Vaccine-induced autoimmunity: the role of molecular mimicry and immune crossreaction

Abstract

Since the early 1800s vaccines have saved numerous lives by preventing lethal infections. However, during the past two decades, there has been growing awareness of possible adverse events associated with vaccinations, cultivating heated debates and leading to significant fluctuations in vaccination rates. It is therefore pertinent for the scientific community to seriously address public concern of adverse effects of vaccines to regain public trust in these important medical interventions. Such adverse reactions to vaccines may be viewed as a result of the interaction between susceptibility of the vaccinated subject and various vaccine components. Among the implicated mechanisms for these reactions is molecular mimicry. Molecular mimicry refers to a significant similarity between certain pathogenic elements contained in the vaccine and specific human proteins. This similarity may lead to immune crossreactivity, wherein the reaction of the immune system towards the pathogenic antigens may harm the similar human proteins, essentially causing autoimmune disease. In this review, we address the concept of molecular mimicry and its application in explaining post vaccination autoimmune phenomena. We further review the principal examples of the influenza, hepatitis B, and human papilloma virus vaccines, all suspected to induce autoimmunity via molecular mimicry. Finally, we refer to possible implications on the potential future development of better, safer vaccines.

Immunizations with Enterotoxigenic Escherichia coli Heat-Stable Toxin Conjugates Engender Toxin-Neutralizing Antibodies in Mice That Also Cross-React with Guanylin and Uroguanylin

“…There is evidence suggesting that exposure to certain virulence factors, either through natural infections or through vaccination, may induce autoimmune diseases. In some of these cases, autoimmunity is suspected to result from molecular mimicry in which antigens of the pathogen resemble host epitopes (31)(32)(33). Thus, avoiding potentially detrimental cross-reactive responses is a high priority when developing new vaccines (32)(33)(34)(35).…”

Inter-Pathogen Peptide Sharing and the Original Antigenic Sin: Solving a Paradox

“…Infections are risk factors for a large spectrum of autoimmune disorders [1 -15]. Likewise, active immunization may also cause collateral autoimmune events [16] and, in addition, result in the production of a waning/weak immunity [17 -24]. The issue is of crucial importance, especially when considering the necessity of reinforcing the immune defence of the human population from the intensifying assault of old and new microbial threats [25 -27].…”

Molecular mimicry, genetic homology, and gene sharing proteomic “molecular fingerprints” using an EBV (Epstein-Barr virus)-derived microarray as a potential diagnostic method in autoimmune disease

“…Other authors have also recently noted significant overlap between proteins in the human immune response expressed by papilloma virus, another DNA virus correlated with SLE and other human autoimmune syndromes [47][48][49][50][51]. Thus, it seems that Bgene sharing^between host immune response genes is not limited to transcription factors and virokines but may include all aspects of the host immune response.…”

“…4). If further studies confirm that virokines such as the BCL-2-encoded EBV protein are poorly antigenic due to the extensive sharing of epitopes with host cytokines, then the host would be vulnerable to the partial agonist and partial antagonist properties of the EBV-encoded proteins such as BCRF-1 acting on the IL-10 receptor, and this could suggest a paradigm for the pathogenic effects of other shared genes [47][48][49][50][51]. In addition, current studies that characterize levels of IL-10 in autoimmune syndromes may in fact be measuring a combination of viral-encoded virokines and host cytokines.…”