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Updated: Jun 27, 2026
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Visualization of SARS-CoV-2 using Immuno RNA-Fluorescence In Situ Hybridization
Published on: December 23, 2020
Exploring Key Regulators of Mitochondrial Dynamics and Immune Response in SARS-CoV-2 Infection
Thatiana Corrêa de Melo1, Hellen Paula Valerio1, Dilza Trevisan-Silva1
1Centre of Excellence in New Target Discovery (CENTD), Butantan Institute, São Paulo 05503-900, Brazil.
Viruses
|June 26, 2026
Summary
SARS-CoV-2 infection alters mitochondria, impacting antiviral responses. The study reveals a link between mitochondrial changes, ISG15, and SUMOylation in regulating immunity during infection.
Area of Science:
- Cellular Biology
- Immunology
- Virology
Background:
- Mitochondria play a key role in antiviral immunity and cellular metabolism.
- The precise mechanisms linking SARS-CoV-2 infection, mitochondrial dynamics, and immune gene regulation are not fully understood.
Purpose of the Study:
- To investigate SARS-CoV-2-induced mitochondrial remodeling and its connection to antiviral gene regulation and post-translational modifications.
- To elucidate the temporal dynamics of mitochondrial changes and immune responses during infection.
Main Methods:
- Confocal and high-content imaging, colocalization analysis, and CellProfiler quantification.
- RT-qPCR, proteomics, cytokine profiling, and conditioned-medium analysis were employed.
- Analysis was performed on SARS-CoV-2-infected lung-derived LC-HK2 cells at 48 and 96 hours post-infection.
Main Results:
- SARS-CoV-2 infection induced a time-dependent mitochondrial phenotype, shifting from fission to fusion and elongation.
- Upregulation of antiviral and ISG15-related transcripts was observed, with limited IFN-α2 secretion.
- Dynamic modulation and colocalization of SUMO2/3 with mitochondrial proteins and MAVS were detected.
Conclusions:
- A coordinated mitochondrial-immune regulatory axis exists during SARS-CoV-2 infection.
- Mitochondrial remodeling is linked to ISG15-associated antiviral responses and SUMO-dependent regulation.
- There is a potential uncoupling between antiviral transcriptional activation and downstream interferon production.
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