The COVID-19 pandemic is spreading around the world and 187 million people have already been affected. One of its after-effects is post-COVID depression, which, according to the latest data, affects up to 40% of people who have had SARS-CoV-2 infection. A very important issue for the mental health of the general population is to look for the causes of this complication and its biomarkers. This will help in faster diagnosis and effective treatment of the affected patients. In our work, we focused on the search for major depressive disorder (MDD) biomarkers, which are also present in COVID-19 patients and may influence the development of post-COVID depression. For this purpose, we searched PubMed, Scopus and Google Scholar scientific literature databases using keywords such as ‘COVID-19’, ‘SARS-CoV-2’, ‘depression’, ‘post-COVID’, ‘biomarkers’ and others. Among the biomarkers found, the most important that were frequently described are increased levels of interleukin 6 (IL-6), soluble interleukin 6 receptor (sIL-6R), interleukin 1 β (IL-1β), tumor necrosis factor α (TNF-α), interferon gamma (IFN-γ), interleukin 10 (IL-10), interleukin 2 (IL-2), soluble interleukin 2 receptor (sIL-2R), C-reactive protein (CRP), Monocyte Chemoattractant Protein-1 (MCP-1), serum amyloid a (SAA1) and metabolites of the kynurenine pathway, as well as decreased brain derived neurotrophic factor (BDNF) and tryptophan (TRP). The biomarkers identified by us indicate the etiopathogenesis of post-COVID depression analogous to the leading inflammatory hypothesis of MDD.

For 2.5 years we have been facing the coronavirus disease (COVID-19) and its health, social and economic effects. One of its known consequences is the development of neuropsychiatric diseases such as anxiety and depression. However, reports of manic episodes related to COVID-19 have emerged. Mania is an integral part of the debilitating illness—bipolar disorder (BD). Due to its devastating effects, it is therefore important to establish whether SARS-CoV-2 infection is a causative agent of this severe mental disorder. In this narrative review, we discuss the similarities between the disorders caused by SARS-CoV-2 and those found in patients with BD, and we also try to answer the question of whether SARS-CoV-2 infection may be a risk factor for the development of this affective disorder. Our observation shows that disorders in COVID-19 showing the greatest similarity to those in BD are cytokine disorders, tryptophan metabolism, sleep disorders and structural changes in the central nervous system (CNS). These changes, especially intensified in severe infections, may be a trigger for the development of BD in particularly vulnerable people, e.g., with family history, or cause an acute episode in patients with a pre-existing BD.