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An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus
09:53

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

Published on: August 25, 2017

Broad target cell selectivity of Kaposi's sarcoma-associated herpesvirus glycoprotein-mediated cell fusion and virion

Johnan A R Kaleeba1, Edward A Berger

  • 1Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 4, Room 237, Bethesda, MD 20892, USA.

Virology
|August 8, 2006
PubMed

Insights

Kaposi's sarcoma-associated herpesvirus (KSHV) entry mechanisms were investigated using cell fusion and virion entry assays. Findings reveal specific cell types are permissive to KSHV, suggesting a novel fusion-entry receptor.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • The entry mechanism of Kaposi's sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8, remains largely undefined.
  • Understanding KSHV entry is crucial for developing targeted therapeutic strategies against KSHV-associated diseases.

Purpose of the Study:

  • To identify and characterize target cells permissive to KSHV entry.
  • To elucidate the molecular basis of KSHV-mediated cell fusion and virion entry.

Main Methods:

  • Utilized a quantitative reporter gene assay for KSHV-glycoprotein-mediated cell fusion across diverse cell types.
  • Employed a virion entry assay with a recombinant KSHV encoding a reporter gene.
  • Assessed surface expression of alpha3beta1 integrin on target cells.

Main Results:

  • Human, non-human primate, and rabbit cell lines demonstrated efficient KSHV target cell activity.
  • Rodent and human lymphoblastoid cell lines exhibited weak permissiveness to KSHV.
  • No correlation was found between target cell permissiveness and alpha3beta1 integrin surface expression.

Conclusions:

  • Target cell permissiveness for KSHV entry is cell-type dependent and species-specific.
  • The findings suggest the existence of a putative KSHV fusion-entry receptor distinct from alpha3beta1 integrin.

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