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SARS-CoV-2 and human retroelements: a case for molecular mimicry?
1Department of Internal Medicine, Nephrology, Goethe University Hospital, Johann Wolfgang Goethe University Frankfurt/Main, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany. B.Koch@med.uni-frankfurt.de.
Human retroelements (RE) and coronaviruses (CoV) share sequences, potentially triggering autoimmunity in COVID-19. SARS-CoV-2 infection deregulates RE expression, contributing to disease pathogenesis and severity.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- The pathogenesis of the late phase of COVID-19 remains unclear, with autoimmunity emerging as a significant factor.
- Deregulation of human retroelements (RE), mobile genetic elements, is observed in various viral infections, including COVID-19.
Purpose of the Study:
- To investigate the relationship between human retroelements and coronaviruses (CoV), particularly SARS-CoV-2.
- To explore the potential role of RE-CoV sequence homology in COVID-19 pathogenesis and autoimmunity.
Main Methods:
- Comparative sequence analysis of CoV genomes and human RE.
- Analysis of RE expression profiles in SARS-CoV-2 infected cells and controls.
- Identification of SARS-CoV-2 epitopes and their homology to RE sequences.
Main Results:
- Coronaviruses, including SARS-CoV-2, contain sequences identical to human RE (up to 35 base pairs).
- Some RE-identical sequences are present in SARS-CoV-2 epitopes linked to COVID-19 severity.
- SARS-CoV-2 infection leads to deregulation of RE expression, notably LINE1 and endogenous retroviruses.
Conclusions:
- Shared coding sequences between CoV and human RE can be targeted by antibodies in COVID-19 patients.
- This sequence homology may induce an autoimmune response through molecular mimicry, contributing to COVID-19 pathogenesis.
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