Day 643: More Original Antigenic Sin

There's a rather odd paper in Clinical Immunology Communications about original antigenic sin, antibody dependent enhancement, and back boosting. While it's a great description of those mechanisms and their history in other coronaviruses, it provides no data or citations about their role in COVID-19, only theoretical possibilities. So it's particularly jarring that they conclude on the basis of nothing at all that OAS and ADE have played no role in undermining the success of the vaccines:

Conclusions and perspectives

From the data thus far, there are no indications that the current SARS-CoV-2 vaccines lead to ADE or that the effectivity would be impaired because of the OAS. Yet, sometimes (social) media reports hint towards a higher risk of SARS-CoV-2 infection following vaccination. Furthermore, the concepts of OAS and ADE should be kept in mind when vaccines against novel SARS-CoV-2 variants are developed and tested, and the same would hold true for pan-coronavirus vaccines.

It should be realized that the effects of OAS not necessarily are negative, under some circumstances it can be beneficial because it can offer protection against antigenically related virus strains. Especially the back boosting aspect of OAS can have a relative protective effect when novel virus variants emerge, such as has been shown for influenza.

Speaking of side-effects, there's also a paper out about myocarditis in recently-vaccinated adolescent males who had received an mRNA-based vaccine and had not had a prior case of COVID:

Of 52 patients who underwent cardiac MRI during the study period, 5 underwent MRI for suspected myocarditis after recent COVID-19 mRNA vaccination without known prior COVID-19. These 5 patients were all males with age ranging from 16 to 19 years (mean, 17.2±1.0 years) who presented within 4 days of the second dose of COVID-19 mRNA vaccine. Troponin levels were elevated in all patients (mean peak troponin I, 6.8±4.1 ng/mL). Alternate possible causes of myocarditis were deemed clinically unlikely based on medical history, physical examination, myocarditis viral panel, and toxicology screen. Cardiac MRI findings were consistent with myocarditis in all 5 patients based on Lake Louise criteria, including early gadolinium enhancement (EGE) and late gadolinium enhancement (LGE) in all patients and corresponding myocardial edema in 4 patients. All 5 patients had a favorable hospital course and were discharged in stable condition with improved or resolved symptoms after mean hospitalization length of 4.8 days. Two patients underwent repeat cardiac MRI that showed persistent, though decreased, LGE. Three patients reported mild intermittent self-resolving chest pain after discharge; 2 patients had no recurrent symptoms after discharge.

That's practically the entire paper, but there's some interesting speculation on Reddit about what the mechanism might be.

Massachusetts cases were up a sixth of a percentage point yesterday, and [p.s.] a fifth today.