Unveiling the Link Between Spike Protein Mimicry and CIDP: The Role of Neurofascin

🧠 Spike Protein Mimicry and Neurofascin: Unveiling the Link to CIDP

Introduction

In recent discussions surrounding COVID-19 vaccines, concerns have been raised about potential neurological side effects. One such concern is the development of Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), a rare autoimmune disorder affecting the peripheral nervous system. Emerging research suggests that molecular mimicry between the spike protein of SARS-CoV-2 and human neural proteins, particularly neurofascin, may play a role in triggering CIDP.

Understanding Neurofascin

Neurofascin is a cell adhesion molecule expressed in neurons, playing a crucial role in the formation and maintenance of the nodes of Ranvier—the gaps between myelin sheaths that facilitate rapid nerve impulse conduction. There are two isoforms:

• Neurofascin-155 (NF155): Predominantly expressed in oligodendrocytes, forming the paranodal junctions in the central nervous system.

• Neurofascin-186 (NF186): Found in neurons, contributing to the juxtaparanodal regions.

These regions are essential for proper nerve function, and disruption can lead to demyelination and neurological deficits.

Molecular Mimicry: Spike Protein and Neurofascin

Molecular mimicry occurs when a foreign antigen shares structural similarities with host proteins, leading the immune system to mistakenly attack its own tissues. Studies have identified short peptide sequences in the SARS-CoV-2 spike protein that resemble epitopes found in neurofascin.

This similarity suggests that antibodies generated against the spike protein could cross-react with neurofascin, potentially leading to autoimmune attacks on the nodes of Ranvier.

Clinical Evidence: CIDP Post-Vaccination

While CIDP is a rare condition, several case reports have documented its onset following COVID-19 vaccination:

• Case Report 1: A 67-year-old male developed progressive tingling and paresthesia in both lower extremities seven days after receiving the third dose of the Sinopharm vaccine. Neurological examination revealed limb weakness with areflexia, and nerve conduction studies confirmed demyelinating neuropathy consistent with CIDP. (BioMed Central)

• Case Report 2: A 39-year-old woman developed distal CIDP following the second dose of the Pfizer-BioNTech COVID-19 vaccine. She experienced general weakness and sensory changes, with subsequent nerve conduction studies supporting the diagnosis of CIDP. (ResearchGate)

These cases highlight the potential for vaccine-induced autoimmune responses, possibly through molecular mimicry mechanisms.

Professor Angus Dalgleish’s Warning

Professor Angus Dalgleish, an expert oncologist, virologist, and immunologist, observed that spike protein epitopes have up to 80% similarity to human antigens in the myelin sheath. He warned authorities about the potential neurological risks, particularly the risk of triggering autoimmune attacks on neurofascin in the nodes of Ranvier.

Unfortunately, his warnings were largely ignored, leaving the potential risks under-acknowledged despite emerging case reports of post-vaccine CIDP.

Conclusion

The concept of molecular mimicry between the SARS-CoV-2 spike protein and neurofascin provides a plausible explanation for the rare occurrence of CIDP following COVID-19 vaccination. While these cases are infrequent, they underscore the importance of continued surveillance and research to understand the full spectrum of vaccine-induced adverse effects.

Patients experiencing neurological symptoms post-vaccination should seek prompt medical evaluation to ensure timely diagnosis and management. Meanwhile, the early warnings from experts like Professor Dalgleish highlight the need for greater responsiveness from health authorities when potential autoimmune risks are identified.