From Anti-EBV Immune Responses to the EBV Diseasome via Cross-reactivity

Kanduc, Darja; Shoenfeld, Yehuda

doi:10.1055/s-0040-1715641

Cited by 13 publications

(17 citation statements)

References 179 publications

(236 reference statements)

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“…Molecular mimicry and epitope spreading are classical, well-documented mechanisms of autoimmunity induction, as confirmed in a recent study which showed massive peptide sharing between EBV epitopes and human proteins [ 15 ].…”

Section: General Mechanisms Of Virus-induced Autoimmunitymentioning

confidence: 90%

“…Molecular mimicry Viral antigens with structural similarity with self-antigens can be presented to and activate autoreactive T-lymphocytes. [8,9,[14][15][16][17][18] Epitope-spreading Over time, persistent viral infection elicits autoantibodies directed not only towards initial antigens but also multiple epitopes of the same antigens or even different antigens, increasing breadth of immune response.…”

Section: Mechanism Description Referencesmentioning

confidence: 99%

“…In general, viral infections can interact with the host immune system through several mechanisms which ultimately lead to the loss of tolerance, the production of autoantibodies, the tissue deposition of immune complexes and consequent tissue damage. These are: structural or functional molecular mimicry, epitope spreading, superantigen production, bystander activation, altered apoptosis and clearance deficit, epigenetic factors, persistent or recurrent viral infection, and innate immunity activation with type I IFN production [ 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 ].…”

Section: General Mechanisms Of Virus-induced Autoimmunitymentioning

confidence: 99%

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Viral Infections and Systemic Lupus Erythematosus: New Players in an Old Story

Quaglia

Merlotti

Andrea

et al. 2021

Viruses

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A causal link between viral infections and autoimmunity has been studied for a long time and the role of some viruses in the induction or exacerbation of systemic lupus erythematosus (SLE) in genetically predisposed patients has been proved. The strength of the association between different viral agents and SLE is variable. Epstein–Barr virus (EBV), parvovirus B19 (B19V), and human endogenous retroviruses (HERVs) are involved in SLE pathogenesis, whereas other viruses such as Cytomegalovirus (CMV) probably play a less prominent role. However, the mechanisms of viral–host interactions and the impact of viruses on disease course have yet to be elucidated. In addition to classical mechanisms of viral-triggered autoimmunity, such as molecular mimicry and epitope spreading, there has been a growing appreciation of the role of direct activation of innate response by viral nucleic acids and epigenetic modulation of interferon-related immune response. The latter is especially important for HERVs, which may represent the molecular link between environmental triggers and critical immune genes. Virus-specific proteins modulating interaction with the host immune system have been characterized especially for Epstein–Barr virus and explain immune evasion, persistent infection and self-reactive B-cell “immortalization”. Knowledge has also been expanding on key viral proteins of B19-V and CMV and their possible association with specific phenotypes such as antiphospholipid syndrome. This progress may pave the way to new therapeutic perspectives, including the use of known or new antiviral drugs, postviral immune response modulation and innate immunity inhibition. We herein describe the state-of-the-art knowledge on the role of viral infections in SLE, with a focus on their mechanisms of action and potential therapeutic targets.

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Section: General Mechanisms Of Virus-induced Autoimmunitymentioning

confidence: 90%

Section: Mechanism Description Referencesmentioning

confidence: 99%

Section: General Mechanisms Of Virus-induced Autoimmunitymentioning

confidence: 99%

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Viral Infections and Systemic Lupus Erythematosus: New Players in an Old Story

Quaglia

Merlotti

Andrea

et al. 2021

Viruses

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“…Likewise, vaccine-induced autoimmunity from autoimmune cross-reactivity is associated with several pathologies including Guillain-Barré syndrome, multiple sclerosis, demyelinating neuropathies, systemic lupus erythematosus, narcolepsy, or postural orthostatic tachycardia syndrome in susceptible subgroups [ 51 ]. Therefore, one of the side effects of introducing a mass vaccination program could be an emergence of autoimmune diseases especially in individuals who are genetically prone for autoimmunity [ 52 , 53 , 54 ]. The composition of SARS-CoV-2 proteins and validation of similarities with human proteins are critical to predict an autoimmune response associated with immunity against host proteins and its clinical manifestations as well as potential adverse effects of vaccination [ 55 ].…”

