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

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...
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...
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
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...
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’...

You might also read

Related Articles

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

Sort by
Same author

Aligning clinical care with consumer priorities: an adult cystic fibrosis centre experience of co-designing a model of care.

Internal medicine journal·2026
Same author

Calcium triggers <i>Cryptococcus neoformans</i> aggregation by forming coordination bonds with capsular glucuronoxylomannan.

bioRxiv : the preprint server for biology·2026
Same author

Amphotericin B Resistance in <i>Lomentospora prolificans</i> is associated with a soluble cell wall component.

bioRxiv : the preprint server for biology·2026
Same author

Inhibitory potential of autologous neutralizing antibodies sets quantitative limits on the rebound-competent HIV-1 reservoir.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Prone Positioning Is a Feasible Approach in the Diagnostic Work-Up of Posterior Pulmonary Nodules and a Means to Limit CT-to-Body Divergence: A Retrospective Cohort Study.

Diseases (Basel, Switzerland)·2026
Same author

Did avian-like pulmonary anatomy increase the susceptibility of dinosaurs to fungal diseases? Extending the "fungal infection mammalian selection" hypothesis.

mBio·2026

Related Experiment Video

Updated: Jun 23, 2026

High Throughput In Vitro Assessment of Latency Reversing Agents on HIV Transcription and Splicing
07:18

High Throughput In Vitro Assessment of Latency Reversing Agents on HIV Transcription and Splicing

Published on: January 22, 2019

Antigen Stimulation Reactivates HIV-1 Proviruses Despite Integration in Repressive Chromatin.

Angelica Camilo-Contreras1, Filippo Dragoni1, Hao Zhang2

  • 1Johns Hopkins University, Department of Medicine, Division of Infectious Diseases, Baltimore, MD, USA.

Biorxiv : the Preprint Server for Biology
|June 22, 2026
PubMed
Summary

Antigen stimulation can reactivate latent HIV-1 proviruses, even those in repressive genomic areas. This suggests that deeply latent viruses can contribute to persistent HIV-1 infection and viral rebound after stopping antiretroviral therapy (ART).

Keywords:
Antigen StimulationHIV-1Quantitative Viral Outgrowth AssayRepressive ChromatinViral LatencyViral reactivation

More Related Videos

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

CRISPR-Cas9-based Genome Engineering to Generate Jurkat Reporter Models for HIV-1 Infection with Selected Proviral Integration Sites
14:27

CRISPR-Cas9-based Genome Engineering to Generate Jurkat Reporter Models for HIV-1 Infection with Selected Proviral Integration Sites

Published on: November 14, 2018

Related Experiment Videos

Last Updated: Jun 23, 2026

High Throughput In Vitro Assessment of Latency Reversing Agents on HIV Transcription and Splicing
07:18

High Throughput In Vitro Assessment of Latency Reversing Agents on HIV Transcription and Splicing

Published on: January 22, 2019

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

CRISPR-Cas9-based Genome Engineering to Generate Jurkat Reporter Models for HIV-1 Infection with Selected Proviral Integration Sites
14:27

CRISPR-Cas9-based Genome Engineering to Generate Jurkat Reporter Models for HIV-1 Infection with Selected Proviral Integration Sites

Published on: November 14, 2018

Area of Science:

  • Virology
  • Immunology
  • Genomics

Background:

  • Intact HIV-1 proviruses accumulate in transcriptionally repressive regions during long-term antiretroviral therapy (ART) and in elite controllers.
  • This enrichment raises questions about the potential for these latent proviruses to reactivate in vivo.

Purpose of the Study:

  • To investigate whether specific antigen stimulation can overcome epigenetic repression and induce reactivation of latent HIV-1 proviruses.
  • To assess the capacity of proviruses integrated into repressive chromatin to produce infectious virus upon stimulation.

Main Methods:

  • Utilized an antigen-restricted quantitative viral outgrowth assay (ag qVOA).
  • Analyzed cells from two people with HIV (PWH) on ART: one on long-term treatment and one elite controller.
  • Tested the effect of cognate antigen stimulation on proviral latency.

Main Results:

  • Antigen-specific stimulation successfully induced viral outgrowth from intact HIV-1 proviruses.
  • Reactivation occurred from proviruses integrated into a pericentromeric transition region and a zinc finger gene.
  • Demonstrated that antigen recognition can reverse latency in proviruses with low inducibility.

Conclusions:

  • Cognate antigen stimulation can overcome epigenetic constraints to reactivate latent HIV-1.
  • Proviruses residing in transcriptionally repressive regions, considered 'deeper latency,' can be induced.
  • These findings imply that deeply latent HIV-1 reservoirs may contribute to residual viremia and viral rebound after ART interruption.