This compiled research article from our German partners may shine light on one of the mechanisms behind post-vaccine syndromes … which may in turn point to possible solutions. Read the full PDF here >

Excerpt below:

A certain group of autoantibodies that are frequently found in post covid syndrome patients are autoantibodies against G-protein coupled receptors (GPCR-AABs), they are also called functional autoantibodies (fAABs). In the case of post covid, agonistic AABs are most common, but there are also antagonistic GPCR-AABs. Wallukat et al. examined sera from 31 patients with long covid symptoms, and functional autoantibodies were detected in all samples [1]. They also seem to play a role in the severity of a covid course [2]. Autoantibodies against ACE2, one of the entry ports into human cells for the SARS-Cov-2 virus, are also present in post covid sufferers in 80-90% of all cases [3]. According to our own experience in various support groups, these autoantibodies are also found in many post-vaccine syndrome sufferers (currently, according to our own estimate, a prevalence of 80-90%). A first official case report also suggests that these autoantibodies may also play a role in post-vaccine syndrome sufferers [4]. There are also initial case reports of post-vaccination dysautonomia that may have been triggered by these autoantibodies [5, 6].

Before the covid pandemic, these functional autoantibodies (fAABs) were predominantly known from the field of cardiovascular and neurodegenerative diseases, for example dementia, type 2 diabetes or cardiomyopathy but also rheumatic diseases [7, 8, 9]. In classical autoimmune diseases, the body’s own immune system turns against the body’s own structures through malformed antibodies, resulting in inflammation and organ damage. Functional autoantibodies, on the other hand, act as agonists at the receptor instead of natural ligands and, when bound, activate it in an uncontrolled and long-lasting manner. Thus, they exhibit a wide range of pharmacological properties [10, 11].

GPCRs are important mediators of signal transduction and as such are involved in numerous bodily functions, such as sensory stimulus processing, various metabolic functions, inflammatory processes, and cell growth and differentiation. Therefore, uncontrolled activation can thus lead to an improbably large number of different disorders. A well-known example is the β1-adrenoceptor which plays a major role in regulating cardiac function. People with agonistic autoantibodies to the β1- adrenoceptor may therefore experience a variety of cardiac symptoms, including dilated cardiomyopathy [12].

Other diseases associated with GPCR-AAB include myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), postural tachycardia syndrome (POTS), and chronic pain syndrome/fibromyalgia [9, 13, 14, 15]. These are all clinical pictures that also occur or develop frequently in post-covid patients and post-vaccine patients [5, 6]. Post-vaccine patients are currently anticipated to have a 10- 20% rate of developing full-blown ME/CFS.

Post vaccine syndromes are likely to be severely under-reported because the vaccination campaign is recent, physicians are often reluctant to associate symptoms with vaccination, and clinicians lack diagnostic markers. However, reactions of this type are also known to occur after other vaccinations and, due to the longer elapsed time period, are also found more frequently in the literature ….

Read the full PDF here >