The main function of the thyroid gland is the production of the prohormone thyroxine (T4) and the active hormone triiodothyronine (T3). In the human body, T3 controls the basal metabolism, with effects on the central nervous, cardiovascular, respiratory, musculoskeletal, and ultimately, the immune system. On a cellular level, thyroid hormones T3 and T4 are known for their diverse effects on cell function, including the regulation of cell proliferation, tissue regeneration, apoptosis, and angiogenesis COVID-19 infection has a remarkably wide range of manifestations. Besides respiratory, gastrointestinal, and cardiovascular effects, various endocrine complications of SARS-CoV-2 infection have been identified, including thyroid dysfunctions. One of the key features of COVID-19 is inflammation. A term often used to describe this inflammation is the "cytokine storm," which is an excessive immune response by the body involving cytokines, contributing to the more severe pathohistological and clinical features associated with it, such as acute respiratory syndrome (ARS), multiple organ failure and autoimmune diseases. The causative agent of COVID-19 infection, SARS-CoV-2, is characterized by a high frequency of genetic recombination and mutations. Among its proteins, protein S ("spike") plays the main pathophysiological role; by binding to host cell proteins, primarily ACE2, TMPRSS2, and integrin αvβ3, it enables the virus to enter the cell through endocytosis or fusion of the viral envelope with the cell membrane. Thyroid follicular cells significantly express these proteins on their surface, making it one of the main targets of SARS-CoV-2 in the body. As complications of COVID-19 infection, thyrotoxicosis, hypothyroidism, destructive and subacute thyroiditis, de novo Graves' disease, atypical thyroiditis, and non-thyroidal illness syndrome (NTIS) have been described. Thyroid dysfunction has been recorded during SARS-CoV-2 infection or even several weeks after recovery. The effects of the "cytokine storm" can also significantly impact those with pre-existing thyroid dysfunctions, especially older adults, whose immune systems may be less resilient, with a higher risk of thromboembolic complications and mortality. It has been shown that thyroid disorders, primarily hypothyroidism, are associated with a higher risk of poor outcomes, admission to intensive care units, and hospitalization in patients with COVID-19; however, this association is significantly influenced by the age of the patients. If patients were on appropriate therapy, there was no statistically significant difference in the observed outcomes. In contrast, it has been shown that hyperthyroidism does not significantly affect the outcome of COVID-19 infection. Individuals with thyroid diseases can be treated for COVID-19 infection just like healthy individuals, without the risk of additional complications during the treatment process. Low levels of FT3 and the FT3/FT4 ratio are indicators of disease severity, while low levels of FT3 are prognostic markers of COVID-19-related mortality. Thyroid disorders have been documented after the administration of all types of COVID-19 vaccines. The most common cases of thyroid disorders have been reported after mRNA vaccines, followed by viral vector vaccines and cases after inactivated vaccines. Moreover, subacute thyroiditis (SAT) was the most common thyroid disorder associated with COVID-19 vaccination, followed by Graves' disease.