CD4 and COVID-19: With less and less protozoal diseases in high-resource countries, an evolving disbalance between Th1 and Th2-pathways may occur and, together with other regulatory CD4+ T cell populations, might have an influence on the host immune response to SARS-CoV-2 and the subsequent organ and tissue damage caused by a hyperinflammatory state, characterized by a cytokine storm in the late phase of COVID-19 [36].