Autoimmune thyroid disease (AITD) is characterized by an autoimmune response to thyroid antigens. It requires a specific genetic background and is triggered by the exposure to environmental factors [1]. Hashimoto’s thyroiditis (HT) and Graves’ disease (GD) are the more common types of AITD: HT is usually associated to serum autoantibodies to thyroid peroxidase (TPO-Ab) and to thyroglobulin (Tg-Ab) and is characterized by thyroid damage that can lead to hypothyroidism, whereas hyperthyroidism of GD is due to autoantibodies that stimulates the thyrotropin receptor (TSH-R-Ab) [1], [2]. These disorders are common worldwide, and their incidence is increasing. The prevalence of HT is 10-12% in the general population, the highest of all autoimmune diseases, whereas that of GD is estimated to be 1-2.5% [2], [3], [4]. As in other autoimmune disorders, AITD is more common in females [3], [4]. The breakdown of self-tolerance to thyroid antigens (TPO, Tg, and the TSH-R) is the main driver of thyroid autoimmunity [5]. Immunogenicity of autoantigens is linked to some specific characteristics, namely genetic polymorphism, a higher numbers of peptides available for binding to major histocompatibility complex (MHC) on antigens presenting cells (APC), and a high level of glycosylation, which favors antigen binding to mannose receptors localized on cell surface on APC [5**], [6]. Because these characteristics are more marked in Tg, its immunogenicity is higher compared to TPO and the TSH-R [6], [7]. The influence of genes and environment is different in HT and GD. Their relevance of genetic factors can be quantified using the sibling risk ratio, which is the ratio of the risk of developing AITD in siblings of patients with AITD compared to the prevalence of AITD in the general population [8], [9]. This ratio is 17 for GD and 28.0 for HT [9]. Since family members share environmental and genetic factors, studies have focused on twins, leading to a more clear definition of the influence of genetic background and environment on the risk of developing AITD [8]. Some twin studies have demonstrated that the genetic background contributes for more than 75% to the risk of developing GD and HT [9]. Thus, the contribution of environmental factors to the onset of AITD accounts for the remaining 20% [7]. Iodine intake, cigarette smoking, stress and infections among other environmental factors have been reported to be associated with the development of AITD [7], [10], [11]. Some studies have shown that infectious disease may trigger autoimmune disorders, including AITD [12].

Starting from December 2019, SARS-CoV-2 infection has spread worldwide, infecting millions of people [13]. Early during the pandemic, it was observed that the thyroid can be involved during the SARS-CoV-2 infection, in the form of subacute thyroid in patients with mild COVID-19 infection and of painless, destructive thyroiditis in hospitalized subjects with a severe infection [14**], [15], [16*]. In addition, some cases of AITD, both GD and HT, have been reported in association with SARS-CoV-2 infection. In this review, we focus on the relationship between SARS-CoV-2 infection and occurrence of AITD.