Clinical implications of human Parvovirus B19 infection on autoimmunity and autoimmune diseases

Parvovirus B19 (B19V) is a human pathogen from the Parvoviridae family that primarily targets and replicates in erythroid progenitor cells (EPCs). While its symptoms are typically self-limiting in healthy individuals, B19V can cause or exacerbate autoimmune diseases in vulnerable patients. This review integrates the involvement of B19V in the development and worsening of several autoimmune diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), hematological disorders (thalassemia, anemia, and thrombocytopenia), vasculitis, antiphospholipid syndrome (APS), dermatological disease (systemic sclerosis, psoriasis), autoimmune thyroid disease, myocarditis, and myasthenia gravis, and autoinflammatory disease of adult-onset Still’s disease (AOSD). B19V contributes to autoimmunity and autoimmune disease onset and progression through mechanisms such as molecular mimicry, immune system disruption, and chronic infection. By summarizing findings from in vitro experiments, clinical case studies, seroprevalence data, and biopsy results, this review highlights the critical connection between B19V and autoimmune disease development. Recognizing the role of B19V in the early diagnosis and management of these conditions is essential, as its presence may influence the disease course and severity. Greater awareness among healthcare professionals and the public is necessary to address the impact of B19V, leading to more accurate diagnoses and better-informed treatment approaches for autoimmune diseases linked to the virus.