Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV)/human herpesvirus-8 is the causative agent of the endothelial cell-derived tumour Kaposi's sarcoma. Herpesviruses possess large complex genomes which provide many options to regulate cellular physiology during the viral life cycle and in the course of tumourigenicity. Novel techniques of systems biology and reverse genetics are increasingly applied to dissect the complex interaction of KSHV with endothelial cells. This review will outline novel results and pitfalls of these technologies in the elucidation of KSHV pathogenicity.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Disease Models, Animal
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Endothelial Cells / metabolism
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Endothelial Cells / virology*
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Gene Expression
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Gene Expression Profiling
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Genes, Viral
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Herpesviridae Infections / etiology
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Herpesviridae Infections / genetics
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Herpesviridae Infections / virology
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Herpesvirus 8, Human / genetics*
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Herpesvirus 8, Human / pathogenicity*
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Host-Pathogen Interactions / genetics
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Humans
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Mice
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Mice, Transgenic
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Proteomics
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Sarcoma, Kaposi / etiology
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Sarcoma, Kaposi / genetics
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Sarcoma, Kaposi / virology
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Signal Transduction
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Systems Biology
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Viral Proteins / genetics
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Viral Proteins / metabolism