Crosstalk among strenuous exercise, IL-6 and S-Protein Based Vaccines for COVID-19 may explain the rare adverse effects of myocarditis and thrombosis in recently vaccinated young people. A prospective observational study.

Abstract

Interleukin 6 (IL-6) is a type of interleukin that functions as both a pro-inflammatory and anti-inflammatory cytokine. It is encoded by the IL6 gene in humans. Both COVID-19 infection and S-Protein Based Vaccines for COVID-19 were found to induce the production of proinflammatory IL-6, and also, strenuous exercise was found to induce IL-6 secretion by the skeletal muscles via lactate. Exercise causes skeletal muscle cells to release IL-6, and it raises the plasma concentration of IL-6 100 times higher than at rest . Exercise-induced IL-6 release is highly correlated with exercise intensity and duration; thus, IL-6 is regarded as an energy sensor released by contracting muscles. but It was found that rare adverse effects such as myocardial infarction and coagulation abnormalities , are rarely associated with S-Protein Based Vaccines for COVID-19. Recently, it was showed in a study that most patients who experienced myocarditis after COVID-19 vaccine were young male youth aged 16 to 29 years had the highest incidence of myocarditis. Interestingly, It was observed that IL-6 was linked to adverse effects such as thrombosis and myocarditis, both of which are similar to that was caused by COVID-19 infection, and that S-Protein Based Vaccines for COVID-19. Here, we propose a testable hypothesis that strenuous exercise could be a risk and cofactor helping in the existing of these adverse effects in young people such as myocarditis and thrombosis via induction the secretion of proinflammatory IL-6. In our prospective observational study we will assess the possible correlation among the strenuous exercise , IL-6, myocarditis and thrombosis. The study will be multi-center and will involve young patient who will be vaccinated with first ,second and third dose of S-Protein Based Vaccines for COVID-19 (Moderna and Pfizer-BioNTech vaccine). Pfizer and BioNTech have successfully developed the BNT162b2 mRNA vaccine, which consists of the full-length S glycoprotein with the K986P and V987P mutation sites. Also, Moderna's mRNA-1273 vaccine contains the coding sequence for a S glycoprotein stabilized by a pair of proline substitutions (K986P/V987P), a transmembrane anchor, and an intact S1-S2 cleavage site

Incidence, risk factors, natural history, and hypothesised mechanisms of myocarditis and pericarditis following covid-19 vaccination: living evidence syntheses and review

“…Findings from 12 studies from the original review 15 were carried forward (Q1=5, 25 26 27 28 29 Q2=2, 29 30 Q3 part 2=10 25 26 27 28 31 32 33 34 35 36 ). From the search update, we identified 34 new reports across all questions (Q1=9, 37 38 39 40 41 42 43 44 45 Q2=5, 37 41 45 46 47 Q3 part 1=1, 48 Q4=3, 39 49 50 Q5=21 9 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 ). We excluded five studies that only reported on combined myocarditis and pericarditis (as we located studies reporting these separately), 71 72 73 74 75 eight studies that did not report on confirmed cases, 76 77 78 79 80 81 82 83 and three studies 84 85 <...…”

“…We included 21 papers, 9 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 including narrative reviews, opinion pieces, letters to the editor, case reports, case series, a retrospective study, and a protocol for a prospective observational study. Across the included papers, we identified 16 hypotheses that are presented in table 4 .…”

Myopericarditis in a Male Adolescent Following the Second Shot of COVID-19 Pfizer m-RNA Vaccine: Typical Example and Analysis of 110 Single Case Reports

“…Several mechanisms have been suggested, but none is convincing on its own. The many suggested mechanisms include: hyper immune or inflammatory reaction after exposure to spike protein, mRNA strand, or unexplained trigger; late onset of hypersensitivity (serum sickness); eosinophilic myocarditis; hyperreactivity to vaccine excipients (e.g., polyethylene glycol and tromethamine or lipid nanoparticle sheath); reaction to mRNA vaccine lipid nanomolecules; self-immunity through mimicry or other pathways; low residual quantity of double strand RNA; unbalanced micro-RNA reaction; release of anti-idiotype antibodies against certain regions of antigen-specific antibodies; activation of pre-existent dysregulated immune pathways in predisposed subjects (leading to polyclonal B cell growth, immune complex development, and inflammation); antibody-dependent amplification of immunity or other forms of immune intensification with re-exposure to the virus after vaccine inoculation; direct cell invasion through the interplay of the spike protein and the angiotensin converting enzyme 2 (ACE2) widely expressed on cardiomyocytes surfaces; cardiac pericyte expression of ACE2 with disabled immune complex on the surface of pericytes along with activation of the complement system; hyperviscosity-induced cardiac problem; and demanding effort induced secretion of proinflammatory interleukin 6 [ 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 ]. A combination of some of these immune-mediated mechanisms is likely involved in m-RNA vaccine-induced myocarditis and pericarditis, of which the first manifestation can be fatal.…”