Update on KSHV epidemiology, Kaposi Sarcoma pathogenesis, and treatment of Kaposi Sarcoma

Uldrick, Thomas S.; Whitby, Denise

doi:10.1016/j.canlet.2011.02.006

Cited by 171 publications

(137 citation statements)

References 138 publications

(173 reference statements)

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“…K aposi's sarcoma-associated herpesvirus (KSHV) is an oncogenic gamma herpesvirus that is the cause of Kaposi's sarcoma (1,2). KSHV infection in cell culture manifests mainly as a latent infection; however, there is a percentage of spontaneous lytic reactivation.…”

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confidence: 99%

Regulation of Viral and Cellular Gene Expression by Kaposi's Sarcoma-Associated Herpesvirus Polyadenylated Nuclear RNA

Rossetto

Tarrant-Elorza

Verma

et al. 2013

J Virol

121

195

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Kaposi's sarcoma-associated herpesvirus (KSHV) is the cause of Kaposi's sarcoma and body cavity lymphoma. In cell culture, KSHV results in a latent infection, and lytic reactivation is usually induced with the expression of K-Rta or by treatment with phorbol 12-myristate 13-acetate (TPA) and/or n-butyrate. Lytic infection is marked by the activation of the entire viral genomic transcription cascade and the production of infectious virus. KSHV-infected cells express a highly abundant, long, noncoding transcript referred to as polyadenylated nuclear RNA (PAN RNA). PAN RNA interacts with specific demethylases and physically binds to the KSHV genome to mediate activation of viral gene expression. A recombinant BACmid lacking the PAN RNA locus fails to express K-Rta and does not produce virus. We now show that the lack of PAN RNA expression results in the failure of the initiation of the entire KSHV transcription program. In addition to previous findings of an interaction with demethylases, we show that PAN RNA binds to protein components of Polycomb repression complex 2 (PRC2). RNA-Seq analysis using cell lines that express PAN RNA shows that transcription involving the expression of proteins involved in cell cycle, immune response, and inflammation is dysregulated. Expression of PAN RNA in various cell types results in an enhanced growth phenotype, higher cell densities, and increased survival compared to control cells. Also, PAN RNA expression mediates a decrease in the production of inflammatory cytokines. These data support a role for PAN RNA as a major global regulator of viral and cellular gene expression.K aposi's sarcoma-associated herpesvirus (KSHV) is an oncogenic gamma herpesvirus that is the cause of Kaposi's sarcoma (1, 2). KSHV infection in cell culture manifests mainly as a latent infection; however, there is a percentage of spontaneous lytic reactivation. Lytic infection is marked by the production of infectious virus, whereas latency is characterized by the lack of infectious virus production and the expression of a limited number of viral transcripts and proteins. One of the most abundant transcripts present in KSHV-infected cells is a long noncoding RNA, referred to as polyadenylated nuclear RNA (PAN RNA) (3, 4).We previously showed that PAN RNA interacts with cell-and virus-encoded factors and mediates the regulation of immune response gene expression (5, 6). Data from our laboratory and others indicated that PAN RNA is a major regulator of viral gene expression through a mechanism that involves a direct interaction with the viral chromosome (5, 7). PAN RNA interacts with the demethylases UTX and JMJD3 to remove the suppressive H3K23me3 mark within the KSHV viral genome. In a recent study describing the transcriptome of KSHV-infected cell lines, PAN RNA was detected in the absence of lytic-phase induction, suggesting that PAN RNA is expressed during chronic latent infection in cell culture (8). This observation suggests that PAN RNA has the potential to influence viral and cellular gene expressio...

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mentioning

confidence: 99%

Regulation of Viral and Cellular Gene Expression by Kaposi's Sarcoma-Associated Herpesvirus Polyadenylated Nuclear RNA

Rossetto

Tarrant-Elorza

Verma

et al. 2013

J Virol

121

195

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“…Kaposi's sarcoma is an angioproliferative multicentric disorder of cells of endothelial origin, described in 1872 by the Hungarian dermatologist Moritz Kaposi [1,2].…”

Section: Discussionmentioning

confidence: 99%

Disseminated KaposiA’s Sarcoma as Initial Event in AIDS

Jordão¹,

Barros²,

Trope³

et al. 2015

J AIDS Clin Res

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“…The best therapeutic results are obtained in the classic KS with only local treatment [12,13] . Treatment of HIV-associated KS requires anti-retroviral therapy, which leads to both immune reconstitution and control of HIV viremia [14] . Radiotherapy is effective and often represents the best local treatment for palliation of pain, bleeding or edema, with response and complete remission rates of more than 90% and 70%, respectively [12] .…”

Section: Discussionmentioning

confidence: 99%

Isolated classic Kaposi Sarcoma in an old female patient

Dilek¹,

Dilek²,

Saral³

et al. 2014

JST

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Kaposi sarcoma (KS) is an angio-proliferative disorder and classified in terms of four clearly differentiated variants. Classic variant is an uncommon disease that it has an overwhelming male predominance and majority of cases patients are positive for HIV infections. We present HIV-negative female patient presenting multiple nodules on palmar and dorsal aspect of right wrist. Considering the male predominance of classic KS and positivity of HIV infections in majority of KS cases the patient presented to contribute to the literature.

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Update on KSHV epidemiology, Kaposi Sarcoma pathogenesis, and treatment of Kaposi Sarcoma

Cited by 171 publications

References 138 publications

Regulation of Viral and Cellular Gene Expression by Kaposi's Sarcoma-Associated Herpesvirus Polyadenylated Nuclear RNA

Regulation of Viral and Cellular Gene Expression by Kaposi's Sarcoma-Associated Herpesvirus Polyadenylated Nuclear RNA

Disseminated KaposiA’s Sarcoma as Initial Event in AIDS

Isolated classic Kaposi Sarcoma in an old female patient

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