KSHV and the pathogenesis of Kaposi sarcoma: listening to human biology and medicine
Don Ganem
Don Ganem
Published April 1, 2010
Citation Information: J Clin Invest. 2010;120(4):939-949. https://doi.org/10.1172/JCI40567.
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KSHV and the pathogenesis of Kaposi sarcoma: listening to human biology and medicine

Abstract

The linkage of Kaposi sarcoma (KS) to infection by a novel human herpesvirus (Kaposi sarcoma–associated herpesvirus [KSHV]) is one of the great successes of contemporary biomedical research and was achieved by using advanced genomic technologies in a manner informed by a nuanced understanding of epidemiology and clinical investigation. Ongoing efforts to understand the molecular mechanisms by which KSHV infection predisposes to KS continue to be powerfully influenced by insights emanating from the clinic. Here, recent developments in KS pathogenesis are reviewed, with particular emphasis on clinical, pathologic, and molecular observations that highlight the many differences between this process and tumorigenesis by other oncogenic viruses.

Authors

Don Ganem

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Figure 4

Structure of transcripts from the major latency locus of KSHV.

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Structure of transcripts from the major latency locus of KSHV. Top panel...
Top panel: Disposition of ORFs in the latency cluster. ORF-73 encodes LANA; ORF-72 encodes v-cyclin (v-CYC); ORF-71 encodes v-FLIP; ORF-K12 encodes kaposin A; DRs 1 and 2 encode direct repeats in which translation of kaposins B and C initiate. LIR, long interspersed repeats. Middle panel: KSHV microRNA (miR) cluster, with pre-miRNAs indicated by arrowheads. Bottom panels: Structures of transcripts directed by the kaposin (or LTd) promoter and by the LANA (or LTc) promoter. Figure modified with permission from RNA (101).