SynthesisPathogens (Basel, Switzerland)2026
Autoantibodies and Molecular Mimicry in Alphavirus Chronic Arthritis: A Systematic Review.
Synthesis in Pathogens (Basel, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Chronic arthritis following arthritogenic alphavirus infections presents symptoms resembling autoimmune rheumatic diseases, raising questions about the underlying mechanisms, including molecular mimicry and autoantibody production. This systematic review evaluated evidence supporting molecular mimicry and the potential role of autoantibodies as predictive biomarkers in alphavirus-induced chronic arthritis. A comprehensive search of PubMed, Scopus and Web of Science was conducted following PRISMA 2020 guidelines and PECO framework. Thirteen studies met the inclusion criteria: four computational studies assessing peptide homology between viral and human proteins, and nine clinical studies evaluating autoantibodies in chronic post-alphavirus arthritis. Computational analyses identified conserved alphavirus peptides with sequence and structural similarity to human proteins implicated in autoimmunity, supporting the hypothesis of molecular mimicry. However, most lacked experimental validation. Clinical studies showed variable detection of autoantibodies, rheumatoid factors, anti-cyclic citrullinated peptide, and antinuclear antibodies in chronic patients, though seropositivity rates were inconsistent and generally low. Only one study reported a significant association between autoantibody levels and disease chronicity. The findings suggest a potential autoimmune component in post-alphavirus arthritis driven by molecular mimicry, though current evidence remains inconclusive due to methodological heterogeneity and limited validation. Autoantibodies may contribute to pathogenesis but are not reliable predictors of chronicity. Future longitudinal studies with standardized assays and validation of computational findings in human models are needed.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.