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

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...
Viral Mutations00:36

Viral Mutations

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 for adaptive...
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...
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...

You might also read

Related Articles

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

Sort by
Same author

Modeling quantifies in vivo neutralization, Fc-mediated killing, and resistance in human clinical trials of five anti-HIV broadly neutralizing antibodies.

bioRxiv : the preprint server for biology·2026
Same author

Towards modeling phage therapy.

PLoS computational biology·2026
Same author

INHERITANCE OF INTRACELLULAR VIRAL RNA IN A MULTISCALE MODEL OF HEPATITIS C INFECTION.

SIAM journal on applied mathematics·2026
Same author

AZD5582 robustly reactivates latently infected cells and clears the majority of those reactivated from the SIV reservoir.

bioRxiv : the preprint server for biology·2026
Same author

Bemnifosbuvir: An HCV NS5B Inhibitor With Multiple Modes of Action.

Clinical pharmacology and therapeutics·2026
Same author

Dynamics of natural and pharmacologic control of an SIV variant with an envelope trafficking defect.

The Journal of experimental medicine·2025

Related Experiment Video

Updated: Jun 21, 2026

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

Modeling sequence evolution in acute HIV-1 infection.

Ha Youn Lee1, Elena E Giorgi, Brandon F Keele

  • 1Theoretical Biology and Biophysics, Los Alamos National Laboratory, Los Alamos, NM 87545, USA.

Journal of Theoretical Biology
|August 8, 2009
PubMed
Summary
This summary is machine-generated.

This study introduces a mathematical model to simulate human immunodeficiency virus type 1 (HIV-1) evolution during acute infection. The model helps assess sequence diversity and identify single-strain infections versus multiple-strain transmissions.

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

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 21, 2026

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

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

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
  • Computational Biology
  • Evolutionary Genetics

Background:

  • Understanding viral evolution during acute infection is crucial for predicting disease progression and transmission.
  • Human immunodeficiency virus type 1 (HIV-1) exhibits rapid evolution within a host, complicating early infection dynamics.
  • Existing phylogenetic methods often trace lineages backward, which can be challenging for early, rapidly diversifying viral populations.

Purpose of the Study:

  • To develop and validate a mathematical model and Monte Carlo (MC) simulation for analyzing viral evolution during acute HIV-1 infection.
  • To estimate sequence diversity, the most recent common ancestor (MRCA), and coalescence time of transmitted HIV-1 strains.
  • To differentiate between single-strain and multiple-strain HIV-1 transmissions based on sequence diversity.

Main Methods:

  • Developed a mathematical model incorporating synchronous and asynchronous viral infection processes.
  • Utilized Monte Carlo (MC) simulations to model viral diversification forward in time, assuming base substitution without selection pressure.
  • Compared model predictions against 306 envelope gene sequences from eight newly infected individuals.

Main Results:

  • Model predictions showed good agreement with sequence data from 68 patients, supporting the hypothesis of single-strain HIV-1 infection with no selection pressure.
  • Sequence diversity in two patients exceeded model predictions, suggesting the transmission of multiple HIV-1 strains.
  • The model successfully estimated sequence diversity and the probability of the MRCA being the transmitted strain or an evolved variant.

Conclusions:

  • The developed forward-time model provides a robust framework for studying early viral evolution and transmission dynamics.
  • The findings indicate that most acute HIV-1 infections originate from a single transmitted strain, but multiple-strain transmissions can occur.
  • The model is adaptable for analyzing longitudinal data to estimate within-host viral evolutionary parameters.