthritis, the virusinduced immune activation leads to the release of pro-inflammatory cytokines, such as interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6), which contribute to the persistent joint inflammation [3]. Similarly, in RA, a dysregulated immune response triggers the production of autoantibodies, such as rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPAs), resulting in chronic synovial inflammation and joint damage [4].

Synovial inflammation

The synovial membrane plays a critical role in joint inflammation in both chronic chikungunya arthritis and RA. Histopathological studies have revealed synovial lining hyperplasia, infiltration of immune cells, and increased vascularity in affected joints of patients with chronic chikungunya arthritis, resembling the characteristic features observed in RA. The infiltrating immune cells, including macrophages, lymphocytes, and plasma cells, contribute to the perpetuation of the inflammatory cascade and joint destruction in both conditions [5].

Joint destruction

Chronic chikungunya arthritis and RA share a common outcome of joint destruction. In chronic chikungunya arthritis, the persistent inflammation, accompanied by the production of matrix metalloproteinase and other destructive enzymes, leads to cartilage degradation and bone erosions. Similarly, in RA, the chronic inflammatory milieu triggers an imbalance between the production and degradation of extracellular matrix components, resulting in progressive joint destruction [6].

Genetic susceptibility

Genetic factors play a role in both chronic chikungunya arthritis and RA. Several studies have identified specific human leukocyte antigen (HLA) associations in patients with chronic chikungunya arthritis, suggesting a genetic predisposition to the development of persistent joint symptoms [7]. Similarly, HLA associations, such as the HLA-DRB1 shared epitope, are well-established risk factors for the development of RA. These genetic susceptibilities contribute to the dysregulation of immune responses and the subsequent joint pathology observed in both conditions [8].

Autoimmunity

Although the exact mechanisms underlying chronic chikungunya arthritis are still under investigation, there is increasing evidence suggesting an autoimmune component in its pathogenesis [9]. Autoantibodies, including RF and ACPAs, are frequently detected in patients with chronic chikungunya arthritis, reminiscent of the autoimmune nature of RA. This autoantibody production may result from molecular mimicry, where viral antigens share similarities with host antigens, triggering an immune response against self-structure [10].

Conclusion

Chronic chikungunya arthritis and rheumatoid arthritis share several common features in their pathogenesis, including immunological dysregulation, synovial inflammation, joint destruction, genetic susceptibility, and the presence of The pathogenesis of chronic chikungunya arthritis shares several common features with rheumatoid arthritis (RA), highlighting the complexity of these chronic joint disorders. Immunological dysregulation, synovial inflammation, joint destruction, genetic susceptibility, and the presence of autoantibodies are among the shared features that contribute to the development and progression of both conditions. The understanding of these shared features provides valuable insights into the underlying mechanisms driving chronic chikungunya arthritis and RA. It underscores the importance of immune dysregulation and the role of pro-inflammatory cytokines and autoantibodies in perpetuating joint inflammation and damage. The similarities in synovial inflammation and joint destruction highlight the common pathways involved in the breakdown of joint integrity.

Genetic susceptibility plays a crucial role in both chronic chikungunya arthritis and RA, emphasizing the influence of genetic factors on immune dysregulation and joint pathology. These genetic associations provide a potential avenue for identifying individuals at risk and developing personalized treatment approaches. The presence of autoantibodies in chronic chikungunya arthritis suggests an autoimmune component, mirroring the autoimmune nature of RA. The phenomenon of molecular mimicry may contribute to the production of autoantibodies and the development of self-directed immune responses, leading to joint inflammation and damage. The identification of shared features between chronic chikungunya arthritis and RA paves the way for potential therapeutic interventions.

Targeting common pathways involved in immune dysregulation, synovial inflammation, and joint destruction may offer new avenues for treatment strategies aimed at reducing inflammation and preventing joint damage in both conditions. Further research is needed to elucidate the specific mechanisms underlying the shared features and to explore additional factors contributing to the pathogenesis of chronic chikungunya arthritis and RA. This knowledge will not only enhance our understanding of these complex diseases but also inform the development of innovative therapeutic approaches that can alleviate symptoms, improve outcomes, and enhance the quality of life for individuals affected by chronic chikungunya arthritis and RA.

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Citation: Schoen RT (2023) Pathogenesis of Chronic Chikungunya Arthritis: Uncovering the Shared Features with Rheumatoid Arthritis. Air Water Borne Dis 12: 189. DOI: 10.4172/2167-7719.1000189

Copyright: © 2023 Schoen RT. 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.

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