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Related Concept Videos

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...
Pinching-off of Coated Vesicles01:32

Pinching-off of Coated Vesicles

Vesicle budding is orchestrated by distinct cytosolic proteins such as adaptor proteins, coat proteins, and GTPases. To initiate vesicle budding, membrane-bending proteins containing crescent-shaped BAR domains bind to the lipid heads in the bilayer and distort the membrane to form a protein-coated vesicle bud. Adaptors proteins such as AP2 for clathrin-coated vesicles can nucleate on the deformed membrane. Finally, coat proteins such as clathrin or COPI and COPII assemble into a coat forming...
Size and Structure of Viral Genomes01:26

Size and Structure of Viral Genomes

Viral genomes exhibit remarkable diversity in size, structure, and composition, influencing their replication strategies and interactions with host cells. These genomes consist of either DNA or RNA and may be linear or circular. Additionally, they can be single-stranded or double-stranded, with each configuration affecting how the virus propagates within a host. RNA viruses, for instance, generally have smaller genomes than DNA viruses, a factor that contributes to their high mutation rates and...
Retrovirus Life Cycles01:10

Retrovirus Life Cycles

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...
Intralumenal Vesicles and Multivesicular Bodies01:38

Intralumenal Vesicles and Multivesicular Bodies

Intraluminal vesicles (ILVs) are small vesicles 50-80 nm in diameter formed during the maturation of early endosomes. A specialized endosome containing numerous ILVs is called a multivesicular body (MVB). ILVs contain internalized molecules such as antigens, nucleic acids, proteins, and metabolites. Some of these molecules are released from the MVBs inside exosomes and are transported to other cells. Other MVBs contain molecules that are retained in the ILVs and are later degraded within the...
Retroviruses02:33

Retroviruses

Retroviruses and retrotransposons both insert copies of their genetic elements into the genome of the host cell. Thus, the viral genes are passed on when the host genome is replicated or translated. A typical retroviral DNA sequence contains 3-4 genes that encode the different proteins required for its structural assembly and function as a molecular parasite. This DNA is transcribed into a single mRNA, which is very similar in structure to conventional mRNAs, i.e., it is capped at the 5’...

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Related Experiment Video

Updated: Jun 3, 2026

Measurement of In Vitro Integration Activity of HIV-1 Preintegration Complexes
10:34

Measurement of In Vitro Integration Activity of HIV-1 Preintegration Complexes

Published on: February 22, 2017

Essential ingredients for HIV-1 budding.

Winfried Weissenhorn1, Heinrich Göttlinger2

  • 1UVHCI UMI 3265 University Joseph Fourier-EMBL-CNRS, 6 rue Jules Horowitz, 38042 Grenoble, France.

Cell Host & Microbe
|March 16, 2011
PubMed
Summary
This summary is machine-generated.

Human immunodeficiency virus type 1 (HIV-1) uses the host cell's ESCRT-III/VPS4 machinery for viral release. New research reveals HIV-1 needs only a small, transient ESCRT-III subset, dependent on VPS4, for efficient viral escape.

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In vitro Uncoating of HIV-1 Cores
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In vitro Uncoating of HIV-1 Cores

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A High-throughput Cre-Lox Activated Viral Membrane Fusion Assay to Identify Inhibitors of HIV-1 Viral Membrane Fusion
07:22

A High-throughput Cre-Lox Activated Viral Membrane Fusion Assay to Identify Inhibitors of HIV-1 Viral Membrane Fusion

Published on: August 14, 2018

Related Experiment Videos

Last Updated: Jun 3, 2026

Measurement of In Vitro Integration Activity of HIV-1 Preintegration Complexes
10:34

Measurement of In Vitro Integration Activity of HIV-1 Preintegration Complexes

Published on: February 22, 2017

In vitro Uncoating of HIV-1 Cores
10:49

In vitro Uncoating of HIV-1 Cores

Published on: November 8, 2011

A High-throughput Cre-Lox Activated Viral Membrane Fusion Assay to Identify Inhibitors of HIV-1 Viral Membrane Fusion
07:22

A High-throughput Cre-Lox Activated Viral Membrane Fusion Assay to Identify Inhibitors of HIV-1 Viral Membrane Fusion

Published on: August 14, 2018

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • The human immunodeficiency virus type 1 (HIV-1) utilizes host cell machinery for its replication and egress.
  • The Endosomal Sorting Complexes Required for Transport (ESCRT)-III complex and its associated ATPase VPS4 are crucial for cellular membrane remodeling events, including scission.

Discussion:

  • This study investigates the precise role of the ESCRT-III/VPS4 machinery in HIV-1 virion release.
  • It elucidates the minimal ESCRT-III components required for viral scission and how VPS4 activity regulates this process.

Key Insights:

  • HIV-1 egress depends on the transient recruitment of a limited subset of ESCRT-III proteins.
  • The membrane scission function mediated by ESCRT-III during HIV-1 release is critically dependent on VPS4 ATPase activity.

Outlook:

  • Further research can explore the specific interactions between HIV-1 components and the minimal ESCRT-III subset.
  • Understanding this mechanism could reveal new therapeutic targets for inhibiting HIV-1 replication and spread.