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Related Concept Videos

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...
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The lysogenic cycle is a crucial viral replication strategy that allows bacteriophages to persist within host cells without immediately destroying them. This process is primarily observed in temperate phages, such as bacteriophage lambda (λ), which infects Escherichia coli. The cycle allows the viral genome to persist across bacterial generations while keeping host cells viable.Integration of the Viral GenomeUpon infection, bacteriophage lambda attaches to the bacterial surface and injects its...
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Viral Replication: Lytic Cycle

Bacteriophages, or phages, are viruses that specifically infect bacteria. Among them, T-even bacteriophages, such as T4, exhibit a well-characterized lytic replication cycle in Escherichia coli (E. coli). This process ensures the rapid proliferation of the virus while ultimately leading to the destruction of the bacterial host.Attachment and DNA InjectionThe infection process begins with the recognition and binding of the T4 phage to the E. coli cell surface. Tail fibers of the phage...
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Lysogenic Cycle of Bacteriophages00:43

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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...
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Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...

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Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
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Published on: October 7, 2011

Fixation probability for lytic viruses: the attachment-lysis model.

Z Patwa1, L M Wahl

  • 1Department of Applied Mathematics, University of Western Ontario, London, Ontario N6A 5B7, Canada.

Genetics
|September 2, 2008
PubMed
Summary

The fixation probability of beneficial mutations in viruses is highly sensitive to life-history traits. Viral adaptation is critically dependent on the timing of population bottlenecks, influencing mutation fixation outcomes.

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Area of Science:

  • Evolutionary biology
  • Virology
  • Population genetics

Background:

  • The fixation probability of beneficial mutations is crucial for understanding adaptation.
  • Life-history traits significantly influence evolutionary dynamics.
  • Lytic viruses are important model organisms for studying adaptation.

Purpose of the Study:

  • To compute the fixation probability of beneficial mutations in lytic viruses using a life-history model.
  • To investigate the impact of different life-history parameters on mutation fixation.
  • To determine the sensitivity of fixation probability to population bottleneck timing.

Main Methods:

  • Developed a life-history model for lytic viruses.
  • Assumed exponentially distributed attachment times and constant lysis times.
  • Incorporated periodic population bottlenecks and constant clearance rates.
  • Calculated fixation probabilities for mutations affecting attachment rate, lysis time, burst size, and clearance probability.

Main Results:

  • Fixation probabilities for beneficial mutations varied significantly based on life-history parameters.
  • The time between population bottlenecks critically influenced fixation probability.
  • Mutations affecting lysis time showed complex dynamics depending on experimental sampling methods.
  • Sensitivity analysis revealed a strong dependence on bottleneck frequency across all mutation types.

Conclusions:

  • Viral adaptation and fixation probability are highly sensitive to life-history assumptions.
  • The timing of population bottlenecks is a key determinant of beneficial allele fixation in viruses.
  • Understanding these dynamics is essential for interpreting experimental evolution studies with lytic viruses.