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Related Concept Videos

Viral Mutations00:36

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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...
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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...
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Among the three main modes of HGT—transformation, conjugation, and transduction—transduction is unique in that it is mediated by bacteriophages, or bacterial viruses.Transduction occurs in two ways. Generalized transduction occurs during the lytic cycle of a bacteriophage infection. In this process, bacteriophages infect bacterial cells, replicate within them, and ultimately cause cell lysis, releasing newly assembled virions. Occasionally, random fragments of the bacterial genome...
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Related Experiment Video

Updated: Oct 4, 2025

A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses
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Evolution during primary HIV infection does not require adaptive immune selection.

David A Swan1, Morgane Rolland2,3, Joshua T Herbeck4

  • 1Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109.

Proceedings of the National Academy of Sciences of the United States of America
|February 11, 2022
PubMed
Summary
This summary is machine-generated.

Host immunity controls human immunodeficiency virus (HIV) viral load but not its evolution. Viral evolution is driven by intrinsic fitness distributions, not adaptive immunity, during primary HIV infection.

Keywords:
HIV primary infectionphylodynamicsphylogeneticsviral dynamics modelingviral evolution

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Area of Science:

  • Virology
  • Evolutionary Biology
  • Immunology
  • Computational Biology

Background:

  • Modern human immunodeficiency virus (HIV) research relies on viral sequencing and population measurements.
  • Linking mechanistic biological processes and evolutionary dynamics during HIV infection is crucial for understanding disease progression.

Purpose of the Study:

  • To develop and validate within-host phylodynamic models of HIV primary infection.
  • To compare model predictions with viral load and evolutionary dynamics data.
  • To elucidate the drivers of viral evolution during primary HIV infection.

Main Methods:

  • Development of multiple within-host phylodynamic models for HIV primary infection.
  • Comparative validation of models against viral load and evolutionary dynamics data.
  • Analysis of viral fitness distributions and selection pressures.

Main Results:

  • The optimal model indicated no positive selection during primary HIV infection.
  • Host adaptive immunity reduced viral load but did not drive viral evolution.
  • Viral fitness distributions, primarily exponential with mostly neutral evolution, were similar in vivo and in vitro, suggesting intrinsic viral properties drive evolution.

Conclusions:

  • Host adaptive immunity controls viral load but not viral evolution during primary HIV infection.
  • Intrinsic viral fitness distributions, rather than adaptive immunity, appear to drive HIV evolution.
  • Accurate mechanistic insights from phylogenetic inference require consideration of viral and immune-cell population dynamics.