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Heparanase is the possible link between monkeypox and Covid-19: robust candidature in the mystic and present
Hayder M Al-Kuraishy1, Ali I Al-Gareeb1, Helal F Hetta2
1Department of Clinical Pharmacology and Therapeutic Medicine, College of Medicine, ALmustansiriyiah University, Baghdad, Iraq.
Abstract:
Heparanase (HPSE) is an endoglycosidase cleaves heparan sulfate (HS) and this contributes to the degradation and remodeling of the extracellular matrix. HS cleaved by HPSE induces activation of autophagy and formation of autophagosommes which facilitate binding of HPSE to the HS and subsequent release of growth factors. The interaction between HPSE and HS triggers releases of chemokines and cytokines which affect inflammatory response and cell signaling pathways with development of hyperinflammation, cytokine storm (CS) and coagulopathy. HPSE expression is induced by both SARS-CoV-2 and monkeypox virus (MPXV) leading to induction release of pro-inflammatory cytokines, endothelial dysfunction and thrombotic events. Co-infection of MPX with SARS-CoV-2 may occur as we facing many outbreaks of MPX cases during Covid-19 pandemic. Therefore, targeting of HPSE by specific inhibitors may reduce the risk of complications in both SARS-CoV-2 and MPXV infections. Taken together, HPSE could be a potential link between MPX with SARS-CoV-2 in Covid-19 era.
Insights
Heparanase (HPSE) plays a key role in severe inflammation and blood clotting during SARS-CoV-2 and monkeypox virus infections. Inhibiting HPSE may reduce disease severity and complications in co-infected patients.
Area of Science:
- Biochemistry
- Virology
- Immunology
Background:
- Heparanase (HPSE) is an enzyme that degrades heparan sulfate (HS) in the extracellular matrix.
- HPSE activity is linked to inflammation, cytokine storm, and coagulopathy.
- Both SARS-CoV-2 and monkeypox virus (MPXV) induce HPSE expression.
Purpose of the Study:
- To investigate the role of HPSE in SARS-CoV-2 and MPXV infections.
- To explore HPSE as a potential therapeutic target for viral co-infections.
Main Methods:
- The study focuses on the molecular interactions and biological consequences of HPSE activity.
- Analysis of HPSE induction by SARS-CoV-2 and MPXV.
- Discussion of potential therapeutic strategies targeting HPSE.
Main Results:
- HPSE cleavage of HS activates autophagy and releases growth factors.
- HPSE triggers pro-inflammatory cytokine release, leading to hyperinflammation and cytokine storm.
- HPSE contributes to endothelial dysfunction and thrombotic events in viral infections.
Conclusions:
- HPSE is implicated in the pathogenesis of both SARS-CoV-2 and MPXV infections.
- Co-infection with SARS-CoV-2 and MPXV may exacerbate HPSE-mediated complications.
- Targeting HPSE with inhibitors could mitigate severe outcomes in these viral infections.
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