
Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16
Published: April 17, 2025
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has been recognized not only for its acute effects but also ability to cause LongCOVID (LCS), a condition characterized by persistent symptoms affecting multiple organ systems. This review examines the molecular and immunological mechanisms underlying LCS, with particular focus on autophagy inhibition, chronic inflammation, oxidative, nitrosative calcium stress, viral persistence autoimmunology. Potential pathophysiological involved in LCS include (1) autoimmune activation, (2) latent persistence, where SARS-CoV-2 continues influence host metabolism, (3) reactivation of pathogens such as Epstein-Barr virus (EBV) or cytomegalovirus (CMV), exacerbating immune metabolic dysregulation, (4) possible inflammatory body fails restore post-infection homeostasis. The manipulation cellular pathways proteins is critical aspect virus’ evade clearance establish long-term dysfunction. Viral NSP13, ORF3a ORF8 have shown disrupt autophagy, thereby impairing promoting evasion. In addition, mitochondrial dysfunction, dysregulated signaling, oxidative HIF-1α activation Nrf2 inhibition create self-sustaining feedback loop that contributes tissue damage symptoms. Therefore understanding basis development effective therapeutic strategies. Targeting glycolysis restoration homeostasis may provide novel strategies mitigate consequences infection. Future research should personalized interventions based dominant perturbations individual patients.
Language: Английский