Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapieFeb 6, 2026

Changes in Blood Cell Makers and Specialized Antibodies After COVID-19 Linking Immune Problems to Blood Vessel Damage

Updated Feb 7, 2026

Abstract

Post-acute sequelae of SARS-CoV-2 infection (PASC) involves persistent symptoms lasting for at least three months after the initial infection.

The pathophysiology of PASC is multifactorial and not fully understood.
Immune dysregulation and hemostatic imbalance may play central roles in complications following COVID-19.
Megakaryocytes are suggested to contribute to ongoing thrombo-inflammatory processes post-infection.
Afucosylated IgG antibodies are linked to heightened immune activation during acute COVID-19.
The persistence of abnormal antibody glycosylation patterns after the acute phase may influence chronic immune and vascular changes in PASC.
Prolonged immune-hemostatic interactions could lead to sustained inflammation and microvascular issues.

Simplified

Post-acute sequelae of SARS-CoV-2 infection (PASC), also referred to as long COVID, encompasses a constellation of persistent symptoms lasting for at least three months after acute SARS-CoV-2 infection and not explained by alternative diagnoses. The multifactorial pathophysiology underlying PASC remains incompletely understood, limiting the development of effective management strategies. Increasing evidence suggests that both immune dysregulation and hemostatic imbalance play central roles in post-COVID-19 complications. Megakaryocytes, key regulators of platelet production and coagulation, have emerged as potential contributors to sustained thrombo-inflammatory processes following SARS-CoV-2 infection. In parallel, afucosylated IgG antibodies have been strongly implicated in exaggerated immune activation and hyperinflammatory responses during acute COVID-19. The persistence of such antibody glycosylation patterns beyond the acute phase raises the possibility that they may also contribute to chronic immune and vascular alterations observed in PASC. This narrative review explores the potential interplay between megakaryocyte dysfunction and afucosylated IgG antibodies in the pathogenesis of PASC. By examining mechanisms identified during acute SARS-CoV-2 infection, we discuss how prolonged immune-hemostatic crosstalk may promote persistent inflammation, endothelial dysfunction, and microvascular abnormalities. Understanding these interconnected pathways may provide mechanistic insight into the heterogeneity of PASC manifestations and help identify novel therapeutic targets for long-term post-COVID-19 sequelae.

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Changes in Blood Cell Makers and Specialized Antibodies After COVID-19 Linking Immune Problems to Blood Vessel Damage

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