Video Experimental Relacionado

Updated: May 6, 2026

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons

Published on: August 23, 2016

Virus Zika e interacciones de proteínas del huésped para comprender los mecanismos moleculares de la patogénesis y el

Xiaodong Han¹, Jiansen Du², Wenhui Li¹

¹College of Life Sciences, Inner Mongolia Agriculture University, Hohhot, Inner Mongolia, China.

Frontiers in cellular and infection microbiology

|February 20, 2026

Abstract:

Zika virus (ZIKV) causes severe neurological disease, including microcephaly and Guillain-Barré syndrome, through complex interactions with host cell proteins. This review synthesizes the 2015-2025 published literature on ZIKV-host protein interactions and their therapeutic targeting. ZIKV enters cells via multiple receptor pathways: adhesion receptors (DC-SIGN, Hsp70), high-affinity entry receptors (ITGB4, GRP78, NCAM1), internalization receptors (integrin αvβ5, sialic acid), and endosomal receptors (AXL, TIM-1, CD300a). Viral structural proteins direct virion assembly, while nonstructural proteins NS1-NS5 suppress immune responses, remodel cellular membranes, and dysregulate gene expression. NS5 uniquely suppresses neurodevelopmental genes and disrupts ciliary function through nuclear localization, directly driving microcephaly pathogenesis. Therapeutic strategies include receptor antagonists, protease inhibitors, and polymerase inhibitors. However, receptor redundancy, viral protein multifunctionality, and pregnancy safety constraints limit clinical translation. This review identifies ZIKV-host protein interactions as therapeutic targets and highlights barriers to drug development.

Palabras clave:

Virus Zika desarrollo de fármacos antivirales patogénesis de flavivirus receptores de entrada de virus interacciones proteína-huésped de virus

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