Related Experiment Video

Updated: Aug 29, 2026

Structure-Guided Design and Development of Novel Cyclophilin A Inhibitors and Ganoderiol-F Derivatives: An In-Silico Approach
10:01

Structure-Guided Design and Development of Novel Cyclophilin A Inhibitors and Ganoderiol-F Derivatives: An In-Silico Approach

Published on: June 23, 2026

Specific inhibition of hepatitis C virus replication by cyclosporin A

Mina Nakagawa1, Naoya Sakamoto, Nobuyuki Enomoto

  • 1Department of Gastroenterology and Hepatology, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.

Biochemical and Biophysical Research Communications
|December 16, 2003
PubMed

Insights

Cyclosporin A (CsA) effectively inhibits hepatitis C virus (HCV) replication in liver cells without harming them. This antiviral effect occurs at concentrations relevant for clinical use, suggesting CsA as a potential therapeutic agent.

Area of Science:

  • Hepatology and Viral Research
  • Pharmacology and Drug Discovery

Background:

  • Hepatitis C virus (HCV) infection presents treatment challenges due to limited therapeutic options.
  • Cyclosporin A (CsA), an immunosuppressant, has shown potential against HCV, but its mechanism remains unclear.

Purpose of the Study:

  • To investigate the antiviral effects of Cyclosporin A (CsA) on hepatitis C virus (HCV) replication.
  • To explore the mechanism of CsA's action against HCV in vitro.

Main Methods:

  • Utilized a human hepatoma cell line (Huh7) engineered with an HCV replicon (Huh7/Rep-Feo).
  • Assessed HCV replication suppression and cell viability following CsA treatment.
  • Compared CsA's effects with FK506 and evaluated interferon-stimulated gene responses.

Main Results:

  • CsA demonstrated dose-dependent suppression of HCV replication with an IC50 of approximately 0.5 microg/ml.
  • CsA treatment did not affect cell growth or viability, indicating specific antiviral activity.
  • FK506 did not inhibit HCV replication, and CsA's action was independent of interferon pathways.

Conclusions:

  • Cyclosporin A specifically inhibits HCV replication in vitro at clinically relevant concentrations.
  • Understanding CsA's precise mechanism against HCV could reveal novel therapeutic targets.

More Related Videos

A Protocol for Analyzing Hepatitis C Virus Replication13:04

A Protocol for Analyzing Hepatitis C Virus Replication

Published on: June 26, 2014

Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors16:49

Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors

Published on: July 16, 2012

Related Concept Videos

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),...
Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
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...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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...