Post-COVID-19 Tissue Remodeling and Multiorgan Damage: Pathogenetic Mechanisms, Structural Alterations, and Long-Term Clinical Consequences of SARS-CoV-2 Infection

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is primarily recognized as an acute respiratory infection; however, accumulated evidence demonstrates that its biological effects extend far beyond the respiratory tract. Materials and Methods. A narrative analytical review of published scientific literature on post-COVID-19 tissue injury was performed. Particular attention was given to studies addressing persistent inflammation, viral persistence, endothelial and microvascular injury, fibrotic remodeling, skeletal muscle pathology, and multiorgan involvement. Publications from peer-reviewed journals and authoritative international sources were evaluated with emphasis on pulmonary, cardiovascular, renal, muscular, neurological, and vascular changes. Results. Post-COVID-19 tissue pathology appears to result from several interacting mechanisms, including residual injury from acute infection, dysregulated immune activation, endothelial damage, microcirculatory impairment, persistent or residual viral material in selected tissues, oxidative stress, mitochondrial dysfunction, and profibrotic signaling. Pulmonary interstitial abnormalities and fibrosis are particularly evident after severe disease, whereas endothelial and microvascular abnormalities may contribute to multisystem symptoms. Skeletal muscle abnormalities, inflammatory changes, impaired energy metabolism, and reduced exercise tolerance have also been reported. Persistent structural damage does not occur uniformly in all patients, and the extent of tissue injury depends on acute disease severity, pre-existing disorders, age, immunological response, and other host-related factors. Conclusion. SARS-CoV-2 infection may produce prolonged structural and functional changes in multiple tissues. Post-COVID-19 complications should therefore be considered a multisystem pathophysiological process rather than exclusively a respiratory sequela. Evaluation of tissue remodeling, endothelial dysfunction, inflammatory activation, and fibrosis may improve understanding of persistent symptoms and support individualized follow-up strategies.