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Related Concept Videos

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Viral Recombination

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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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Retroviruses02:33

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Retroviruses and retrotransposons both insert copies of their genetic elements into the genome of the host cell. Thus, the viral genes are passed on when the host genome is replicated or translated. A typical retroviral DNA sequence contains 3-4 genes that encode the different proteins required for its structural assembly and function as a molecular parasite. This DNA is transcribed into a single mRNA, which is very similar in structure to conventional mRNAs, i.e., it is capped at the 5’...
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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 Mutations

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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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Infection01:20

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When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
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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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Updated: Oct 23, 2025

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When Viruses Cross Developmental Pathways.

Pankaj Trivedi1, Sandesh Kumar Patel2, Diana Bellavia2

  • 1Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy.

Frontiers in Cell and Developmental Biology
|August 23, 2021
PubMed
Summary
This summary is machine-generated.

Oncogenic viruses disrupt developmental pathways, driving cancer. Understanding these viral interactions can lead to more effective, targeted antiviral therapies with fewer side effects.

Keywords:
HedgehogNotchWNTimmune evasionmicroRNAoncogenic virusestargeted therapies

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Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Aberrant regulation of developmental pathways is fundamental to tumorigenesis.
  • Tumor cells exhibit hallmarks like sustained proliferation and metastasis, often due to dysregulated Hedgehog, Notch, or WNT signaling.
  • Human tumor viruses contribute to cancer by encoding oncogenic proteins, altering the microenvironment, and inducing genomic instability.

Purpose of the Study:

  • To elucidate the mechanisms by which oncogenic viruses intersect with and modulate developmental pathways.
  • To understand the role of viral immune evasion in accelerating tumor growth via developmental pathway compromise.
  • To identify targets for improved antiviral therapies by exploring virus-developmental pathway cross-signaling.

Main Methods:

  • Review of literature on oncogenic viruses and developmental pathway regulation.
  • Analysis of viral oncogenic proteins and their impact on cellular signaling.
  • Investigation of viral modulation of coding and non-coding gene regulatory pathways.

Main Results:

  • Oncogenic viruses can hijack developmental pathways (Hedgehog, Notch, WNT) to promote cancer hallmarks.
  • Viral immune evasion strategies can further dysregulate developmental pathways, accelerating tumor progression.
  • Current antiviral therapies targeting viral replication show limited efficacy and significant side effects.

Conclusions:

  • Elucidating virus-developmental pathway interactions is critical for understanding viral tumorigenesis.
  • Targeting the cross-signaling between oncogenic viruses and developmental pathways offers a promising strategy for next-generation antiviral therapies.
  • A deeper understanding will enable the development of more targeted and effective antiviral treatments with improved safety profiles.