Impacts of Viral Infections on Autoimmune Thyroid Diseases: A Narrative Review

Abstract

Autoimmune thyroid diseases (AITDs), primarily Hashimoto’s thyroiditis (HT) and Graves’ disease (GD), represent the most prevalent organ-specific autoimmune disorders worldwide. Their development results from a multifactorial interaction among genetic susceptibility, immune dysregulation, hormonal influences, and environmental triggers. Among environmental factors, viral infections have gained major attention because of their ability to disrupt immune tolerance and initiate autoreactive immune responses against thyroid antigens. This narrative review summarizes current evidence regarding the contribution of viral infections to the pathogenesis and progression of AITDs, with emphasis on immunopathogenic mechanisms, epidemiological associations, and clinical implications. A structured literature search was conducted using PubMed, Scopus, and Google Scholar databases. Priority was given to systematic reviews, meta-analyses, cohort studies, mechanistic investigations, and landmark original articles published in peer-reviewed journals. Evidence indicates that Epstein–Barr virus (EBV) and hepatitis C virus (HCV) demonstrate the strongest associations with thyroid autoimmunity, whereas SARS-CoV-2, cytomegalovirus (CMV), human herpesvirus-6 (HHV-6), enteroviruses, and parvovirus B19 show variable but biologically plausible associations. Proposed mechanisms include molecular mimicry, bystander activation, epitope spreading, aberrant HLA class II expression, polyclonal B-cell activation, apoptosis-mediated release of thyroid antigens, and chronic cytokine-driven inflammation. Viral infections appear to function primarily as environmental triggers in genetically predisposed individuals rather than independent causative agents. In Iraq and other regions with persistent infectious disease burden, understanding virus-associated thyroid autoimmunity may improve early detection and preventive strategies. Further prospective multicenter studies integrating virological, immunological, and genetic analyses are required to establish causality and guide targeted interventions.