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Related Concept Videos

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...
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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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Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the retrovirus to...
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Viruses are extraordinarily diverse in shape and size, but they all have several structural features in common. All viruses have a core that contains a DNA- or RNA-based genome. The core is surrounded by a protective coat of proteins called the capsid. The capsid is composed of subunits called capsomeres. The capsid and genome-containing core are together known as the nucleocapsid.
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Receptor-mediated Endocytosis

Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
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Updated: Jun 15, 2026

Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1
11:56

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Published on: August 24, 2015

Cholesterol-binding viral proteins in virus entry and morphogenesis.

Cornelia Schroeder1

  • 1Max Planck Institute for Molecular Cell Biology and Genetics, Pfotenhauerstr. 108, D-01307, Dresden, Germany. cornelia.schroeder@mpi-cbg.de

Sub-Cellular Biochemistry
|March 10, 2010
PubMed
Summary
This summary is machine-generated.

Viral proteins like HIV gp41, influenza M2, and Semliki Forest virus E1 bind cholesterol, impacting virus entry, assembly, and budding. This cholesterol interaction is crucial for viral lifecycle and pathogenesis.

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Area of Science:

  • Virology
  • Molecular Biology
  • Biochemistry

Background:

  • Cholesterol binding by viral proteins is implicated in virus entry and morphogenesis.
  • Few viral cholesterol-binding proteins have been characterized, including those in HIV, influenza A virus, and Semliki Forest virus.

Purpose of the Study:

  • To explore the role of cholesterol binding in viral proteins.
  • To investigate the mechanisms and implications of cholesterol-protein interactions in viral lifecycle.

Main Methods:

  • Characterization of viral proteins and their interaction with cholesterol.
  • Site-directed mutagenesis to study the function of cholesterol recognition consensus (CRAC) motifs.
  • Analysis of viral fusion, assembly, and budding processes.
  • Use of cholesterol affinity columns and artificial membranes.

Main Results:

  • HIV gp41 uses a CRAC motif for cholesterol binding, essential for fusion.
  • Influenza A virus M2 protein binds cholesterol via CRAC motifs, influencing assembly and virulence.
  • Semliki Forest virus E1 protein directly binds cholesterol, affecting budding and host range.

Conclusions:

  • Cholesterol binding is a significant factor in the lifecycle of various viruses.
  • Viral proteins utilize specific motifs, such as CRAC, to interact with cholesterol.
  • Targeting these cholesterol-binding interactions could offer new antiviral strategies.