Molecular Insights into the MAPK Cascade during Viral Infection: Potential Crosstalk between HCQ and HCQ Analogues

Figure 3

Immunomodulation by Sars-CoV-2 infection and potential inhibitors. In COVID-19 patients, as elegantly reviewed in [45, 46, 48], SARS-Cov-2 infection causes a highly generalized proinflammatory state, the so-called “cytokine storm” by activated macrophages that produce proinflammatory cytokines, such as IL-6, IL-2, IL-10, and TNF-alpha, with a reduction in IFN-gamma production by CD4+ T cells. In parallel, a higher neutrophil count, a lower number of lymphocytes, and lymphopenia are observed. HCQ/CQ have been shown to downregulate cytokine production in different diseases [49], acting on the MAPK cascade in human epithelial cells upon coronavirus infection [54], thus contributing to impair the cytokine storm.