Received April 19, 2022; Revised May 17, 2022; Accepted May 17, 2022
Despite numerous data on the absence or weak expression of the main functional receptor of SARS-CoV-2 angiotensin-converting enzyme 2 (ACE2) by T cells, it was recently demonstrated that the new coronavirus can efficiently infect T lymphocytes. Here, we analyze the data on the alternative (ACE2-independent) pathways of cell infection, identified T cell subpopulations that serve as the most plausible targets of SARS-CoV-2, discuss the mechanisms of virus–cell interaction, including both infectious and non-infectious pathways of T lymphocyte regulation, and estimate the role of the virus-dependent damage of T lymphocytes in COVID-19 pathogenesis. Particular attention is paid to regulatory T cells as potential targets of SARS-CoV-2, as well as to the possible involvement of exosomes in the sensitivity of peripheral T cells to the virus.
KEY WORDS: SARS-CoV-2, T lymphocytes, ACE2, CD147, TregDOI: 10.1134/S0006297922060086