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The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
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In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fulfill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.
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Related Experiment Video

Updated: Mar 25, 2026

Establishment and Quantification of De Novo Lytic Infection by Cell-free Kaposi's Sarcoma-Associated Herpesvirus
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KSHV Genome Replication and Maintenance.

Pravinkumar Purushothaman1, Prerna Dabral1, Namrata Gupta1

  • 1Department of Microbiology and Immunology, School of Medicine, University of Nevada, Reno Reno, NV, USA.

Frontiers in Microbiology
|February 13, 2016
PubMed
Summary
This summary is machine-generated.

Kaposi's sarcoma-associated herpesvirus (KSHV) latency relies on the LANA protein for viral episome replication and segregation. This review details LANA's molecular mechanisms in maintaining KSHV persistence.

Keywords:
KSHVLANALBSlatencyori-Aori-Ppre-RCreplication

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Area of Science:

  • Virology
  • Molecular Biology
  • Oncology

Background:

  • Kaposi's sarcoma-associated herpesvirus (KSHV), or human herpesvirus 8 (HHV8), causes severe malignancies in immunocompromised individuals.
  • KSHV establishes lifelong infections with latent and lytic cycles.
  • During latency, the viral episome is tethered to host chromosomes and replicates with cell division.

Purpose of the Study:

  • To review the molecular mechanisms of KSHV genome replication, segregation, and latency maintenance.
  • To highlight the central role of Latency-associated nuclear antigen (LANA) in these processes.

Main Methods:

  • Review of existing literature on KSHV latency and LANA function.
  • Analysis of LANA's interactions with viral and cellular components.
  • Discussion of LANA's role in DNA replication and segregation.

Main Results:

  • LANA is crucial for tethering the KSHV episome to host chromosomes via binding to LANA binding sites (LBS) and cellular nucleosomal proteins.
  • LANA modulates cellular signaling pathways and recruits host factors for replication and segregation.
  • The KSHV terminal repeat (TR) region is vital for latent DNA replication and episome segregation, facilitated by LANA binding.

Conclusions:

  • LANA is a key determinant of KSHV latent infection, essential for episome replication and stable inheritance.
  • Understanding LANA's mechanisms provides insights into KSHV pathogenesis and potential therapeutic targets.