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Updated: Oct 17, 2025

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons
09:11

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

Published on: August 23, 2016

21.0K

Cell membrane skeletal protein 4.1R participates in entry of Zika virus into cells

Shan Su1, Xin Liu2, Ren-Rong Tian3

  • 1Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences /Key Laboratory of Bioactive Peptides of Yunnan Province, KIZ-CUHK Joint Laboratory of Bioresources and Molecular Research in Common Diseases, Center for Biosafety Mega-Science, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, China; School of Life Sciences, Zhengzhou University, Zhengzhou 450001, China.

Virus Research
|October 12, 2021
PubMed

Insights

Zika virus (ZIKV) infection relies on the host cell protein 4.1R. This protein is crucial for viral entry and replication, highlighting a potential therapeutic target for ZIKV.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Zika virus (ZIKV), a mosquito-borne flavivirus, causes severe congenital abnormalities and neurological disorders.
  • No specific antiviral treatments or vaccines are currently available for ZIKV.
  • Viruses utilize host cell membrane skeletal proteins for critical life cycle stages like entry and release.

Purpose of the Study:

  • To identify host cell proteins interacting with ZIKV.
  • To investigate the role of identified host proteins in ZIKV infection.
  • To explore potential therapeutic targets for ZIKV.

Main Methods:

  • Immunoprecipitation assays to detect protein interactions.
  • ZIKV envelope (E) protein and host cell membrane skeleton protein 4.1R interaction analysis.
  • Assessment of viral titer and protein synthesis following 4.1R deletion.

Main Results:

  • The Axl receptor and ZIKV envelope (E) protein were found to interact with host cell membrane skeleton protein 4.1R.
  • Deletion of 4.1R significantly reduced ZIKV titer.
  • Viral protein synthesis was notably decreased in the absence of 4.1R.

Conclusions:

  • Host cell membrane skeleton protein 4.1R is essential for ZIKV infection.
  • 4.1R plays a significant role in the ZIKV life cycle, potentially during viral entry.
  • Targeting 4.1R could be a novel strategy for ZIKV treatment.
Keywords:
4.1R proteinMembrane skeleton proteinVirus-host cell protein interactionZika virus

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