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  • Article
    Information-Theoretic Approach in Allometric Scaling Relations of Dna and Proteins
    (Wiley, 2022) Adiguzel, Yekbun
    Allometric scaling relations can be observed in between molecular parameters. Hence, we looked for presence of such relation among sizes (i.e., lengths) of proteins and genes. Protein lengths exist in the literature as the number of amino acids. They can also be derived from the mRNA lengths. Here, we looked for allometric scaling relation by using such data and simultaneously, the data was compared with the sizes of genes and proteins that were obtained from our modified information-theoretic approach. Results implied presence of scaling relation in the calculated results. This was expected due to the implemented modification in the information-theoretic calculation. Relation in the literature-based data was lacking high goodness of fit value. It could be due to physical factors and selective pressures, which ended up in deviations of the literature-sourced values from those in the model. Genome size is correlated with cell size. Intracellular volume, which is related to the DNA size, would require certain number of proteins, the sizes of which can therefore be correlated with the protein sizes. Cell sizes, genome sizes, and average protein and gene sizes, along with the number of proteins, namely the expression levels of the genes, are the physical factors, and the molecular factors influence those physical factors. The selective pressures on those can act through the connection between those physical factors and limit the dynamic ranges. Biological measures could be prone to such forces and are likely to deviate from expected models, regardless of the validity of assumptions, unless those are also implemented in the models. Yet, present discrepancies could be pointing at the need for model improvement, data imperfection, invalid assumptions, etc. Still, current work highlights possible use of information-theoretic approach in allometric scaling relations' studies.
  • Review
    Citation - WoS: 6
    Citation - Scopus: 6
    Shared Pathogenicity Features and Sequences Between Ebv, Sars-Cov and Hla Class I Molecule-Binding Motifs With a Potential Role in Autoimmunity
    (Humana Press inc, 2023) Adiguzel, Yekbun; Mahroum, Naim; Muller, Sylviane; Blank, Miri; Halpert, Gilad; Shoenfeld, Yehuda
    Epstein-Barr virus (EBV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are extraordinary in their ability to activate autoimmunity as well as to induce diverse autoimmune diseases. Here we reviewed the current knowledge on their relation. Further, we suggested that molecular mimicry could be a possible common mechanism of autoimmunity induction in the susceptible individuals infected with SARS-CoV-2. Molecular mimicry between SARS-CoV-2 and human proteins, and EBV and human proteins, are present. Besides, relation of the pathogenicity associated with both coronavirus diseases and EBV supports the notion. As a proof-of-the-concept, we investigated 8mer sequences with shared 5mers of SARS-CoV-2, EBV, and human proteins, which were predicted as epitopes binding to the same human leukocyte antigen (HLA) supertype representatives. We identified significant number of human peptide sequences with predicted-affinities to the HLA-A*02:01 allele. Rest of the peptide sequences had predicted-affinities to the HLA-A*02:01, HLA-B*40:01, HLA-B*27:05, HLA-A*01:01, and HLA-B*39:01 alleles. Carriers of these serotypes can be under a higher risk of autoimmune response induction upon getting infected, through molecular mimicry-based mechanisms common to SARS-CoV-2 and EBV infections. We additionally reviewed established associations of the identified proteins with the EBV-related pathogenicity and with the autoimmune diseases.
  • Article
    Citation - WoS: 4
    Citation - Scopus: 4
    Molecular/Antigenic Mimicry and Immunological Cross-Reactivity Explains Sars-Cov Autoimmunity
    (Elsevier, 2025) Adiguzel, Yekbun; Bogdanos, Dimitros P.; Shoenfeld, Yehuda
    COVID-19 pandemic is over, but its effects on chronic illnesses remain a challenging issue. Understanding the influence of SARS-COV-2-mediated autoimmunity and overt autoimmune disease is of paramount importance, as it can provide a critical mass of information regarding both infection-mediated (and vaccination-induced) autoimmune phenomena in susceptible individuals during the disease course, and short or long-term post-disease sequelae. The high prevalence of organ and non-organ specific autoantibody positivity in patients with COVID-19 led to studies attempting to delineate the origin and the underlying mechanism responsible for their induction nature, identifying novel autoantigens, and the self-epitope sequences which could be the impetus for the initiating autoreactive responses. Herein, we provide a meticulous review of the studies reporting those mimicking sequences that have been experimentally validated, based on the assumption that molecular mimicry and immunological crossreactivity may account for autoantibody development. Most reports are based on bioinformatics approaches, and only a disproportionally small number of studies currently demonstrate immunological crossreactivity. We took the opportunity to further review and searched for the linear human epitope sequences of human, through the epitopes deposited at the Immune Epitope Database. This included an analysis of autoimmune disease as the disease data to comprehensively understand the subject matter. The critical overview of the findings underscore the urgent and immense need for further research to gain a comprehensive understanding of the mechanisms involved and the anticipated appraisal that molecular mimicry and immunological crossreactivity is indeed central to the loss of immunological tolerance during SARS-COV-2 infection.