Section: Raised Concerns Of Current Sars-cov-2 Vaccinesmentioning

confidence: 99%

Does COVID-19 Vaccination Warrant the Classical Principle “ofelein i mi vlaptin”?

et al. 2021

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The current severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic warrants an imperative necessity for effective and safe vaccination, to restrain Coronavirus disease 2019 (COVID-19) including transmissibility, morbidity, and mortality. In this regard, intensive medical and biological research leading to the development of an arsenal of vaccines, albeit incomplete preconditioned evaluation, due to emergency. The subsequent scientific gap raises some concerns in the medical community and the general public. More specifically, the accelerated vaccine development downgraded the value of necessary pre-clinical studies to elicit medium- and long-term beneficial or harmful consequences. Previous experience and pathophysiological background of coronaviruses’ infections and vaccine technologies, combined with the global vaccines’ application, underlined the obligation of a cautious and qualitative approach, to illuminate potential vaccination-related adverse events. Moreover, the high SARS-CoV-2 mutation potential and the already aggregated genetical alterations provoke a rational vagueness and uncertainty concerning vaccines’ efficacy against dominant strains and the respective clinical immunity. This review critically summarizes existing evidence and queries regarding SARS-CoV-2 vaccines, to motivate scientists’ and clinicians’ interest for an optimal, individualized, and holistic management of this unprecedented pandemic.

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“…[1][2][3][4][5][6][7][8][9][10][11] Pathologically, cross-reactions between pathogen and human proteins might lead to thrombocytopenia, altered spermatogenesis, schizophrenia and neuropsychiatric diseases, neurodegeneration, lymphomas, sudden death, microcephaly and Guillain-Barré syndrome, pneumonia, multiple sclerosis, immunodeficiency, developmental disorders, autoinflammatory disease, arthritis, hemochromatosis, myasthenia gravis, and systemic lupus erythematosus. 4,8,[12][13][14][15][16][17][18][19][20][21][22][23][24][25][26] As a matter of fact, pathogen-derived immunoreactive epitopes are mostly composed of peptide sequences present in human proteins, 10,18,21,23,26 thus documenting that the immune system does not exert any negative selection of selfreactive lymphocytes. 27,28 Hence, it comes as a logical consequence that peptide sharing between infectious antigens and human proteins can cause cross-reactions in the human host, possibly leading to a multitude of postinfection autoimmune pathologies.…”

Section: Introductionmentioning

confidence: 99%

Lack of Molecular Mimicry between Nonhuman Primates and Infectious Pathogens: The Possible Genetic Bases

Kanduc

2021

Global Medical Genetics

Self Cite

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Recently, it was found that proteomes from poliovirus, measles virus, dengue virus, and severe acute respiratory syndrome-related Coronavirus 2 (SARS-CoV-2) have high molecular mimicry at the heptapeptide level with the human proteome, while heptapeptide commonality is minimal or absent with proteomes from nonhuman primates, that is, gorilla, chimpanzee, and rhesus macaque. To acquire more data on the issue, analyses here have been expanded to Ebola virus, Francisella tularensis, human immunodeficiency virus-1 (HIV-1), Toxoplasma gondii, Variola virus, and Yersinia pestis. Results confirm that heptapeptide overlap is high between pathogens and Homo sapiens, but not between pathogens and primates. Data are discussed in light of the possible genetic bases that differently model primate phenomes, thus possibly underlying the zero/low level of molecular mimicry between infectious agents and primates. Notably, this study might help address preclinical vaccine tests that currently utilize primates as animal models, since autoimmune cross-reactions and the consequent adverse events cannot occur in absentia of shared sequences.

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From Anti-EBV Immune Responses to the EBV Diseasome via Cross-reactivity

Cited by 13 publications

References 179 publications

Viral Infections and Systemic Lupus Erythematosus: New Players in an Old Story

Viral Infections and Systemic Lupus Erythematosus: New Players in an Old Story

Does COVID-19 Vaccination Warrant the Classical Principle “ofelein i mi vlaptin”?

Lack of Molecular Mimicry between Nonhuman Primates and Infectious Pathogens: The Possible Genetic Bases

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