Chemokines and chemokine receptors during COVID-19 infection

Abstract

Graphical abstract

Innate Receptor Activation Patterns Involving TLR and NLR Synergisms in COVID-19, ALI/ARDS and Sepsis Cytokine Storms: A Review and Model Making Novel Predictions and Therapeutic Suggestions

“…It does not appear that either of these approaches has been systematically investigated in COVID-19, ALI-ARDS or sepsis, and even the use of melatonin in COVID-19 was initiated in apparent ignorance of its multiple TLR/NLR-moderating effects. Since many individual TLR and NLR antagonists are being investigated, and some are in clinical trials, (reviewed in [267]), such multipronged therapies are quite feasible.…”

“…As noted in several places above (most notably in the Introduction and Section 2.8), interferon release is severely impaired in COVID-19, which facilitates SARS-CoV-2 infectivity and replication. A number of groups have therefore suggested, correctly in light of the IRAP model, that patients with severe COVID-19 need interferon supplementation [267][268][269][270][271][272], a therapeutic approach that would very likely be harmful in other cytokine release syndromes in which interferon is overproduced. An alternative suggested by the IRAP model might be to stimulate a natural interferon release using RIG1, NOD1 and, perhaps, TLR3 agonists (Figure 12).…”

The Link between Electrical Properties of COVID-19 and Electromagnetic Radiation

“…Step V. Activation and the disorganized immune response: Besides modifying cellular processes to support COVID-19 propagation, the stress responses to apoptosis triggered by an electrical and an electromagnetic radiation events activity may have deleterious consequences for the host cell leads to inflammatory in response to virus such as the cytokines, chemokines in plasma, and chemokine-receptor, and interfere with several receptors signaling pathway [6]. Because the COVID-19 seems is an electrically excitable virus has a structure that permits virus to pass chemical signal or an electrical signal to another virus or to the host cell that actively responds to effects some change brings it about and a stimulus such as B cell, T cells, Cytokine, chemokine, chemokine receptor, cytokines, and mast cell that (involved in the development of asthma or allergic rhinitis).…”

“…As known COVID-19 is adept at evasion host immune responses [4] and interfere with several receptor signaling pathways such as chemokine receptors to produce an active inflammatory response [5,6]. Our previous work has shown the electrical properties of COVID-19 [7].…”

Involvement of Interleukin-1 Receptor-Associated Kinase 4 and Interferon Regulatory Factor 5 in the Immunopathogenesis of SARS-CoV-2 Infection: Implications for the Treatment of COVID-19

“…Effective treatments are required for COVID-19 hyperinflammatory syndrome, occurring characteristically 7-14 days after first symptoms (1) and variously described as "macrophage activation syndrome" (2), "cytokine storm" (3) or "acute respiratory distress syndrome" (4). Its immunological hallmarks are excessive elevation of predominantly proinflammatory cytokines, chemokines (5), and other bioactive molecules, such as HMGB1 (6) and reactive oxygen species (7). Upregulated cytokines include IL-6, TNF-α, IFN-γ, IL-1β, IL-15, IL-23, and IL-10, and chemokines, CXCL8(IL-8), CXCL9(MIG), CXCL10(IP10), CCL2(MCP-1), CCL3(MIP-1α), CCL5(RANTES), CCL7(MCP-3), CCL8(MCP-2), CCL11(eotaxin-1), and CCL20(MIP-3α) (1,2,(8)(9)(10)(11).…”