ArticleInternational immunopharmacology2022
Viral load is associated with mitochondrial dysfunction and altered monocyte phenotype in acute severe SARS-CoV-2 infection.
Article in International immunopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
- Phospholipase A2 Isoforms in Lung Immunity and Respiratory Infections: Potential Targets for Next-Generation Therapy.International journal of molecular sciences · 2026Review
- Impact of nutrition on long COVID.Sports medicine and health science · 2026Review
- Induction of dysfunctional CD14Frontiers in immunology · 2026Article
- Impaired Peripheral Blood Mononuclear Cell (PBMC) Mitochondrial Respiration Is Associated with Mortality and Long COVID Syndrome Severity in COVID-19 Patients.International journal of molecular sciences · 2025Article
- Pattern Recognition Receptors (PRRs) Expression and Activation in COVID-19 and Long COVID: From SARS-CoV-2 Escape Mechanisms to Emerging PRR-Targeted Immunotherapies.Microorganisms · 2025Review
- HIF-1α Pathway in COVID-19: A Scoping Review of Its Modulation and Related Treatments.International journal of molecular sciences · 2025Article
- Long-term mitochondrial and metabolic impairment in lymphocytes of subjects who recovered after severe COVID-19.Cell biology and toxicology · 2025Article
- Does COVID-19 Trigger the Risk for the Development of Parkinson's Disease? Therapeutic Potential of Vitamin C.Molecular neurobiology · 2024Review
- Optimizing cardiopulmonary rehabilitation duration for long COVID patients: an exercise physiology monitoring approach.GeroScience · 2024Article
- Precision nutrition to reset virus-induced human metabolic reprogramming and dysregulation (HMRD) in long-COVID.NPJ science of food · 2024Review
- Inhalation of ACE2-expressing lung exosomes provides prophylactic protection against SARS-CoV-2.Nature communications · 2024Article
- Altered mitochondrial respiration in peripheral blood mononuclear cells of post-acute sequelae of SARS-CoV-2 infection.Mitochondrion · 2024Article
- Mitochondria in COVID-19: from cellular and molecular perspective.Frontiers in physiology · 2024Review
- Elevated CD39+T-Regulatory Cells and Reduced Levels of Adenosine Indicate a Role for Tolerogenic Signals in the Progression from Moderate to Severe COVID-19.International journal of molecular sciences · 2023Article
- Article
- The Role of Cluster of Differentiation 39 (CD39) and Purinergic Signaling Pathway in Viral Infections.Pathogens (Basel, Switzerland) · 2023Review
- Endotoxin tolerance and low activation of TLR-4/NF-κB axis in monocytes of COVID-19 patients.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Non-alcoholic fatty liver disease and COVID-19: Harmless companions or disease intensifier?World journal of gastroenterology · 2023Review
- Aberrant phenotype of circulating antigen presenting cells in giant cell arteritis and polymyalgia rheumatica.Frontiers in immunology · 2023Article
- Mild to moderate post-COVID-19 alters markers of lymphocyte activation, exhaustion, and immunometabolic responses that can be partially associated by physical activity level- an observational sub-analysis fit- COVID study.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
18 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Monocytes play a major role in the initial innate immune response to SARS-CoV-2. Although viral load may correlate with several clinical outcomes in COVID-19, much less is known regarding their impact on innate immune phenotype. We evaluated the monocyte phenotype and mitochondrial function in severe COVID-19 patients (n = 22) with different viral burden (determined by the median of viral load of the patients) at hospital admission. Severe COVID-19 patients presented lower frequency of CD14 + CD16- classical monocytes and CD39 expression on CD14 + monocytes, and higher frequency of CD14 + CD16 + intermediate and CD14-CD16 + nonclassical monocytes as compared to healthy controls independently of viral load. COVID-19 patients with high viral load exhibited increased GM-CSF, PGE-2 and lower IFN-α as compared to severe COVID-19 patients with low viral load (p < 0.05). CD14 + monocytes of COVID-19 patients with high viral load presented higher expression of PD-1 but lower HLA-DR on the cell surface than severe COVID-19 patients with low viral load. All COVID-19 patients presented decreased monocyte mitochondria membrane polarization, but high SARS-CoV-2 viral load was associated with increased mitochondrial reactive oxygen species. In this sense, higher viral load induces mitochondrial reactive oxygen species generation associated with exhaustion profile in CD14 + monocytes of severe COVID-19 patients. Altogether, these data shed light on new pathological mechanisms involving SARS-CoV-2 viral load on monocyte activation and mitochondrial function, which were associated with COVID-19 severity.
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