Affiliation:
1. Seoul National University College of Medicine
2. University of Ottawa
3. IIAIGC Study Center
4. Haider Associates
5. Metropolitan Hospital New York
6. McGill University Health Centre
7. Ewha Womans University
8. KyungHee University College of Life Science
9. Chosun University
10. Aston University
Abstract
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces immune-mediated diseases. Interactions between the host and virus govern induction, resulting in multiorgan impacts. In 2021, as normal life was challenging during the pandemic era, we analyzed SCI journals according to L. Wittgenstein's Tractatus Logi-co-Philosophicus. The pathophysiology of coronavirus disease 2019 (COVID-19) involves the following steps: 1) the angiotensin-converting enzyme (ACE2) and Toll-like receptor (TLR) pathways: 2) the neuropilin (NRP) pathway, with seven papers and continuing with twenty-four: 3) the sterile alpha motif (SAM) and histidine-aspartate domain (HD)-containing protein 1 (SAMHD1) tetramerization pathway, with two papers and continuing with twelve: 4) inflammasome activation pathways, with five papers and continuing with thirteen: 5) the cytosolic DNA sensor cyclic-GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) (cGAS–STING) signaling pathway, with six papers and successful with eleven: 6) the spike protein pathway, with fourteen and continuing with twenty-three: 7) the immunological memory engram pathway, with thirteen papers and successive with eighteen: 8) the excess acetylcholine pathway, with three papers and successful with nine. We reconfirmed that COVID-19 involves seven (1-7) pathways and a new pathway involving excess acetylcholine. Therefore, it is necessary to therapeutically alleviate and block the pathological course harmoniously with modulating innate lymphoid cells (ILCs) if diverse SARS-CoV-2 variants are subsequently encountered in the future.
Publisher
Research Square Platform LLC