Review
Parvovirus B19-associated arthropathy: a contemporary narrative review
L. Bianchi1, J. Ciaffi2, D. Giuggioli3, F. Ursini4
- Rheumatology Unit, Department of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, Modena, Italy. lorenzo.bianchi12@studio.unibo.it
- Medicine & Rheumatology Unit, IRCCS Istituto Ortopedico Rizzoli, Bologna; and Department of Biomedical and Neuromotor Sciences (DIBINEM), Alma Mater Studiorum Università di Bologna, Italy.
- Rheumatology Unit, Department of Medical and Surgical Sciences for Children and Adults, University of Modena and Reggio Emilia, Modena, Italy.
- Medicine & Rheumatology Unit, IRCCS Istituto Ortopedico Rizzoli, Bologna; and Department of Biomedical and Neuromotor Sciences (DIBINEM), Alma Mater Studiorum Università di Bologna, Italy.
CER19866
Review
Received: 01/03/2026
Accepted : 04/05/2026
In Press: 05/08/2026
Abstract
Parvovirus B19 is a common and frequently under-recognised cause of acute-onset inflammatory polyarthropathy in adults, with a clinical phenotype that can closely mimic early rheumatoid arthritis. This review synthesises the adult-focused literature on epidemiology, immunopathogenesis, clinical presentation, diagnostic strategy, and management of parvovirus B19-associated arthropathy, with attention to the renewed circulation observed in recent years and its implications for clinical practice. In adults, joint involvement typically manifests as abrupt, painful, symmetric polyarticular disease with predominant small-joint involvement, often accompanied by morning stiffness and, occasionally, minimal extra-articular features. Most cases follow a self-limited, non-erosive course, yet a minority experience prolonged symptoms, creating a diagnostic grey zone in which rheumatoid arthritis overdiagnosis and inappropriate immunosuppression may occur. Diagnostic uncertainty is amplified by the limitations of routine testing: immunoglobulin M may persist for months or reappear, immunoglobulin G reflects past exposure, low-level parvovirus B19 DNA can be detectable long after acute infection, and transient antinuclear antibodies/rheumatoid factor positivity may misleadingly support an autoimmune label. Mechanistically, available data support a multifactorial model involving innate immune activation, immune-complex formation, molecular mimicry, and persistence of viral material within non-permissive tissues, although their relative contributions remain incompletely defined. We propose a structured, pragmatic framework integrating clinical pattern recognition, epidemiological context, disciplined interpretation of serology/polymerase chain reaction, and short-term reassessment to assist in distinguishing parvovirus B19 arthropathy from evolving autoimmune inflammatory arthritis.
