Plasminogen activator inhibitor-1 regulates Zika virus infection DOI Creative Commons
Miloš Stojanov,

Yen-Chi Chiu,

Amal Fahmi

и другие.

Research Square (Research Square), Год журнала: 2025, Номер unknown

Опубликована: Март 20, 2025

Abstract Zika virus (ZIKV) infection can lead to severe congenital outcomes, yet the mechanisms governing its entry into host cells remain understood. ZIKV is a flavivirus known exploit multiple cellular receptors and cofactors, particularly in neural cells, where result syndrome (CZS). Here we show that plasminogen activator inhibitor-1 (PAI-1), serine protease inhibitor involved hemostasis, directly interacts with particles critically enhances viral replication diverse cell types, including human progenitor three-dimensional organoids. Our findings reveal PAI-1 may contribute through distinct or complementary pathways, underscoring virus’s versatile mechanisms. Inhibition of via tiplaxtinin (TPX) dramatically reduces load impedes infectious particle release, demonstrating dose-dependent effect especially potent models relevant CZS. These results highlight as an essential mediator pathogenesis suggest targeting function could represent novel therapeutic avenue. Given risk future outbreaks devastating impact CZS, interventions aimed at hold promise for reducing global burden infection.

Язык: Английский

Plasminogen activator inhibitor-1 regulates Zika virus infection DOI Creative Commons
Miloš Stojanov,

Yen-Chi Chiu,

Amal Fahmi

и другие.

Research Square (Research Square), Год журнала: 2025, Номер unknown

Опубликована: Март 20, 2025

Abstract Zika virus (ZIKV) infection can lead to severe congenital outcomes, yet the mechanisms governing its entry into host cells remain understood. ZIKV is a flavivirus known exploit multiple cellular receptors and cofactors, particularly in neural cells, where result syndrome (CZS). Here we show that plasminogen activator inhibitor-1 (PAI-1), serine protease inhibitor involved hemostasis, directly interacts with particles critically enhances viral replication diverse cell types, including human progenitor three-dimensional organoids. Our findings reveal PAI-1 may contribute through distinct or complementary pathways, underscoring virus’s versatile mechanisms. Inhibition of via tiplaxtinin (TPX) dramatically reduces load impedes infectious particle release, demonstrating dose-dependent effect especially potent models relevant CZS. These results highlight as an essential mediator pathogenesis suggest targeting function could represent novel therapeutic avenue. Given risk future outbreaks devastating impact CZS, interventions aimed at hold promise for reducing global burden infection.

Язык: Английский

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