Correction: Ago HITS-CLIP Expands Understanding of Kaposi's Sarcoma-associated Herpesvirus miRNA Function in Primary Effusion Lymphomas

ABSTRACT Kaposi's sarcoma-associated herpesvirus (KSHV) latently infects KS tumors, primary effusion lymphomas (PELs), and PEL cell lines. K12 (T0.7) is the most abundant transcript expressed in latent KSHV infection. We characterize here the K12 transcript from a PEL tumor prior to passage in cell culture. The PEL tumor KSHV K12 transcript contained additional complex nucleotide repeat elements compared to the previously described K12 message of the BCBL-1 PEL cell line. The PEL tumor lacked kaposin B, the predominant BCBL-1 K12 protein product, but encoded kaposins A and C. The K12 transcript was spliced and the splicing event occurred in all KSHV isolates tested. The 5′ end of the K12 transcript was mapped by 5′ RACE (rapid amplification of cDNA ends) and S1 nuclease protection assays and was at the site of an active promoter. This work demonstrates that the K12 transcript contains variable, complex repeat elements, is spliced and is expressed from a novel KSHV promoter.

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Evidence for Multiple Subpopulations of Herpesvirus-Latently Infected Cells

mBio ◽

10.1128/mbio.03473-21 ◽

2022 ◽

Author(s):

Justin T. Landis ◽

Ryan Tuck ◽

Yue Pan ◽

Carson N. Mosso ◽

Anthony B. Eason ◽

...

Keyword(s):

Kaposi's Sarcoma ◽

Kaposi’S Sarcoma ◽

Resistance To Therapy ◽

Latently Infected ◽

Infected Cells ◽

Kaposi's Sarcoma Associated Herpesvirus ◽

Kaposi’S Sarcoma Associated Herpesvirus ◽

Primary Effusion Lymphomas

Latency is the defining characteristic of the Herpesviridae and central to the tumorigenesis phenotype of Kaposi’s sarcoma-associated herpesvirus (KSHV). KSHV-driven primary effusion lymphomas (PEL) rapidly develop resistance to therapy, suggesting tumor instability and plasticity.

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Epstein-Barr Virus Inhibits Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication in Primary Effusion Lymphomas

Journal of Virology ◽

10.1128/jvi.02743-06 ◽

2007 ◽

Vol 81 (11) ◽

pp. 6068-6078 ◽

Cited By ~ 35

Author(s):

Dongsheng Xu ◽

Tricia Coleman ◽

Jun Zhang ◽

Ashley Fagot ◽

Catherine Kotalik ◽

...

Keyword(s):

Kaposi's Sarcoma ◽

Epstein Barr Virus ◽

Kaposi’S Sarcoma ◽

Lytic Replication ◽

Transcription Activator ◽

Barr Virus ◽

Kaposi's Sarcoma Associated Herpesvirus ◽

Epstein Barr ◽

Kaposi’S Sarcoma Associated Herpesvirus ◽

Primary Effusion Lymphomas

ABSTRACT The majority of AIDS-associated primary effusion lymphomas (PEL) are latently infected with both Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV). PELs harboring two viruses have higher oncogenic potential, suggesting functional interactions between EBV and KSHV. The KSHV replication and transcription activator (K-RTA) is necessary and sufficient for induction of KSHV lytic replication. EBV latent membrane protein 1 (LMP-1) is essential for EBV transformation and establishment of latency in vitro. We show EBV inhibits chemically induced KSHV lytic replication, in part because of a regulatory loop in which K-RTA induces EBV LMP-1 and LMP-1 in turn inhibits K-RTA expression and furthermore the lytic gene expression of KSHV. Suppression of LMP-1 expression in dually infected PEL cells enhances the expression of K-RTA and lytic replication of KSHV upon chemical induction. Because LMP-1 is known to inhibit EBV lytic replication, KSHV-mediated induction of LMP-1 would potentiate EBV latency. Moreover, KSHV infection of EBV latency cells induces LMP-1, and K-RTA is involved in the induction. Both LMP-1 and K-RTA are expressed during primary infection by EBV of KSHV latency cells. Our findings provide evidence that an interaction between EBV and KSHV at molecular levels promotes the maintenance and possibly establishment of viral latency, which may contribute to pathogenesis of PELs.

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