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Viral Replication: Lytic Cycle01:20

Viral Replication: Lytic Cycle

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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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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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Viral Replication: Lysogenic Cycle01:16

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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...
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Viral Recombination00:57

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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.
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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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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...
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Assays for the Specific Growth Rate and Cell-binding Ability of Rotavirus
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Enterovirus replication: go with the (counter)flow.

Jules Nchoutmboube1, Lauren A Ford-Siltz1, George A Belov1

  • 1Department of Veterinary Medicine and Virginia-Maryland Regional College of Veterinary, Medicine, University of Maryland, College Park, MD, USA.

Trends in Microbiology
|March 10, 2015
PubMed
Summary
This summary is machine-generated.

Enteroviruses hijack cellular lipid pathways to build replication sites. Disrupting this PI4P-cholesterol cycle halts virus production, offering new therapeutic targets.

Keywords:
cholesterol–PI4P exchangedrug repurposingenterovirus replication organelleslipid traffickingoxysterol binding protein (OSBP)

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Area of Science:

  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • (+)RNA viruses establish unique membranous replication compartments.
  • The mechanisms viruses use to acquire and maintain specific lipid compositions are poorly understood.

Purpose of the Study:

  • To elucidate how enteroviruses induce and maintain their distinct membranous replication domains.
  • To identify host factors and lipid pathways critical for enterovirus replication.

Main Methods:

  • Investigated the role of lipid transfer proteins and kinases in enterovirus-induced membrane rearrangements.
  • Utilized genetic and pharmacological approaches to perturb the PI4P-cholesterol exchange cycle.

Main Results:

  • Enteroviruses exploit the oxysterol-binding protein 1 (OSBP1) and PI4 kinase-dependent PI4P-cholesterol cycle.
  • Blocking the OSBP1-mediated lipid flow significantly inhibits enterovirus replication.

Conclusions:

  • The PI4P-cholesterol exchange cycle is essential for creating and maintaining enterovirus replication sites.
  • Targeting this dynamic lipid flow represents a promising antiviral strategy against enteroviruses.