Purpose of Review <p>This review explores the critical interactions between Zika virus (ZIKV) and human cell receptors, focusing on their roles in viral entry, pathogenesis, and potential therapeutic interventions.</p> Recent Findings <p>Recent studies have identified several key receptors involved in ZIKV infection, including phosphatidylserine receptors (TYRO- 3, AXL, TIM- 1), C-type lectin receptors (DC-SIGN, CLEC5 A), immunoglobulin superfamily cell adhesion molecule (NCAM1), integrin αVβ5, glycosaminoglycans (GAGs), receptor tyrosine kinases (EGFR), and Fc gamma receptors (FCγR). These interactions play a pivotal role in ZIKV's cellular tropism and immune evasion mechanisms, highlighting their importance in viral pathogenesis and making them promising targets for therapeutic development.</p> Summary <p>ZIKV, a mosquito-borne flavivirus first identified in 1947, typically causes mild symptoms in adults, such as fever, rash, conjunctivitis, and joint pain. However, it has gained global attention due to its association with severe clinical outcomes, including congenital abnormalities like microcephaly and neurological disorders such as Guillain-Barré syndrome. A comprehensive understanding of the molecular mechanisms underlying ZIKV-receptor interactions is crucial for developing targeted therapies. Further research is needed to elucidate the precise roles of these receptors in infection and to evaluate their potential as drug targets for preventing and treating ZIKV-associated diseases.</p>

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Unlocking the Gate: Keys to Understanding Zika Virus Interactions with Human Cell Receptors

  • Janina N. Robles-Minutti,
  • Mario A. Cuapa-González,
  • Luis Márquez-Domínguez,
  • Margarita M. P. Arenas-Hernández,
  • Gerardo Santos-López

摘要

Purpose of Review

This review explores the critical interactions between Zika virus (ZIKV) and human cell receptors, focusing on their roles in viral entry, pathogenesis, and potential therapeutic interventions.

Recent Findings

Recent studies have identified several key receptors involved in ZIKV infection, including phosphatidylserine receptors (TYRO- 3, AXL, TIM- 1), C-type lectin receptors (DC-SIGN, CLEC5 A), immunoglobulin superfamily cell adhesion molecule (NCAM1), integrin αVβ5, glycosaminoglycans (GAGs), receptor tyrosine kinases (EGFR), and Fc gamma receptors (FCγR). These interactions play a pivotal role in ZIKV's cellular tropism and immune evasion mechanisms, highlighting their importance in viral pathogenesis and making them promising targets for therapeutic development.

Summary

ZIKV, a mosquito-borne flavivirus first identified in 1947, typically causes mild symptoms in adults, such as fever, rash, conjunctivitis, and joint pain. However, it has gained global attention due to its association with severe clinical outcomes, including congenital abnormalities like microcephaly and neurological disorders such as Guillain-Barré syndrome. A comprehensive understanding of the molecular mechanisms underlying ZIKV-receptor interactions is crucial for developing targeted therapies. Further research is needed to elucidate the precise roles of these receptors in infection and to evaluate their potential as drug targets for preventing and treating ZIKV-associated diseases.