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Abstract

Long COVID (LC) is characterized by prolonged, diverse symptoms affecting multiple organ systems, including but not limiting to the immune, neurological, and cardiovascular systems. This mini review explores the biological abnormalities underpinning LC, focusing on immune dysregulation, chronic inflammation, oxidative stress, and mitochondrial dysfunction as key contributors to its persistence. Recent studies indicate that LC may involve sustained elevation of pro-inflammatory cytokines, autoimmunity, and T-cell exhaustion, all of which perpetuate a state of low-grade chronic inflammation. Additionally, oxidative and nitrosative stress linked to mitochondrial damage exacerbates fatigue, mood and cognitive symptoms, while hormonal imbalances and metabolic disturbances further complicate the clinical profile. Neurological involvement is marked by neuroinflammation and endothelial dysfunction, potentially escalating the risk of long-term neurodegenerative disorders. Understanding these mechanisms is crucial for developing biomarkers and targeted therapies that address the underlying pathology of LC. This review highlights current findings on the molecular and cellular pathways associated with LC and underscores the need for integrative research to enhance therapeutic strategies and patient care.

Article Type

Review

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