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Related Concept Videos

LTR Retrotransposons03:08

LTR Retrotransposons

18.1K
LTR retrotransposons are class I transposable elements with long terminal repeats flanking an internal coding region. These elements are less abundant in mammals compared to other class I transposable elements. About 8 percent of human genomic DNA comprises LTR retrotransposons. Some of the common examples of LTR retrotransposons are Ty elements in yeast and Copia elements in Drosophila.
The internal coding region of LTR retrotransposons and their mechanism of transposition closely resembles a...
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Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

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As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
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Related Experiment Video

Updated: May 5, 2026

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
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Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

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Sp140L Is a Novel Herpesvirus Restriction Factor.

Jana M Cable, Wiyada Wongwiwat, Jenna C Grabowski

    Biorxiv : the Preprint Server for Biology
    |December 23, 2024
    PubMed
    Summary

    Epstein-Barr Virus (EBV) uses EBNA-LP to evade host defenses. Speckled proteins like SP140L act as restriction factors, and EBNA-LP counters them to establish infection.

    Area of Science:

    • Virology
    • Immunology
    • Genetics

    Background:

    • Herpesviruses, including Epstein-Barr Virus (EBV), must overcome host DNA sensing for infection.
    • EBNA-LP, the first latency protein, is crucial for B cell transformation but its immune evasion role is unknown.

    Purpose of the Study:

    • To elucidate the role of EBNA-LP in evading host antiviral responses.
    • To identify host restriction factors targeted by EBNA-LP.

    Main Methods:

    • Single-cell RNA sequencing of EBNA-LP-Knockout (LPKO) B cells infected with EBV.
    • Genetic manipulation of SP100 and SP140L expression.
    • Analysis of viral gene transcription and cellular proliferation.

    Main Results:

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  • Speckled proteins, particularly SP100 and primate-specific SP140L, act as restriction factors against EBV.
  • Loss of SP100 or SP140L reverses EBV restriction, suppresses interferon-stimulated genes, and restores viral transcription and proliferation.
  • SP140L is also targeted by Herpesvirus Saimiri ORF3 protein, suggesting broader antiviral relevance.

    • Conclusions:

    • EBNA-LP counters SP100 and SP140L to facilitate EBV infection.
    • SP140L acts as a DNA sensing and transcriptional suppression factor in an IFN-independent innate immune response.
    • This mechanism is likely important for infection by other nuclear DNA viruses.