review · Frontiers in Pharmacology
Patients with COVID-19 face a heightened risk of developing blood-clotting complications such as coagulopathy and thrombosis, which correlate with raised D-dimer levels and potentially homocysteine. Multiple genetic variations influence these pathways. By analysing genome-wide association data and tissue-specific gene expression, a molecular interaction network was constructed around key single-nucleotide polymorphisms linked to conditions such as pulmonary embolism, stroke, and vascular diseases. The network structured into three distinct functional clusters representing D-dimer and fibrinogen regulation, homocysteine regulation, and arterial or venous thromboembolism. Within this network, the F2 and F5 genes serve as critical connecting nodes linking the separate functional groups. Evaluating these specific genetic markers through patient genotyping offers a potential method to identify COVID-19 patients who possess the highest vulnerability to severe thrombotic complications.
Blood clots pose a severe and potentially fatal risk to individuals suffering from COVID-19. Uncovering the specific genetic variants and biological networks linked to elevated clotting markers provides a clearer understanding of individual susceptibility. This knowledge could enable healthcare providers to forecast which patients are most vulnerable to life-threatening clotting complications, supporting targeted clinical monitoring and earlier medical interventions.
This early-stage molecular mapping research could inform the development of targeted diagnostic genotyping panels for clinical laboratories and healthcare providers. Such assays would screen COVID-19 patients to predict their predisposition to severe thrombotic events. Because the findings are based on network analysis and existing genetic association data, substantial clinical validation and regulatory assessment would be required before diagnostic tools can reach clinical practice.
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COVID-19 is caused by Severe Acute Respiratory Syndrome Coronavirus-2, which has infected over thirty eight million individuals worldwide. Emerging evidence indicates that COVID-19 patients are at a high risk of developing coagulopathy and thrombosis, conditions that elevate levels of D-dimer. It is believed that homocysteine, an amino acid that plays a crucial role in coagulation, may also contribute to these conditions. At present, multiple genes are implicated in the development of these disorders. For example, single-nucleotide polymorphisms (SNPs) in FGG, FGA, and F5 mediate increases in D-dimer and SNPs in ABO, CBS, CPS1 and MTHFR mediate differences in homocysteine levels, and SNPs in TDAG8 associate with Heparin-induced Thrombocytopenia. In this study, we aimed to uncover the genetic basis of the above conditions by examining genome-wide associations and tissue-specific gene expression to build a molecular network. Based on gene ontology, we annotated various SNPs with five ancestral terms: pulmonary embolism, venous thromboembolism, vascular diseases, cerebrovascular disorders, and stroke. The gene-gene interaction network revealed three clusters that each contained hallmark genes for D-dimer/fibrinogen levels, homocysteine levels, and arterial/venous thromboembolism with F2 and F5 acting as connecting nodes. We propose that genotyping COVID-19 patients for SNPs examined in this study will help identify those at greatest risk of complications linked to thrombosis.
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DOI: 10.3389/fphar.2020.587451
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