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Related Concept Videos

Inhibitors of Viral Protein Synthesis01:30

Inhibitors 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...
Inhibitors Of Virion Release01:25

Inhibitors 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...
Inhibitors of Virion Maturation and Assembly01:19

Inhibitors 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...

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Related Experiment Video

Updated: Jun 26, 2026

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
11:28

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Published on: October 7, 2011

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Zinc Influx Restricts Enterovirus D68 Replication.

Shunan Liu1, Xia Cao1, Haoran Guo2

  • 1Department of Pharmacology, School of Pharmacy, Jilin University, Changchun, China.

Frontiers in Microbiology
|November 1, 2021
PubMed
Summary

Zinc ions show significant antiviral activity against Enterovirus D68 (EV-D68) by inhibiting viral replication and production. Enhancing zinc influx presents a promising therapeutic strategy for treating EV-D68 infections.

Keywords:
EV-D68antiviral agentsenteroviruspyrrolidine dithiocarbamatezinc influx

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Last Updated: Jun 26, 2026

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Area of Science:

  • Virology
  • Infectious Diseases
  • Drug Discovery

Background:

  • Enterovirus D68 (EV-D68) is a significant respiratory pathogen responsible for severe disease and neurological complications.
  • Global outbreaks since 2014 highlight the urgent need for effective EV-D68 therapeutics, as no approved antiviral agents or vaccines currently exist.

Purpose of the Study:

  • To investigate the antiviral potential of zinc ions against EV-D68 infection.
  • To explore the mechanisms underlying zinc's antiviral activity and its therapeutic implications.

Main Methods:

  • In vitro assessment of zinc salt activity against EV-D68.
  • Evaluation of viral RNA replication, protein synthesis, virion production, and cytopathic effects.
  • Analysis of zinc chloride (ZnCl2) effects on viral attachment and protein VP1 synthesis.
  • Investigation of zinc ionophore effects on anti-EV-D68 activity.

Main Results:

  • Zinc ions demonstrated potent antiviral activity against EV-D68 in vitro, suppressing viral RNA replication, protein synthesis, and infectious virion production.
  • Zinc treatment inhibited cytopathic effects with low cytotoxicity (EC50=0.033mM).
  • Zinc chloride moderately inhibited viral attachment, and enhanced zinc influx via ionophores boosted antiviral efficacy.

Conclusions:

  • Zinc ions possess substantial antiviral properties against EV-D68.
  • Enhancing cellular zinc influx is a viable therapeutic strategy for managing EV-D68 infections.