Related Experiment Video

Updated: Aug 20, 2026

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)
07:02

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)

Published on: September 14, 2010

Dissection of the Kaposi's sarcoma-associated herpesvirus gene expression program by using the viral DNA replication

Michael Lu1, Jacqueline Suen, Carolina Frias

  • 1HIV and AIDS Malignancy Branch, National Cancer Institute, National Institutes of Health, Building 10, Room 10S255 MSC1868, Bethesda, MD 20892, USA.

Journal of Virology
|November 27, 2004
PubMed

Insights

Kaposi

Area of Science:

  • Virology
  • Molecular Biology
  • Oncology

Background:

  • Kaposi's sarcoma-associated herpesvirus (KSHV) establishes latency and can reactivate into a lytic replication cycle.
  • Understanding KSHV gene expression dynamics during lytic replication is crucial for therapeutic development.
  • Previous studies using viral microarrays provided insights but lacked precise kinetic resolution for gene expression.

Purpose of the Study:

  • To differentiate KSHV genes requiring viral DNA replication from those expressed independently.
  • To elucidate the kinetic profiles of KSHV gene expression during TPA-induced lytic replication.
  • To investigate the role of viral DNA replication in the expression of KSHV lytic genes and viral gene homologs.

Main Methods:

  • Treatment of KSHV-infected primary effusion lymphoma cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) to induce lytic replication.
  • Utilizing cidofovir (CDV), a KSHV DNA polymerase inhibitor, to block viral DNA replication.
  • Analyzing the expression levels of various KSHV genes and viral cellular gene homologs under different treatment conditions (TPA, TPA+CDV).

Main Results:

  • Immediate-early and early lytic genes (e.g., ORF50, K8 bZIP, ORF57) were largely unaffected by CDV, indicating expression independent of DNA replication.
  • Late capsid and tegument genes (e.g., ORF25, ORF26, ORF64, ORF67) were sensitive to CDV, requiring DNA replication for maximal expression.
  • Latency-associated transcript ORF73 was constitutively expressed, unaffected by TPA or CDV. Expression of some viral cellular gene homologs was CDV-sensitive, while others were not.

Conclusions:

  • KSHV gene expression can be categorized into DNA replication-dependent and -independent pathways.
  • This study provides a kinetic framework for KSHV lytic gene expression, distinguishing early/regulatory from late/structural genes.
  • The findings offer insights into KSHV replication strategies and pathogenesis, identifying specific viral gene homologs expressed during distinct phases of the lytic cycle.

More Related Videos

Quantitative Fluorescence In Situ Hybridization (FISH) and Immunofluorescence (IF) of Specific Gene Products in KSHV-Infected Cells06:21

Quantitative Fluorescence In Situ Hybridization (FISH) and Immunofluorescence (IF) of Specific Gene Products in KSHV-Infected Cells

Published on: August 27, 2019

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus09:53

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus

Published on: August 25, 2017

Related Concept Videos

Cytomegalovirus Disease01:27

Cytomegalovirus Disease

Cytomegalovirus (CMV) disease is caused by human cytomegalovirus, a double-stranded DNA virus of the Herpesviridae family. While primary CMV infection is often asymptomatic in immunocompetent individuals, the virus can cause severe disease in neonates and immunocompromised patients. CMV is the most common cause of congenital viral infection in the United States, and a major pathogen in solid organ and hematopoietic stem cell transplant recipients.CMV is transmitted via bodily fluids, sexual...
Antiviral Nucleoside Inhibitors01:22

Antiviral Nucleoside Inhibitors

Antiviral Nucleoside InhibitorsAntiviral nucleoside inhibitors are structural analogs of natural nucleosides that interfere with viral DNA or RNA synthesis. These compounds selectively target viral polymerases due to their resemblance to host nucleosides, thereby disrupting viral genome replication.Mechanism of Acyclovir ActionAcyclovir is a guanosine analog with a three-carbon acyclic side chain. It selectively targets herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2),...
Retrovirus Life Cycles01:10

Retrovirus Life Cycles

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 retrovirus to...
Herpes01:28

Herpes

Herpes simplex type 1 (HSV‑1) is a widespread pathogen responsible for orolabial lesions. It is an enveloped, double-stranded DNA (dsDNA) virus belonging to the family Herpesviridae. Once the virus infects a host cell, its double‑stranded DNA genome is delivered into the nucleus, where a coordinated cascade of immediate‑early, early, and late gene expression directs viral DNA replication, structural protein synthesis, and virion assembly. After primary infection of epithelial cells, HSV-1...
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...
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...