COVID-19 Demonstrates That Inflammation Is a Hyperviscous State.

Area of Science:

• Hematology
• Virology
• Pathophysiology

Background:

• Severe coronavirus disease-2019 (COVID-19) complications are linked to blood hyperviscosity.
• Hyperviscosity arises from elevated fibrinogen levels, creating a syndrome affecting various blood flow conditions.
• This condition increases thrombosis risk and impairs tissue perfusion.

Purpose of the Study:

• To elucidate the mechanisms by which COVID-19-induced hyperviscosity contributes to disease severity and long-term effects.
• To explore the role of viral genetic factors in triggering hyperviscosity and immune responses.

Main Methods:

• Review of existing literature on COVID-19 pathophysiology, focusing on hematological changes.
• Analysis of the severe acute respiratory syndrome coronavirus 2 genome for specific genetic sequences.
• Correlation of hyperviscosity markers with clinical outcomes and organ-specific damage in COVID-19 patients.

Main Results:

• COVID-19-associated hyperviscosity significantly increases arterial and venous thrombosis risk, counteracting anticoagulation.
• Reduced tissue perfusion due to hyperviscosity leads to lung, heart, and brain damage, including hypoxemia, myocarditis, and demyelination.
• Viral genetic factors, specifically oligonucleotide sequences, activate innate immunity, elevating fibrinogen and contributing to pathology.

Conclusions:

• Blood hyperviscosity is a critical factor in severe COVID-19 pathogenesis, driving thrombosis and organ dysfunction.
• Hyperviscosity contributes to long-COVID symptoms through mechanisms like capillary rarefaction and endothelial damage.
• Targeting hyperviscosity and associated immune activation may offer therapeutic strategies for COVID-19 and its sequelae.