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Summary

Kaposi's sarcoma-associated herpesvirus (KSHV) terminal repeats (TR) length regulates viral gene expression by controlling bromodomain-containing protein 4 (BRD4) recruitment. Shorter TR sequences impair KSHV reactivation and viral gene transcription.

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Area of Science:

Virology
Molecular Biology
Epigenetics

Background:

Kaposi's sarcoma-associated herpesvirus (KSHV) possesses a terminal repeats (TR) sequence crucial for gene regulation.
The TR sequence functions as a gene enhancer, recruiting bromodomain-containing protein 4 (BRD4) to modulate transcription.

Purpose of the Study:

To investigate the role of KSHV TR copy number in viral gene expression and reactivation.
To elucidate the mechanism by which TR influences BRD4 recruitment and transcriptional activity.

Main Methods:

Generation of recombinant KSHV with reduced TR copy numbers (TR5 vs. TR21).
Analysis of viral gene expression, reactivation efficiency, and BRD4 recruitment in infected cells.
Utilizing auxin-inducible LANA degradation to assess LANA's role in BRD4 occupancy.
In vitro experiments with purified proteins to study LANA, BRD4, and TR DNA interactions.

Main Results:

Reducing KSHV TR copy number significantly attenuated viral gene expression and impaired reactivation.
Lower TR copy numbers decreased BRD4 recruitment to viral gene promoters, reducing transcriptional activity.
KSHV reactivation efficiency correlated with the size of LANA nuclear bodies (NBs), which are influenced by TR length.
LANA is essential for BRD4 occupancy on latent chromatin and facilitates LANA-BRD4 liquid-liquid phase separation (LLPS) in a TR-dependent manner.

Conclusions:

KSHV TR length is a critical determinant of enhancer activity, influencing BRD4 recruitment and viral gene expression.
LANA binding to TR forms an enhancer domain that regulates KSHV episome transcription and replication outcomes.
Transcription memory and TR length dynamically control KSHV replication potential through enhancer strength modulation.