Air & Water Borne Diseases
Open Access

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.

1. Castro-Hermida JA, González-Losada YA, Ares-Mazás E(2002) Prevalence of and risk factors involved in the spread of neonatal bovine cryptosporidiosis in Galicia (NW Spain). Vet Parasitol 106:1-10.

Indexed at, Google Scholar, Crossref

2. Chavatte-Palmer P, Velazquez MA, Jammes H, Duranthon V(2018) Review: epigenetics, developmental programming and nutrition in herbivores. Animal 12: 363–371.

Indexed at, Google Scholar, Crossref

3. Wu G, Bazer FW, Wallace JM, Spencer TE (2006) Board-invited review: intrauterine growth retardation: implications for the animal sciences. J Anim Sci 84: 2316–2337.

Indexed at, Google Scholar, Crossref

4. Wu Y, Cheng Z, Bai Y, Ma X(2019) Epigenetic mechanisms of maternal dietary protein and amino acids affecting growth and development of offspring. Curr Protein Pept Sci 20:727–735.

Indexed at, Google Scholar, Crossref

5. Tao S, Dahl GE (2013) Invited review: heat stress effects during late gestation on dry cows and their calves. J Dairy Sci 96:4079–4093.

Indexed at, Google Scholar, Crossref

6. Alharthi AS, Lopreiato V, Dai H (2019) Short communication: supply of methionine during late pregnancy enhances whole-blood innate immune response of Holstein calves partly through changes in mRNA abundance in polymorphonuclear leukocytes. J Dairy Sci 102:10599–10605.

Indexed at, Google Scholar, Crossref

7. Diallo B, Sissoko D, Loman NJ (2016) Resurgence of Ebola Virus Disease in Guinea Linked to a Survivor With Virus Persistence in Seminal Fluid for More Than 500 Days . Clin Infect Dis 63:13-53.

Indexed at, Google Scholar, Crossref

8. Dokubo EK, Wendland A, Mate SE (2018) Persistence of Ebola virus after the end of widespread transmission in Liberia: an outbreak report .Lancet Infect Dis 18:10-15.

Indexed at, Google Scholar, Crossref

9. Baseler L, Chertow DS, Johnson KM (2017) The Pathogenesis of Ebola Virus Disease.  Annu Rev Pathol 12:3-87.

Indexed at, Google Scholar, Crossref

10. Kreuels B, Wichmann D, Emmerich P (2014) A case of severe Ebola virus infection complicated by gram-negative septicemia. N Engl J Med 371:23-94.

Indexed at, Google Scholar, Crossref