How does SARS-CoV-2 cause lymphopenia when T cells barely express ACE-2 receptors?

In a recent review published in the journal Cell Communication and Signaling , a team of researchers in Egypt and the United States explored the direct and indirect mechanisms of T lymphocyte-linked adaptive anti-viral immune responses that might contribute to lymphopenia associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections. Schematic representation of possible mechanisms of lymphopenia in SARS-CoV-2 viral infection. Study: SARS-CoV-2-associated lymphopenia: possible mechanisms and the role of CD147 Although the spread and severity of the coronavirus disease 2019 (COVID-19) pandemic have been contained after worldwide vaccination efforts, SARS-CoV-2 continues to evolve due to accumulating mutations in its ribonucleic acid (RNA).

While some of these mutations have led to lower virulence and transmissibility, others have also helped the virus evade vaccine-induced immunity. The major immunopathological characteristics observed when SARS-CoV-2 triggers host immunity are low adaptive immune responses and uncontrolled inflammatory responses, including cytokine storms and abnormal interferon production. Of particular concern is the decrease in lymphocytes observed in patients with severe COVID-19.

The invasion of a cell by SARS-CoV-2 occurs when the spike protein binds to the angiotensin-converting enzyme-2 (ACE-2) receptor on the cell surface. Given that T helper cells (CD4 + ) and cytotoxic T cells (CD8 + ) do not express many ACE-2 receptors on.