Abstract
Kaposi’s sarcoma-associated herpesvirus (KSHV/human herpesvirus 8) is a γ-herpesvirus linked to Kaposi’s sarcoma (KS) and two lymphoproliferative disorders, primary effusion lymphoma (PEL or body-cavity B-lymphoma [BCBL]) and a subset of Multicentric Castleman’s Disease. During lytic growth, pervasive viral transcription generating a variety of transcripts with uncertain protein-coding potential has been described on a genome-wide scale in β- and γ-herpesviruses. One class of such RNAs is called long non-coding RNAs (lncRNAs). KSHV encodes a viral lncRNA known as polyadenylated nuclear RNA (PAN RNA), a copious early gene product. PAN RNA has been implicated in KSHV gene expression, replication, and immune modulation. PAN RNA expression is required for optimal expression of the entire KSHV lytic gene expression program. Latent KSHV episomes are coated with viral latency-associated nuclear antigen (LANA). LANA rapidly dissociates from episomes during reactivation. Here we review recent studies suggesting that PAN RNA may function as a viral lncRNA, including a role in the facilitation of LANA-episomal dissociation during lytic replication.
Highlights
Recent new developments in epigenetic control of transcriptional programs by chromatin modifiers are highlighted by findings that long non-coding RNA, previously thought to be “transcription noise”, interact with chromatin-associated proteins to modulate their functions [1,2].long non-coding RNAs (lncRNAs) interactions have been reported with most classes of proteins that associate with chromatin including transcription factors [3], chromatin remodelers [4], and histone methylases and demethylases [5,6]
Non-coding RNAs can be classified as either housekeeping or regulatory ncRNA, and based on transcript size, regulatory ncRNA can be further grouped into two subclasses; small non-coding RNA (20–200 nt) and long non-coding RNA
Pathogen-encoded lncRNAs have been reported for several virus groups, including herpesviruses
Summary
Recent new developments in epigenetic control of transcriptional programs by chromatin modifiers are highlighted by findings that long non-coding RNA (lncRNA), previously thought to be “transcription noise”, interact with chromatin-associated proteins to modulate their functions [1,2]. LncRNA interactions have been reported with most classes of proteins that associate with chromatin including transcription factors [3], chromatin remodelers [4], and histone methylases and demethylases [5,6]. The most dominant function explored in lncRNA studies relates to epigenetic regulation of target genes This role is typically associated with gene repression, which has been studied in many cellular lncRNAs including ANRIL, HOTAIR, H19, and XIST [6,9,10,11,12]. These lncRNAs exhibit their repression function through interactions with histone modifying enzymes. The programmers of chromatin remodeling are enzymes involved in histone modifications, namely histone methylases and demethylases, regulation of such enzymes by lncRNAs through recruitment or assembly of specific complexes may have profound local effects on chromatin modification
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