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Hepatitis

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...

Cofactors and Coenzymes

Cofactors and Coenzymes

Enzymes require additional components for proper function. There are two such classes of molecules: cofactors and coenzymes. Cofactors are metallic ions and coenzymes are non-protein organic molecules. Both of these types of helper molecule can be tightly bound to the enzyme or bound only when the substrate binds.

Cofactors and Coenzymes

Cofactors and Coenzymes

Enzymes are proteins made of amino acids. The functional group of each constituent amino acid catalyzes a wide variety of chemical reactions via ionic interactions or acid-base reactions. However, amino acids cannot catalyze oxidation-reduction and group transfer reactions and need to be aided by non-protein components called cofactors. Cofactors are also referred to as the chemical teeth of an enzyme.
Cofactors can be metallic ions or organic molecules called coenzymes. These types of helper...

Cofactors and Coenzymes

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Inhibitors of Viral Protein Synthesis

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Inhibitors Of Virion Release

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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...

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Updated: Jun 15, 2026

A Protocol for Analyzing Hepatitis C Virus Replication

A Protocol for Analyzing Hepatitis C Virus Replication

Published on: June 26, 2014

Potential roles for cellular cofactors in hepatitis C virus replication complex formation.

Kristi L Berger¹, Glenn Randall

¹Department of Microbiology; The University of Chicago, Chicago, IL, USA.

Communicative & Integrative Biology

|March 3, 2010

Summary

Hepatitis C virus (HCV) replication requires phosphatidylinositol 4-kinase III alpha (PI4K-IIIalpha). Targeting PI4K-IIIalpha may offer new antiviral strategies against chronic HCV infection.

Keywords:

HCV replication membrane trafficking membranous web phosphatidylinositol kinase

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Published on: May 10, 2022

Area of Science:

Virology
Cell Biology
Biochemistry

Background:

Hepatitis C virus (HCV) chronically infects over 130 million people globally.
Current HCV therapies have limitations, necessitating novel antiviral strategies.
Identifying host cellular cofactors is crucial for expanding therapeutic targets.

Purpose of the Study:

To investigate the role of host cellular cofactors in hepatitis C virus (HCV) replication.
To identify specific host genes essential for HCV infection and replication.
To elucidate the mechanism by which phosphatidylinositol 4-kinase III alpha (PI4K-IIIalpha) contributes to HCV replication.

Main Methods:

Conducted an RNA interference screen of host membrane trafficking genes in HCV infection.
Utilized small interfering RNAs (siRNAs) to silence PI4K-IIIalpha expression.
Examined the co-localization of PI4K-IIIalpha with viral replication markers.
Assessed the impact of PI4K-IIIalpha silencing on the formation of the membranous web, a hallmark of HCV replication.

Main Results:

Identified phosphatidylinositol 4-kinase III alpha (PI4K-IIIalpha) as essential for HCV replication.
Demonstrated that PI4K-IIIalpha co-localizes with viral replication markers.
Showed that silencing PI4K-IIIalpha prevents the formation of the membranous web, crucial for viral replication complexes.
Observed that PI4K-IIIalpha is involved in establishing HCV replication complexes.

Conclusions:

Phosphatidylinositol 4-kinase III alpha (PI4K-IIIalpha) plays a critical role in establishing hepatitis C virus (HCV) replication complexes.
PI4K-IIIalpha may nucleate replication complex formation by mediating protein-phospholipid interactions at cellular membranes.
Targeting PI4K-IIIalpha represents a potential therapeutic strategy for developing new antiviral treatments for HCV.