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Looking at Kaposi's Sarcoma-Associated Herpesvirus-Host Interactions from a microRNA Viewpoint.

ABSTRACT: Kaposi's sarcoma-associated herpesvirus (KSHV), also called human herpesvirus 8, belongs to the gamma herpesviruses and is the etiological agent of Kaposi's sarcoma, primary effusion lymphoma, and some types of multicentric Castleman's disease. In vivo, KSHV mainly infects B cells and endothelial cells. The interactions between KSHV and its host cells determine the outcome of viral infection and subsequent viral pathogenesis. MicroRNAs (miRNAs) are small, non-coding RNAs that are important in fine-tuning cellular signaling. During infection, KSHV modulates the expression profiles and/or functions of a number of host miRNAs, for example hsa-miR-132 and hsa-miR-146a. Meanwhile, KSHV itself encodes 12 pre-miRNAs, including miR-K12-11, which is the functional ortholog of the host miR-155. A number of cellular and viral targets of deregulated cellular miRNAs and viral miRNAs are found in KSHV-infected cells, which suggests that miRNAs may be important in mediating KSHV-host interactions. In this review, we summarize our current understanding of how KSHV modulates the expression and/or functions of host miRNAs; we review in detail the functions of miR-K12-11 as the ortholog of miR-155; and we examine the functions of viral miRNAs in KSHV life cycle control, immune evasion, and pathogenesis.

SUBMITTER: Liang D

PROVIDER: S-EPMC3258008 | biostudies-literature | 2011

REPOSITORIES: biostudies-literature

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Looking at Kaposi's Sarcoma-Associated Herpesvirus-Host Interactions from a microRNA Viewpoint.

Liang Deguang D Lin Xianzhi X Lan Ke K

Frontiers in microbiology 20120111

Kaposi's sarcoma-associated herpesvirus (KSHV), also called human herpesvirus 8, belongs to the gamma herpesviruses and is the etiological agent of Kaposi's sarcoma, primary effusion lymphoma, and some types of multicentric Castleman's disease. In vivo, KSHV mainly infects B cells and endothelial cells. The interactions between KSHV and its host cells determine the outcome of viral infection and subsequent viral pathogenesis. MicroRNAs (miRNAs) are small, non-coding RNAs that are important in fi ...[more]

PMID: 22275910

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Project description:UnlabelledThe human oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV) expresses a set of ∼20 viral microRNAs (miRNAs). miR-K10a stands out among these miRNAs because its entire stem-loop precursor overlaps the coding sequence for the Kaposin (Kap) A/C proteins. The ectopic expression of KapA has been reported to lead to transformation of rodent fibroblasts. However, these experiments inadvertently also introduced miR-K10a, which raises the question whether the transforming activity of the locus could in fact be due to miR-K10a expression. To answer this question, we have uncoupled miR-K10a and KapA expression. Our experiments revealed that miR-K10a alone transformed cells with an efficiency similar to that when it was coexpressed with KapA. Maintenance of the transformed phenotype was conditional upon continued miR-K10a but not KapA protein expression, consistent with its dependence on miRNA-mediated changes in gene expression. Importantly, miR-K10a taps into an evolutionarily conserved network of miR-142-3p targets, several of which are expressed in 3T3 cells and are also known inhibitors of cellular transformation. In summary, our studies of miR-K10a serve as an example of an unsuspected function of an mRNA whose precursor is embedded within a coding transcript. In addition, our identification of conserved miR-K10a targets that limit transformation will point the way to a better understanding of the role of this miRNA in KSHV-associated tumors.ImportanceKaposi's sarcoma-associated herpesvirus (KSHV) is a human tumor virus. The viral Kaposin locus has known oncogenic potential, which has previously been attributed to the encoded KapA protein. Here we show that the virally encoded miR-K10a miRNA, whose precursor overlaps the KapA-coding region, may account for the oncogenic properties of this locus. Our data suggest that miR-K10a mimics the cellular miRNA miR-142-3p and thereby represses several known inhibitors of oncogenic transformation. Our work demonstrates that functional properties attributed to a coding region may in fact be carried out by an embedded noncoding element and sheds light on the functions of viral miR-K10a.

Dataset Information

Looking at Kaposi's Sarcoma-Associated Herpesvirus-Host Interactions from a microRNA Viewpoint.

Publications

Looking at Kaposi's Sarcoma-Associated Herpesvirus-Host Interactions from a microRNA Viewpoint.

Similar Datasets

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