Abstract
Analyses of the peptide sharing between five common human viruses (Borna disease virus, influenza A virus, measles virus, mumps virus and rubella virus) and the human proteome highlight a massive viral vs. human peptide overlap that is mathematically unexpected. Evolutionarily, the data underscore a strict relationship between viruses and the origin of eukaryotic cells. Indeed, according to the viral eukaryogenesis hypothesis and in light of the endosymbiotic theory, the first eukaryotic cell (our lineage) originated as a consortium consisting of an archaeal ancestor of the eukaryotic cytoplasm, a bacterial ancestor of the mitochondria and a viral ancestor of the nucleus. From a pathologic point of view, the peptide sequence similarity between viruses and humans may provide a molecular platform for autoimmune crossreactions during immune responses following viral infections/immunizations.
Conflict of interest statement: None to declare.
References
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Articles in the same Issue
- Frontmatter
- Reviews
- Complexity of type IV collagens: from network assembly to function
- Structural and mechanistic aspects of S-S bonds in the thioredoxin-like family of proteins
- Oxidative stress and antioxidants in the pathophysiology of malignant melanoma
- Research Articles/Short Communications
- Genes and Nucleic Acids
- Dynamic characteristics of the mitochondrial genome in SCNT pigs
- Protein Structure and Function
- Conversion of chenodeoxycholic acid to cholic acid by human CYP8B1
- Molecular Medicine
- The comparative biochemistry of viruses and humans: an evolutionary path towards autoimmunity
- MiR-23a-3p-regulated abnormal acetylation of FOXP3 induces regulatory T cell function defect in Graves’ disease
- Cell Biology and Signaling
- Evidence for a protective role of the CX3CL1/CX3CR1 axis in a model of amyotrophic lateral sclerosis
- LncRNA TINCR/microRNA-107/CD36 regulates cell proliferation and apoptosis in colorectal cancer via PPAR signaling pathway based on bioinformatics analysis
- Regulatory effect of hsa-miR-5590-3P on TGFβ signaling through targeting of TGFβ-R1, TGFβ-R2, SMAD3 and SMAD4 transcripts
Articles in the same Issue
- Frontmatter
- Reviews
- Complexity of type IV collagens: from network assembly to function
- Structural and mechanistic aspects of S-S bonds in the thioredoxin-like family of proteins
- Oxidative stress and antioxidants in the pathophysiology of malignant melanoma
- Research Articles/Short Communications
- Genes and Nucleic Acids
- Dynamic characteristics of the mitochondrial genome in SCNT pigs
- Protein Structure and Function
- Conversion of chenodeoxycholic acid to cholic acid by human CYP8B1
- Molecular Medicine
- The comparative biochemistry of viruses and humans: an evolutionary path towards autoimmunity
- MiR-23a-3p-regulated abnormal acetylation of FOXP3 induces regulatory T cell function defect in Graves’ disease
- Cell Biology and Signaling
- Evidence for a protective role of the CX3CL1/CX3CR1 axis in a model of amyotrophic lateral sclerosis
- LncRNA TINCR/microRNA-107/CD36 regulates cell proliferation and apoptosis in colorectal cancer via PPAR signaling pathway based on bioinformatics analysis
- Regulatory effect of hsa-miR-5590-3P on TGFβ signaling through targeting of TGFβ-R1, TGFβ-R2, SMAD3 and SMAD4 transcripts