Severe acute respiratory syndrome coronaviruses contributing to mitochondrial dysfunction: Implications for post-COVID complications

Kabekkodu, Shama Prasada; Chakrabarty, Sanjiban; Jayaram, Pradyumna; Mallya, Sandeep; Thangaraj, Kumarasamy; Singh, Keshav K.; Satyamoorthy, Kapaettu

doi:10.1016/j.mito.2023.01.005

Cited by 20 publications

(9 citation statements)

References 115 publications

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“…Preexisting mitochondrial impairment, which is a feature of obesity and type 2 diabetes ( 349 ), might be a key mechanism that aggravates disease severity and contributes to PASC and long-lasting metabolic alterations in these populations. SARS-CoV-2 infection profoundly impacts mitochondrial structure and function ( 350 ). Mitochondria are key not only for energy production, but also for biosynthesis of fatty acids, regulation of cell cycle, apoptosis, innate immune response, and ketogenesis ( 85 , 254 , 351 ).…”

Section: Connecting the Dotsmentioning

confidence: 99%

Diabetes Mellitus, Energy Metabolism, and COVID-19

Conte,

Cipponeri,

Roden

2023

Endocrine Reviews

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Obesity, diabetes mellitus (mostly type 2), and COVID-19 show mutual interactions because they are not only risk factors for both acute and chronic COVID-19 manifestations, but also because COVID-19 alters energy metabolism. Such metabolic alterations can lead to dysglycemia and long-lasting effects. Thus, the COVID-19 pandemic has the potential for a further rise of the diabetes pandemic. This review outlines how preexisting metabolic alterations spanning from excess visceral adipose tissue to hyperglycemia and overt diabetes may exacerbate COVID-19 severity. We also summarize the different effects of SARS-CoV-2 infection on the key organs and tissues orchestrating energy metabolism, including adipose tissue, liver, skeletal muscle, and pancreas. Last, we provide an integrative view of the metabolic derangements that occur during COVID-19. Altogether, this review allows for better understanding of the metabolic derangements occurring when a fire starts from a small flame, and thereby help reducing the impact of the COVID-19 pandemic.

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Section: Connecting the Dotsmentioning

confidence: 99%

Diabetes Mellitus, Energy Metabolism, and COVID-19

Conte,

Cipponeri,

Roden

2023

Endocrine Reviews

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“…Mitochondria are engaged in the antiviral response through the activation of mitochondrial antiviral-signaling protein (MAVS) by cytosolic viral sensors such as RIG-1 [ 76 , 77 ] to induce apoptosis in infected cells [ 76 ]. These interactions are influenced by mitochondrial redox status and are generally thought to promote viral replication [ 78 ] and contribute to post-COVID-19 mitochondrial dysfunction [ 79 ]. In other studies, SARS-CoV-2 is able to inhibit mitochondrial gene transcription and trigger the integrated stress response [ 80 ] and associated interferon responses [ 81 ].…”

Section: Discussionmentioning

confidence: 99%

Prior Influenza Infection Mitigates SARS-CoV-2 Disease in Syrian Hamsters

Di Pietro,

Haberman,

Lindenbach

et al. 2024

Viruses

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Seasonal infection rates of individual viruses are influenced by synergistic or inhibitory interactions between coincident viruses. Endemic patterns of SARS-CoV-2 and influenza infection overlap seasonally in the Northern hemisphere and may be similarly influenced. We explored the immunopathologic basis of SARS-CoV-2 and influenza A (H1N1pdm09) interactions in Syrian hamsters. H1N1 given 48 h prior to SARS-CoV-2 profoundly mitigated weight loss and lung pathology compared to SARS-CoV-2 infection alone. This was accompanied by the normalization of granulocyte dynamics and accelerated antigen-presenting populations in bronchoalveolar lavage and blood. Using nasal transcriptomics, we identified a rapid upregulation of innate and antiviral pathways induced by H1N1 by the time of SARS-CoV-2 inoculation in 48 h dual-infected animals. The animals that were infected with both viruses also showed a notable and temporary downregulation of mitochondrial and viral replication pathways. Quantitative RT-PCR confirmed a decrease in the SARS-CoV-2 viral load and lower cytokine levels in the lungs of animals infected with both viruses throughout the course of the disease. Our data confirm that H1N1 infection induces rapid and transient gene expression that is associated with the mitigation of SARS-CoV-2 pulmonary disease. These protective responses are likely to begin in the upper respiratory tract shortly after infection. On a population level, interaction between these two viruses may influence their relative seasonal infection rates.

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“…Mitochondrial dysfunction can be part of the postacute sequelae of COVID-19 [63]. Several studies have indicated that patients with post-COVID complications, showing chronic fatigue, neuropsychiatric and neurometabolic disturbances, could be affected by disorders of mitochondrial metabolic pathways [64][65][66].…”

Section: Discussionmentioning

confidence: 99%

Association of Inflammatory Mediators with Mitochondrial DNA Variants in Geriatric COVID-19 Patients

2024

Aging dis

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COVID-19 remains a serious concern for elderly individuals with underlying comorbidities. SARS-CoV-2 can target and damage mitochondria, potentially leading to mutations in mitochondrial DNA (mtDNA). This study aimed to evaluate single nucleotide substitutions in mtDNA and analyze their correlation with inflammatory biomarkers in elderly COVID-19 patients. A total of 30 COVID-19 patients and 33 older adult controls without COVID-19 (aged over 65 years) were enrolled. mtDNA was extracted from buffy coat samples and sequenced using a chip-based resequencing system (MitoChip v2.0) which detects both homoplasmic and heteroplasmic mtDNA variants (40-60% heteroplasmy), and allows the assessment of lowlevel heteroplasmy (<10% heteroplasmy). Serum concentrations of IL-6, IFN-α, TNF-α and IL-10 were determined in patients by a high-sensitivity immunoassay. We found a higher burden of total heteroplasmic variants in COVID-19 patients compared to controls with a selective increment in ND1 and COIII genes. Lowlevel heteroplasmy was significantly elevated in COVID-19 patients, especially in genes of the respiratory complex I. Both heteroplasmic variant burden and low-level heteroplasmy were associated with increased levels of IL-6, TNF-α, and IFN-α. These findings suggest that SARS-CoV-2 may induce mtDNA mutations that are related to the degree of inflammation.

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Severe acute respiratory syndrome coronaviruses contributing to mitochondrial dysfunction: Implications for post-COVID complications

Cited by 20 publications

References 115 publications

Diabetes Mellitus, Energy Metabolism, and COVID-19

Diabetes Mellitus, Energy Metabolism, and COVID-19

Prior Influenza Infection Mitigates SARS-CoV-2 Disease in Syrian Hamsters

Association of Inflammatory Mediators with Mitochondrial DNA Variants in Geriatric COVID-19 Patients

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