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Related Concept Videos

Viral Recombination00:57

Viral Recombination

Cells are sometimes infected by more than one virus at once. When two viruses disassemble to expose their genomes for replication in the same cell, similar regions of their genomes can pair together and exchange sequences in a process called recombination. Alternatively, viruses with segmented genomes can swap segments in a process called reassortment.
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...
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...
Lytic Cycle of Bacteriophages01:30

Lytic Cycle of Bacteriophages

Bacteriophages, also known as phages, are specialized viruses that infect bacteria. A key characteristic of phages is their distinctive “head-tail” morphology. A phage begins the infection process (i.e., lytic cycle) by attaching to the outside of a bacterial cell. Attachment is accomplished via proteins in the phage tail that bind to specific receptor proteins on the outer surface of the bacterium. The tail injects the phage’s DNA genome into the bacterial cytoplasm. In the lytic replication...
Lysogenic Cycle of Bacteriophages00:43

Lysogenic Cycle of Bacteriophages

In contrast to the lytic cycle, phages infecting bacteria via the lysogenic cycle do not immediately kill their host cell. Instead, they combine their genome with the host genome, allowing the bacteria to replicate the phage DNA along with the bacterial genome. The incorporated copy of the phage genome is called the prophage. Some prophages can re-activate and enter the lytic cycle. This often occurs in response to a perturbation, such as DNA damage, but can also transpire in the absence of...
Viral Structure00:56

Viral Structure

Viruses are extraordinarily diverse in shape and size, but they all have several structural features in common. All viruses have a core that contains a DNA- or RNA-based genome. The core is surrounded by a protective coat of proteins called the capsid. The capsid is composed of subunits called capsomeres. The capsid and genome-containing core are together known as the nucleocapsid.

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Updated: May 22, 2026

Isolation of Fidelity Variants of RNA Viruses and Characterization of Virus Mutation Frequency
18:10

Isolation of Fidelity Variants of RNA Viruses and Characterization of Virus Mutation Frequency

Published on: June 16, 2011

Increased burst size in multiply infected cells can alter basic virus dynamics.

Kara W Cummings1, David N Levy, Dominik Wodarz

  • 1Department of Ecology and Evolutionary Biology, University of California, 321 Steinhaus Hall, 92617, Irvine, CA, USA.

Biology Direct
|May 10, 2012
PubMed
Summary

Coinfection dynamics in viral infections can significantly alter disease progression. Increased viral output from multiply infected cells impacts treatment efficacy and drug resistance, suggesting a need for load-dependent therapeutic strategies.

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Area of Science:

  • Virology
  • Mathematical Biology
  • Immunology

Background:

  • Mathematical models often assume single-virus infection per cell, neglecting coinfection.
  • Coinfection, where cells harbor multiple viruses, is evident in human immunodeficiency virus (HIV) and other viral infections.
  • Previous models assumed viral output is cell-limited, unaffected by coinfection.

Purpose of the Study:

  • To investigate the impact of increased viral burst size in coinfected cells on viral dynamics.
  • To explore how coinfection influences infection establishment and viral growth patterns.
  • To assess the implications of coinfection for antiviral therapy effectiveness and drug resistance.

Main Methods:

  • Developed and analyzed a mathematical model incorporating increased burst size for coinfected cells.
  • Simulated viral infection dynamics under varying initial virus loads and coinfection scenarios.
  • Evaluated the influence of coinfection prevalence on antiviral drug efficacy.

Main Results:

  • Increased burst size in coinfected cells fundamentally alters model predictions compared to single-infection models.
  • Infection establishment can depend on initial viral load, not solely the basic reproductive ratio.
  • Viral growth can accelerate over time, deviating from simple exponential growth.
  • Antiviral drug effectiveness may depend on the viral load at therapy initiation due to coinfection prevalence.
  • Drug resistance is influenced by both viral genotype and the extent of coinfection.

Conclusions:

  • Increased burst size in coinfected cells significantly changes fundamental viral infection dynamics.
  • Model predictions offer a basis for experimental validation to differentiate infection scenarios.
  • Findings highlight the importance of considering coinfection in viral dynamics and treatment strategies.