Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Harmonizing standards and resources for the medical genome.

Nature·2026
Same author

Segmentation-free analysis of live-cell imaging data reveals how T cell modifications influence cancer cell aggregation dynamics.

Scientific reports·2026
Same author

Toward mechanistic virtual immune cells.

Nature biotechnology·2026
Same author

Host Genetic Regulation of NLRP3 Inflammasome Cytokines Reveals Immune and Vascular Pathways in HIV.

medRxiv : the preprint server for health sciences·2026
Same author

Paracrine signals from HIV-1-infected immune cells reprogram cervical cancer pathways.

iScience·2026
Same author

A multi-omics study reveals pathway-level insights and predictive biomarkers in pediatric TB.

Clinical proteomics·2026

Related Experiment Video

Updated: Dec 28, 2025

Humanized NOD/SCID/IL2rγnull (hu-NSG) Mouse Model for HIV Replication and Latency Studies
07:10

Humanized NOD/SCID/IL2rγnull (hu-NSG) Mouse Model for HIV Replication and Latency Studies

Published on: January 7, 2019

16.1K

A Quantitative Genetic Interaction Map of HIV Infection.

David E Gordon1, Ariane Watson2, Assen Roguev3

  • 1Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; Quantitative Biosciences Institute (QBI), University of California, San Francisco, San Francisco, CA 94158, USA; Gladstone Institutes, San Francisco, CA 94158, USA.

Molecular Cell
|February 22, 2020
PubMed
Summary

Researchers mapped HIV-host genetic interactions using a viral host-dependency epistasis map (vE-MAP). This revealed the CNOT complex

Keywords:
CCR4-NOTCNOT complexIRF7combinatorial geneticsepistasis maphost-pathogen network biologyinnate immunityinterferon stimulated genevE-MAPviral infection genetic screen

More Related Videos

A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses
14:23

A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses

Published on: August 31, 2014

16.0K
Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models
09:54

Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models

Published on: December 3, 2019

10.4K

Related Experiment Videos

Last Updated: Dec 28, 2025

Humanized NOD/SCID/IL2rγnull (hu-NSG) Mouse Model for HIV Replication and Latency Studies
07:10

Humanized NOD/SCID/IL2rγnull (hu-NSG) Mouse Model for HIV Replication and Latency Studies

Published on: January 7, 2019

16.1K
A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses
14:23

A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses

Published on: August 31, 2014

16.0K
Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models
09:54

Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models

Published on: December 3, 2019

10.4K

Area of Science:

  • Virology
  • Genetics
  • Immunology

Background:

  • Understanding host-pathogen interactions is crucial for developing antiviral therapies.
  • Genetic interactions reveal cellular pathways essential for viral replication.

Purpose of the Study:

  • To develop a quantitative platform for mapping genetic interactions in viral infections.
  • To construct a comprehensive viral host-dependency epistasis map (vE-MAP) for HIV.
  • To identify novel host factors and pathways critical for HIV infection.

Main Methods:

  • Developed a platform for quantitative genetic interaction mapping using viral infectivity as a readout.
  • Constructed a vE-MAP of 356 human genes involved in HIV function, involving over 63,000 pairwise genetic perturbations.
  • Utilized gene knockouts and functional assays in primary T cells.

Main Results:

  • The vE-MAP provides an extensive view of genetic dependencies in HIV infection.
  • The CNOT complex (including CNOT1, 10, and 11) was identified as a central player.
  • Knockout of CNOT components suppressed HIV infection by upregulating innate immunity pathways.
  • IRF7 deletion rescued the HIV suppression phenotype, uncovering a novel host signaling pathway.

Conclusions:

  • The vE-MAP is a powerful tool for identifying drug targets and studying viral mutations.
  • The CNOT complex and the IRF7-mediated pathway are critical for HIV pathogenesis.
  • The vE-MAP platform is adaptable for studying diverse viral infections and host-pathogen interactions.