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Decoding SARS-CoV-2 hijacking of host mitochondria in COVID-19 pathogenesis
Keshav K Singh1, Gyaneshwer Chaubey2, Jake Y Chen3
1Department of Genetics, School of Medicine, University of Alabama at Birmingham, Kaul Genetics Building, Birmingham, Alabama.
American Journal of Physiology. Cell Physiology
|June 9, 2020
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) hijacks host mitochondria using viral RNA and proteins. This mitochondrial manipulation by SARS-CoV-2 promotes virus replication and COVID-19 pathogenesis.
Area of Science:
- * Virology
- * Cell Biology
- * Immunology
Background:
- * The COVID-19 pandemic necessitates understanding SARS-CoV-2 pathogenesis.
- * Mitochondria play crucial roles in cellular functions and immunity.
- * Viral interference with host cell mitochondria is a key area of investigation.
Purpose of the Study:
- * To elucidate the mechanisms by which SARS-CoV-2 manipulates host mitochondrial function.
- * To explore the role of viral RNA and protein localization in mitochondria during infection.
- * To investigate the implications of mitochondrial dysfunction in COVID-19 severity, particularly in vulnerable populations.
Main Methods:
- * Review and analysis of existing data on SARS-CoV-1 and SARS-CoV-2.
- * Hypothesis generation based on viral RNA and protein interactions with mitochondria.
- * Examination of ACE2 regulation and open-reading frame (ORF) functions in mitochondrial manipulation.
Main Results:
- * SARS-CoV-2 RNA and proteins localize to mitochondria, hijacking cellular functions.
- * Viral manipulation of mitochondria involves ACE2 regulation and direct action by ORFs like ORF-9b.
- * Mitochondrial dysfunction induced by SARS-CoV-2 can lead to cytoplasmic release of mitochondrial DNA (mtDNA), inflammasome activation, and immune suppression.
Conclusions:
- * SARS-CoV-2 actively manipulates host mitochondria to evade immunity and promote viral replication.
- * Age-related decline in mitochondrial function and ACE2 may increase vulnerability to severe COVID-19.
- * Targeting virus-mitochondria interactions offers potential therapeutic strategies for COVID-19.
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