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Related Concept Videos

Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Retroviruses02:33

Retroviruses

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’...
S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

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).
Two states at the origin of replication
In eukaryotes, the initiation of replication occurs at many sites on the chromosomes, called the origins of replication.
S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

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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Viral Recombination00:57

Viral Recombination

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.
LTR Retrotransposons03:08

LTR Retrotransposons

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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Related Experiment Video

Updated: Jul 10, 2026

Establishment and Quantification of De Novo Lytic Infection by Cell-free Kaposi's Sarcoma-Associated Herpesvirus
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Establishment and Quantification of De Novo Lytic Infection by Cell-free Kaposi's Sarcoma-Associated Herpesvirus

Published on: August 15, 2025

An autonomous replicating element within the KSHV genome.

Subhash C Verma1, Ke Lan, Tathagata Choudhuri

  • 1Department of Microbiology and Tumor Virology Program of the Abramson Comprehensive Cancer Center, School of Medicine, University of Pennsylvania, 201E Johnson Pavilion, 3610 Hamilton Walk, Philadelphia, PA 19104, USA.

Cell Host & Microbe
|November 17, 2007
PubMed
Summary
This summary is machine-generated.

Kaposi's sarcoma-associated herpesvirus (KSHV) can replicate its DNA independently of the viral LANA protein. A specific DNA region, the long unique region (LUR), recruits host replication machinery to enable this LANA-independent replication.

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Functional Imaging of Viral Transcription Factories Using 3D Fluorescence Microscopy
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Functional Imaging of Viral Transcription Factories Using 3D Fluorescence Microscopy

Published on: January 18, 2018

Area of Science:

  • Virology
  • Molecular Biology
  • Epigenetics

Background:

  • Herpesviridae family viruses, including Kaposi's sarcoma-associated herpesvirus (KSHV), establish lifelong latent infections.
  • KSHV genomes exist as circular episomes, requiring replication for propagation during host cell division.
  • Viral latency-associated nuclear antigen (LANA) has been considered essential for KSHV episome replication.

Purpose of the Study:

  • To investigate potential LANA-independent mechanisms for KSHV latent DNA replication.
  • To identify specific viral DNA elements that can initiate replication without LANA.
  • To elucidate the role of host cellular machinery in KSHV episome maintenance.

Main Methods:

  • Plasmid-based replication assays using KSHV genomic regions.
  • Deletion analysis of LANA-binding sequences and eukaryotic origins of replication.
  • Immunoprecipitation and depletion studies to assess host replication protein involvement (ORC2, MCM3).

Main Results:

  • A cis-acting DNA element within the KSHV long unique region (LUR) initiated plasmid replication independently of LANA.
  • Replication occurred even in plasmids lacking LANA-binding sites or known eukaryotic origins.
  • Host replication proteins ORC2 and MCM3 were recruited to the LUR element.
  • Depletion of cellular ORC2 abolished LUR-dependent plasmid replication.

Conclusions:

  • KSHV possesses a LANA-independent mechanism for initiating latent DNA replication.
  • The LUR element can directly recruit host cellular replication machinery (ORC2, MCM3) to drive episome replication.
  • This finding reveals a novel pathway for KSHV genome propagation during latency, independent of viral trans-acting factors.