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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...
Antiviral Nucleoside Inhibitors01:22

Antiviral Nucleoside Inhibitors

Antiviral Nucleoside InhibitorsAntiviral nucleoside inhibitors are structural analogs of natural nucleosides that interfere with viral DNA or RNA synthesis. These compounds selectively target viral polymerases due to their resemblance to host nucleosides, thereby disrupting viral genome replication.Mechanism of Acyclovir ActionAcyclovir is a guanosine analog with a three-carbon acyclic side chain. It selectively targets herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2),...
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 19, 2026

Early Viral Entry Assays for the Identification and Evaluation of Antiviral Compounds
09:29

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Punicalagin Inhibits African Swine Fever Virus Replication by Targeting Early Viral Stages and Modulating

Renhao Geng1,2, Dan Yin1,2, Yingnan Liu3

  • 1College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China.

Veterinary Sciences
|September 27, 2024
PubMed
Summary

Punicalagin, a compound from pomegranate peel, effectively inhibits African swine fever virus (ASFV) replication by blocking early viral stages and inactivating the virus. This natural compound shows promise for developing new drugs against ASFV.

Keywords:
African swine fever virusNF-κB/STAT3/NLRP3library screenpunicalaginreplication stages

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Area of Science:

  • Veterinary Virology
  • Natural Product Chemistry
  • Immunology

Background:

  • African swine fever (ASF) poses a significant threat to the global swine industry, with no effective vaccines currently available.
  • Developing antiviral drugs is a critical strategy for controlling African swine fever virus (ASFV) outbreaks.

Purpose of the Study:

  • To screen for compounds inhibiting ASFV replication.
  • To investigate the antiviral mechanism of punicalagin against ASFV.

Main Methods:

  • Screening of a 536-compound antiviral library.
  • Cell-based assays (MA-104, PK-15, WSL, 3D4/21 cells) to assess viral inhibition.
  • Time-of-addition, virucidal assays, RT-qPCR, and Western blot to elucidate the mechanism of action.
  • Analysis of the NF-κB/STAT3/NLRP3 inflammasome pathway.

Main Results:

  • Punicalagin significantly inhibited ASFV replication across multiple cell lines.
  • Punicalagin interfered with early viral replication, including attachment and internalization.
  • Direct virucidal activity of punicalagin against ASFV was confirmed.
  • Punicalagin modulated the NF-κB/STAT3/NLRP3 inflammasome pathway and reduced ASFV-induced inflammation.

Conclusions:

  • Punicalagin exhibits potent anti-ASFV activity.
  • The mechanism involves inhibition of early viral replication and modulation of host inflammatory responses.
  • Punicalagin holds potential as a therapeutic agent for African swine fever.