Related Experiment Video
Updated: Jun 21, 2026
09:11
Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons
Published on: August 23, 2016
20.8K
ZDHHC11 Suppresses Zika Virus Infections by Palmitoylating the Envelope Protein
Dingwen Hu1, Haimei Zou2, Weijie Chen3
1State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China.
Viruses
|January 21, 2023
Summary
Zika virus (ZIKV) infection is worsened by inhibiting palmitoylation. The enzyme ZDHHC11 palmitoylates the ZIKV envelope protein, suppressing viral infection.
Area of Science:
- Virology
- Biochemistry
- Molecular Biology
Background:
- Zika virus (ZIKV), a flavivirus, causes neurodegenerative diseases and male infertility.
- Palmitoylation, a post-translational modification, is crucial in biological processes and viral infections.
- The role of palmitoylation in ZIKV infection regulation was previously uninvestigated.
Purpose of the Study:
- To investigate the role of palmitoylation in ZIKV infection.
- To identify the specific protein modification and the enzyme involved.
- To elucidate the mechanism by which palmitoylation affects ZIKV replication.
Main Methods:
- Inhibition of palmitoylation using 2-bromopalmitate (2-BP).
- Identification of the palmitoylated site on the ZIKV envelope protein (Cys308).
- Screening and identification of the palmitoyl transferase (ZDHHC11) interacting with ZIKV envelope protein.
Main Results:
- Inhibition of palmitoylation enhanced ZIKV infection.
- ZIKV envelope protein was confirmed to be palmitoylated at Cys308.
- ZDHHC11 was identified as the primary enzyme catalyzing ZIKV envelope protein palmitoylation.
- ZDHHC11 suppressed ZIKV infection in an enzymatic activity-dependent manner.
- Knockdown of ZDHHC11 led to increased ZIKV infection.
Conclusions:
- ZIKV envelope protein undergoes a novel post-translational modification via palmitoylation.
- ZDHHC11 suppresses ZIKV infection through the palmitoylation of the ZIKV envelope protein.
- This study reveals a new mechanism for controlling ZIKV pathogenesis.
Related Concept Videos
01:30Inhibitors of Viral Protein Synthesis
Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
01:25Inhibitors Of Virion Release
Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...
01:19Inhibitors of Virion Maturation and Assembly
As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...