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Review
, 120 (4), 939-49

KSHV and the Pathogenesis of Kaposi Sarcoma: Listening to Human Biology and Medicine

Affiliations
Review

KSHV and the Pathogenesis of Kaposi Sarcoma: Listening to Human Biology and Medicine

Don Ganem. J Clin Invest.

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.

Figures

Figure 1
Figure 1. Kaposi sarcoma.
(A) Gross lesions of KS on the palate of a patient with AIDS. (B) Nodular skin lesion seen in KS. (C) Histopathology of a nodular KS lesion, showing fascicles of elongated spindle cells and numerous slit-like neovascular spaces. (D) High-power image of KS spindle cells. All images reproduced from the CDC’s open-access Public Health Image Library.
Figure 2
Figure 2. Phylogenetic tree of selected major herpesviruses.
HSV, herpes simplex virus; VZV, varicella-zoster virus; HCMV, human cytomegalovirus; HHV, human herpesvirus; HVS, herpesvirus saimiri (a simian virus). Figure reproduced with permission from Journal of Virology (193).
Figure 3
Figure 3. Phenotypic effect of latent KSHV infection in primary endothelial cells in culture.
BEC, blood vessel endothelial cell; LEC, lymphatic endothelial cell. Left column: mock infection; right column: KSHV infection. One week after infection, cells were photographed under brightfield imaging (original magnification, ×40).
Figure 4
Figure 4. Structure of transcripts from the major latency locus of KSHV.
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).

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