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

Viral Mutations00:36

Viral Mutations

33.0K
A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material...
33.0K
Size and Structure of Viral Genomes01:26

Size and Structure of Viral Genomes

1.2K
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...
1.2K
Retrovirus Life Cycles01:10

Retrovirus Life Cycles

43.0K
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...
43.0K
Retroviruses02:33

Retroviruses

12.1K
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’...
12.1K
Viruses with RNA Genomes01:29

Viruses with RNA Genomes

1.5K
RNA viruses are categorized into positive-strand, negative-strand, or double-stranded groups based on their genomic structure and replication mechanisms. This classification dictates how they exploit host cellular machinery for protein synthesis and replication. Some RNA viruses also utilize reverse transcription as part of their life cycle, further diversifying their replication strategies.Positive-Strand RNA VirusesPositive-strand RNA viruses have genomes that function directly as messenger...
1.5K
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

5.2K
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...
5.2K

You might also read

Related Articles

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

Sort by
Same author

Prognostic value of circulating tumor DNA in pancreatic cancer: a systematic review and meta-analysis.

Aging·2020
Same author

The role of ferroptosis regulators in the prognosis, immune activity and gemcitabine resistance of pancreatic cancer.

Annals of translational medicine·2020
Same author

The vascular endothelial growth factor trap aflibercept induces vascular dysfunction and hypertension via attenuation of eNOS/NO signaling in mice.

Acta pharmacologica Sinica·2020
Same author

MBNL1 regulates isoproterenol-induced myocardial remodelling in vitro and in vivo.

Journal of cellular and molecular medicine·2020
Same author

Platelets Stimulate Liver Regeneration in a Rat Model of Partial Liver Transplantation.

Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society·2020
Same author

Mutant p53 in Cancer Progression and Targeted Therapies.

Frontiers in oncology·2020

Related Experiment Video

Updated: May 1, 2026

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

15.2K

HIV-1 mutates to evade IFITM1 restriction.

Shilei Ding1, Qinghua Pan2, Shan-Lu Liu3

  • 1Lady Davis Institute, Jewish General Hospital, Montreal, QC, Canada H3T 1E2; Department of Microbiology and Immunology, McGill University, Montreal, QC, Canada H3A 2B4.

Virology
|April 15, 2014
PubMed
Summary

Human immunodeficiency virus type 1 (HIV-1) evades Interferon-induced transmembrane protein 1 (IFITM1) restriction through specific mutations. These mutations enhance viral replication by promoting cell-to-cell transmission, not by overcoming IFITM1

Keywords:
Cell-to-cell transmissionEscape mutationsHIV-1IFITM1

More Related Videos

Pairwise Growth Competition Assay for Determining the Replication Fitness of Human Immunodeficiency Viruses
11:19

Pairwise Growth Competition Assay for Determining the Replication Fitness of Human Immunodeficiency Viruses

Published on: May 4, 2015

12.4K
Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors
05:46

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors

Published on: April 9, 2014

20.3K

Related Experiment Videos

Last Updated: May 1, 2026

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

15.2K
Pairwise Growth Competition Assay for Determining the Replication Fitness of Human Immunodeficiency Viruses
11:19

Pairwise Growth Competition Assay for Determining the Replication Fitness of Human Immunodeficiency Viruses

Published on: May 4, 2015

12.4K
Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors
05:46

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors

Published on: April 9, 2014

20.3K

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Interferon-induced transmembrane (IFITM) proteins are crucial innate immune factors that restrict viral infections.
  • Human immunodeficiency virus type 1 (HIV-1) is susceptible to IFITM-mediated restriction, but the mechanisms by which viruses overcome this barrier are not fully understood.

Purpose of the Study:

  • To investigate how HIV-1 evolves to evade restriction by Interferon-induced transmembrane protein 1 (IFITM1).
  • To identify specific viral mutations that confer resistance to IFITM1 and elucidate the underlying mechanisms.

Main Methods:

  • Passaging HIV-1 in IFITM1-expressing cells to select for resistant variants.
  • Whole-genome sequencing to identify mutations in resistant HIV-1 strains.
  • Functional assays to assess the impact of identified mutations on viral replication and transmission.

Main Results:

  • Selection of IFITM1-resistant HIV-1 strains revealed mutations in the vpu and envelope genes.
  • A combination of mutations, Vpu34 and EnvG367E, was found to enable efficient HIV-1 replication in IFITM1-expressing cells.
  • These mutations enhance viral replication not by counteracting IFITM1-induced downregulation of p24 expression, but by promoting cell-to-cell virus transmission.

Conclusions:

  • HIV-1 can acquire mutations to overcome IFITM1 restriction.
  • Enhanced cell-to-cell transmission is a key mechanism by which HIV-1 evades IFITM1-mediated innate immunity.
  • Understanding these viral evasion strategies is critical for developing effective antiviral therapies.