"Long COVID-19, also known as post-acute sequelae of SARS-CoV-2 infection (PASC) or post COVID-19 condition, is a post-viral syndrome affecting people who have recovered from COVID-19 infection. Symptoms are similar to those experienced by patients with chronic inflammatory response syndrome (CIRS) rather than myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) 6."
"Long COVID-19, also known as post-acute sequelae of SARS-CoV-2 infection (PASC) or post COVID-19 condition, is a post-viral syndrome affecting people who have recovered from COVID-19 infection. Symptoms are similar to those experienced by patients with chronic inflammatory response syndrome (CIRS) rather than myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) 6."
"The aetiopathogenetic mechanisms by which the SARS-CoV-2 infection determines the post-acute sequelae have not yet been fully clarified. Various hypotheses include direct organ damage caused by the virus, innate immune response with release of inflammatory cytokines or the development of a pro-coagulative state. According to some authors, anti-idiotype antibodies play a possible role in the pathogenesis of the disease 5. Basophil function may affect the course of the disease 7,8, and mast cell activation may play a role in long COVID-19 9,10."
"Post-Acute COVID-19 Vaccination Syndrome"
"Recent literature highlights a significant pathophysiological overlap between Post-Acute Sequelae of SARS-CoV-2 (PACS) and Post-Acute COVID-19 Vaccination Syndrome (PACVS), suggesting a pivotal role for renin-angiotensin system (RAS) dysregulation and G-protein-coupled receptor (GPCR)-mediated autoimmunity. In both clinical entities, the interaction of the Spike protein with ACE2 may precipitate a systemic shift toward the pro-inflammatory Angiotensin II/AT1R axis, thereby exacerbating endotheliitis and microvascular dysfunction. Clinically, these mechanisms manifest as autonomic dysfunction (e.g., POTS, postural orthostatic tachycardia syndrome), myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), and peripheral neuropathies 19."
"Recent literature highlights a significant pathophysiological overlap between Post-Acute Sequelae of SARS-CoV-2 (PACS) and Post-Acute COVID-19 Vaccination Syndrome (PACVS), suggesting a pivotal role for renin-angiotensin system (RAS) dysregulation and G-protein-coupled receptor (GPCR)-mediated autoimmunity. In both clinical entities, the interaction of the Spike protein with ACE2 may precipitate a systemic shift toward the pro-inflammatory Angiotensin II/AT1R axis, thereby exacerbating endotheliitis and microvascular dysfunction. Clinically, these mechanisms manifest as autonomic dysfunction (e.g., POTS, postural orthostatic tachycardia syndrome), myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), and peripheral neuropathies 19."
"Most of the management is supportive in nature, depending on the exact clinical manifestations. Regarding COVID-19 vaccination and post-COVID symptoms, one observational and retrospective study 16 showed that in patients with long COVID-19, subsequent vaccination increases the probability that long COVID-19 will persist for up to a year or more (probability between 29% and 44%)."
"Long COVID-19, also known as post-acute sequelae of SARS-CoV-2 infection (PASC) or post COVID-19 condition, is a post-viral syndrome affecting people who have recovered from COVID-19 infection. Symptoms are similar to those experienced by patients with chronic inflammatory response syndrome (CIRS) rather than myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) 6."
"Long COVID-19, also known as post-acute sequelae of SARS-CoV-2 infection (PASC) or post COVID-19 condition, is a post-viral syndrome affecting people who have recovered from COVID-19 infection. Symptoms are similar to those experienced by patients with chronic inflammatory response syndrome (CIRS) rather than myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) 6."
"The aetiopathogenetic mechanisms by which the SARS-CoV-2 infection determines the post-acute sequelae have not yet been fully clarified. Various hypotheses include direct organ damage caused by the virus, innate immune response with release of inflammatory cytokines or the development of a pro-coagulative state. According to some authors, anti-idiotype antibodies play a possible role in the pathogenesis of the disease 5. Basophil function may affect the course of the disease 7,8, and mast cell activation may play a role in long COVID-19 9,10."
"One emerging driver of long-COVID-19 is the persistence of SARS-CoV-2 spike protein fragments that function as "xeno-AMPs" (foreign antimicrobial peptides) 17. These degradation products destabilise membranes of host immune cells, inducing chronic hyperinflammation 17. By mimicking host defence peptides, these viral remnants perturb the immune landscape long after the acute infection has resolved, offering a compelling molecular basis for the systemic dysregulation observed in many patients 17."
"Persistent amyloid coagulopathy is a leading aetiological hypothesis for Long COVID. Evidence suggests the SARS-CoV-2 spike protein triggers structurally anomalous, fibrin-amyloid microclots that resist fibrinolysis and obstruct capillary beds. This mechanical blockage impairs tissue oxygenation and maintains chronic endothelial inflammation. This microvascular dysfunction may explain systemic symptoms (like brain fog and chronic fatigue), marking a transition from acute infection to chronic pathology 18."
