Upon entry of SARS-CoV-2 into the respiratory tract, an orchestrated network between the airway epithelial cells, the alveolar macrophages, the innate lymphocytes, neutrophils and dendritic cells, the toll-like receptors (TLRs) 3, 7, 8; and the pathogen-associated molecular patterns (PAMPs) by the pattern recognition receptors (PRRs) occurs to create an anti-viral state along the lungs. However, the viral infection otherwise results in the increased leukocytes and the pro-inflammatory cytokines (i.e., the cytokine storm) like the interleukin 1-β (IL1-β), the interleukin-1 receptor antagonist (IL-1RA), IL-2, IL7 to IL-10, granulocyte colony stimulating factor (G-CSF), interferon-γ (IFN-γ) inducer protein (IP10), monocyte chemotactic protein-1 (MCP1), the macrophage inflammatory protein-1α (MIP-1α), MIP1β, tumor necrosis factor (TNFα), basic fibroblast growth factor-2 (FGF-2), granulocyte colony stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GMCSF), platelet derived growth factor (PDGFB), and vascular endothelial growth factor A (VEGFA). Therefore, blocking the signal pathways of human cells required for the SARS-CoV-2 replication may impart an anti-viral effect.