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Network Analysis and Transcriptome Profiling Identify Autophagic and Mitochondrial Dysfunctions in SARS-CoV-2
Komudi Singh1, Yun-Ching Chen1, Shahin Hassanzadeh2
1Bioinformatics and Computational Biology Laboratory, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, United States.
Frontiers in Genetics
|April 2, 2021
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uniquely disrupts host cell autophagy and mitochondrial processes, impairing antiviral defenses. Targeting these pathways may offer new therapeutic strategies against SARS-CoV-2 infection.
Area of Science:
- Cellular biology
- Virology
- Host-pathogen interactions
Background:
- Understanding host cell responses to viral infections is crucial for identifying pathogenesis mechanisms.
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes significant global health challenges.
Purpose of the Study:
- To analyze the transcriptional response of host cells to SARS-CoV-2 infection.
- To identify specific biological processes and pathways uniquely affected by SARS-CoV-2 compared to other respiratory viruses.
- To explore potential therapeutic targets based on observed host cell perturbations.
Main Methods:
- Analysis of gene expression profiles in SARS-CoV-2, MERS-CoV, and influenza A virus (IAV) infected lung cell lines (A549, Calu3).
- Validation of findings in infected human nasopharyngeal samples.
- Examination of age-stratified human data to assess antiviral signaling responses.
Main Results:
- SARS-CoV-2 infection specifically perturbed inflammatory, mitochondrial, and autophagy processes, unlike MERS-CoV or IAV.
- Downregulation of genes involved in mTOR expression, mitochondrial function, lysosome acidification, and autophagy was observed in both cell lines and human samples.
- Impaired autophagic flux and reduced upregulation of antiviral signaling genes (chemokines, interferon-stimulated genes) were noted in SARS-CoV-2 infected cells and human samples, particularly in older individuals.
Conclusions:
- Host cell autophagy and mitochondrial dysfunction are key features of SARS-CoV-2 pathogenesis.
- Intervention strategies targeting lysosome acidification or autophagic flux warrant investigation.
- Age-related differences in antiviral responses highlight the complexity of SARS-CoV-2 infection.