"Recent literature highlights a significant pathophysiological overlap between Post-Acute Sequelae of SARS-CoV-2 (PACS) and Post-Acute COVID-19 Vaccination Syndrome (PACVS), suggesting a pivotal role for renin-angiotensin system (RAS) dysregulation and G-protein-coupled receptor (GPCR)-mediated autoimmunity. In both clinical entities, the interaction of the Spike protein with ACE2 may precipitate a systemic shift toward the pro-inflammatory Angiotensin II/AT1R axis, thereby exacerbating endotheliitis and microvascular dysfunction. Clinically, these mechanisms manifest as autonomic dysfunction (e.g., POTS, postural orthostatic tachycardia syndrome), myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), and peripheral neuropathies 19."
"Recent literature highlights a significant pathophysiological overlap between Post-Acute Sequelae of SARS-CoV-2 (PACS) and Post-Acute COVID-19 Vaccination Syndrome (PACVS), suggesting a pivotal role for renin-angiotensin system (RAS) dysregulation and G-protein-coupled receptor (GPCR)-mediated autoimmunity. In both clinical entities, the interaction of the Spike protein with ACE2 may precipitate a systemic shift toward the pro-inflammatory Angiotensin II/AT1R axis, thereby exacerbating endotheliitis and microvascular dysfunction. Clinically, these mechanisms manifest as autonomic dysfunction (e.g., POTS, postural orthostatic tachycardia syndrome), myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), and peripheral neuropathies 19."
"Recent literature highlights a significant pathophysiological overlap between Post-Acute Sequelae of SARS-CoV-2 (PACS) and Post-Acute COVID-19 Vaccination Syndrome (PACVS), suggesting a pivotal role for renin-angiotensin system (RAS) dysregulation and G-protein-coupled receptor (GPCR)-mediated autoimmunity. In both clinical entities, the interaction of the Spike protein with ACE2 may precipitate a systemic shift toward the pro-inflammatory Angiotensin II/AT1R axis, thereby exacerbating endotheliitis and microvascular dysfunction. Clinically, these mechanisms manifest as autonomic dysfunction (e.g., POTS, postural orthostatic tachycardia syndrome), myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), and peripheral neuropathies 19."
"One emerging driver of long-COVID-19 is the persistence of SARS-CoV-2 spike protein fragments that function as "xeno-AMPs" (foreign antimicrobial peptides) 17. These degradation products destabilise membranes of host immune cells, inducing chronic hyperinflammation 17. By mimicking host defence peptides, these viral remnants perturb the immune landscape long after the acute infection has resolved, offering a compelling molecular basis for the systemic dysregulation observed in many patients 17."
"One emerging driver of long-COVID-19 is the persistence of SARS-CoV-2 spike protein fragments that function as "xeno-AMPs" (foreign antimicrobial peptides) 17. These degradation products destabilise membranes of host immune cells, inducing chronic hyperinflammation 17. By mimicking host defence peptides, these viral remnants perturb the immune landscape long after the acute infection has resolved, offering a compelling molecular basis for the systemic dysregulation observed in many patients 17."
"Persistent amyloid coagulopathy is a leading aetiological hypothesis for Long COVID. Evidence suggests the SARS-CoV-2 spike protein triggers structurally anomalous, fibrin-amyloid microclots that resist fibrinolysis and obstruct capillary beds. This mechanical blockage impairs tissue oxygenation and maintains chronic endothelial inflammation. This microvascular dysfunction may explain systemic symptoms (like brain fog and chronic fatigue), marking a transition from acute infection to chronic pathology 18."
"Post-Acute COVID-19 Vaccination Syndrome"
Expected headings
"Foreign antimicrobial peptides"
"Amyloid fibrin microclots"
"Post-Acute COVID-19 Vaccination Syndrome"
"It can manifest weeks or months after the apparent clinical resolution of the acute phase of the disease. Dyspnoea and fatigue are among the most common symptoms 1,2. However, the signs, symptoms and possible clinical manifestations are grouped into two classes 3,4:"
"Recent literature highlights a significant pathophysiological overlap between Post-Acute Sequelae of SARS-CoV-2 (PACS) and Post-Acute COVID-19 Vaccination Syndrome (PACVS), suggesting a pivotal role for renin-angiotensin system (RAS) dysregulation and G-protein-coupled receptor (GPCR)-mediated autoimmunity. In both clinical entities, the interaction of the Spike protein with ACE2 may precipitate a systemic shift toward the pro-inflammatory Angiotensin II/AT1R axis, thereby exacerbating endotheliitis and microvascular dysfunction. Clinically, these mechanisms manifest as autonomic dysfunction (e.g., POTS, postural orthostatic tachycardia syndrome), myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), and peripheral neuropathies 19."