Long COVID a New Derivative in the Chaos of SARS-CoV-2 Infection: The Emergent Pandemic?

Abstract

Coronavirus disease 2019 (COVID-19) is a multisystem illness caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), which can manifest with a multitude of symptoms in the setting of end-organ damage, though it is predominantly respiratory. However, various symptoms may remain after acute SARS-CoV-2 infection, and this condition is referred to as “Long COVID” (LC). Patients with LC may develop multi-organ symptom complex that remains 4–12 weeks after the acute phase of illness, with symptoms intermittently persisting over time. The main symptoms are fatigue, post-exertional malaise, cognitive dysfunction, and limitation of functional capacity. Pediatric patients developed the main symptoms of LC like those described in adults, although there may be variable presentations of LC in children. The underlying mechanisms of LC are not clearly known, although they may involve pathophysiological changes generated by virus persistence, immunological alterations secondary to virus–host interaction, tissue damage of inflammatory origin and hyperactivation of coagulation. Risk factors for developing LC would be female sex, more than five early symptoms, early dyspnea, previous psychiatric disorders, and alterations in immunological, inflammatory and coagulation parameters. There is currently no specific treatment for LC, but it could include pharmacological treatments to treat symptoms, supplements to restore nutritional, metabolic, and gut flora balance, and functional treatments for the most disabling symptoms. In summary, this study aims to show the scientific community the current knowledge of LC.

Persisting Endothelial Cell Activation and Hypercoagulability after COVID-19 Recovery—The Prospective Observational ROADMAP-Post COVID-19 Study

“…Long-COVID-19 emerges as a new aspect of the public health crisis triggered by the pandemic [32]. Delayed arterial thrombosis or venous thromboembolism post-COVID-19 is an emerging health problem [33][34][35].…”

Long COVID: The Nature of Thrombotic Sequelae Determines the Necessity of Early Anticoagulation

“…demonstrated that during early recovery, those who went on to develop PASC generally had higher levels of cytokine biomarkers including TNF-α, IFN-γ–induced protein 10 and IL-6 ( Peluso et al., 2021 ), consistent with increased immune activation. Some speculate that persistent viral RNA shedding triggers chronic immune activation ( Desimmie et al., 2021 ; Fernández-Lázaro et al., 2021 ). Immune system dysregulation in long COVID is characterized by increased interferon gamma (IFN-γ) and interleukin (IL)-2, pathological changes in CD4 + , CD8 + lymphocyte subsets, monocyte CD14 + and CD16 + subsets, and defects in B lymphocytes and monocytes.…”

“…Immune system dysregulation in long COVID is characterized by increased interferon gamma (IFN-γ) and interleukin (IL)-2, pathological changes in CD4 + , CD8 + lymphocyte subsets, monocyte CD14 + and CD16 + subsets, and defects in B lymphocytes and monocytes. Increased oxidative phosphorylation and reactive oxygen species-related inflammatory responses displace TNF-α and IL-6-driven inflammatory responses, driving persistent symptoms and progression of long COVID ( Fernández-Lázaro et al., 2021 ). Thus chronic persistent inflammation in long COVID may stimulate ECs, platelets and other inflammatory cells, promote the upregulation of procoagulant factors, and destroy the protective function of vascular endothelium, thereby causing abnormal coagulation ( Figure 1 ) .…”

Skeletal Muscle in Hypoxia and Inflammation: Insights on the COVID-19 Pandemic

“…The long-term consequences of the SARS-CoV-2 infection remain largely unclear. Indeed, knowledge acquired in these 2 years of pandemia allows to differentiate acute COVID-19 from the SARS-CoV-2 infection sequelae and the Long COVID Syndrome (132). Patients with acute COVID-19 manifest signs and symptoms up to 4 weeks after the onset of the infection; Patients with COVID-19 sequelae are often elderly adult males with associated comorbidities who developed a severe acute SARS-CoV-2 infection leading to structural systemic damage (132).…”