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Heparanase 2 Modulation Inhibits HSV-2 Replication by Regulating Heparan Sulfate
James Hopkins1,2, Ipsita Volety1,3, Farreh Qatanani1
1Department of Ophthalmology and Visual Sciences, College of Medicine, University of Illinois Chicago, Chicago, IL 60612, USA.
Viruses
|January 8, 2025
Summary
The herpes simplex virus type 2 (HSV-2) uses heparanase (HPSE) to spread. A related protein, HPSE 2, blocks this process by regulating heparan sulfate (HS) availability, impacting viral replication.
Area of Science:
- Virology
- Molecular Biology
- Biochemistry
Background:
- Heparanase (HPSE) cleaves heparan sulfate (HS) on cell surfaces, aiding herpes simplex virus type 2 (HSV-2) release.
- HPSE 2 is an HPSE isoform that binds HS but lacks enzymatic activity.
Purpose of the Study:
- To investigate the role of HPSE 2 in HSV-2 replication.
- To elucidate the mechanism by which HPSE 2 influences viral pathogenesis.
Main Methods:
- Assessing HPSE 2 protein levels during HSV-2 infection.
- Manipulating HPSE 2 expression using plasmid transfection and siRNA.
- Evaluating the impact of HPSE 2 on HPSE activity and HS cleavage.
- Quantifying effects on viral entry and egress.
Main Results:
- HSV-2 infection significantly increases HPSE 2 protein levels.
- Elevated HPSE 2 reduces HPSE-mediated HS cleavage, hindering viral egress.
- Reduced HPSE 2 levels enhance HS cleavage, impeding viral entry.
- HPSE 2 acts as a competitive inhibitor of HPSE, modulating HS availability.
Conclusions:
- HPSE 2 plays a dual role in regulating HSV-2 replication by controlling cell surface HS availability.
- Modulation of HPSE 2 offers a potential strategy to impede HSV-2 pathogenesis.
- HPSE 2's functions extend to potential tumor suppression, highlighting its broader biological significance.
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