ReviewFrontiers in cellular and infection microbiology2026
Decoupling musculoskeletal damage from antiviral control: the NLRP3 inflammasome in arthritogenic alphavirus infection.
Review in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Abstract
Mosquito-borne arthritogenic alphaviruses, including chikungunya virus (CHIKV), Ross River virus (RRV), and Mayaro virus (MAYV), cause acute febrile polyarthralgia and can leave a substantial proportion of patients with persistent or relapsing musculoskeletal disease. In many cohorts, chronic arthritis continues after systemic viremia has declined, suggesting that late tissue pathology is sustained largely by host inflammatory programs rather than by ongoing productive viral replication. This Mini Review examines the NLRP3 inflammasome as a pathogenic node linking viral danger sensing to chronic joint and bone damage, and considers whether this pathway can be targeted to reduce tissue injury while preserving antiviral control. Across CHIKV, RRV, and MAYV models, pattern-recognition receptor signaling provides NF-κB-dependent priming of NLRP3, pro-IL-1β, and pro-IL-18, whereas K
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