![]() ![]() On the other hand, in vitro evidence suggests that spike protein could impair pericyte and endothelial cell function via ACE2 and thus contribute to myocarditis. What the researchers did was create a pseudovirus a protein shell with spike proteins but no viral RNA inside. This is what carries instructions for making the spike protein that lets the virus enter human cells. As myocarditis has also been observed in response to other vaccines, such as vaccines against influenza and smallpox, and non-mRNA vaccines against COVID-19, the circulating spike protein could be a biomarker of immune dysregulation leading to myocarditis, rather than a causal agent of this. The new study, however, is the first to directly show that the spike proteins themselves are able to cause harm, and also confirms that COVID-19 is primarily a vascular disease that damages blood vessel walls. ![]() It remains unclear if spike protein has a direct role in the pathogenesis of myocarditis furthermore, it was detected in the majority of but not all patients with myocarditis. The most compelling difference in adolescents who developed post-vaccine myocarditis compared with the asymptomatic cohort was the presence of a surprisingly high level of full-length unbound spike protein that remained detectable for up to 3 weeks after vaccination and somehow eluded antibody recognition despite the lack of significant differences between the two groups in antibody production and neutralization capacity. ChulaCov19 is a prefusion non-stabilized SARS-CoV-2 spike-protein-encoding, nucleoside-modified mRNA, lipid nanoparticle encapsulated vaccine that we report to be stable when stored at 28 ☌. They found that antibody-bound S1 protein could be detected in about 30% of the two cohorts of vaccinated adolescents but in none of the analyzed adults from a separate cohort ( n = 13 >18 years of age) after the second vaccine dose this suggested an age difference in the processing and clearance of the spike protein translated from the mRNA vaccine, which will need to be confirmed with further investigation of a larger number of participants. To identify the potential stimuli for this innate inflammation, the authors used ultra-sensitive single-molecule array antigen assays to detect the levels of spike protein and cleaved spike protein (S1) in free form or bound to antibodies. However, the participants with post-vaccine myocarditis presented a cytokine profile indicative of innate immune cell activation, an increase in neutrophils, and a decrease in platelets compared with the profile of the asymptomatic cohort. The authors found no difference in the antibody responses (antibody serotypes and function) of the two cohorts or significant differences in T cell responses. ![]() The participants included in the study were mostly male (80% of the myocarditis cohort 40% of the control cohort) and mostly between 12 and 21 years of age, and most of the patients developed myocarditis within a week after the second vaccine dose. presented the results of extensive immune profiling of 16 patients hospitalized for myocarditis after mRNA vaccination against COVID-19, compared with that of 45 healthy, asymptomatic, age-matched control participants, at 3 weeks after the second vaccination dose. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |