Limits...
Cellular versus viral microRNAs in host-virus interaction.

Ghosh Z, Mallick B, Chakrabarti J - Nucleic Acids Res. (2008)

Bottom Line: There have been reported evidences of host-cellular miRNAs modulating the expression of various viral genes, thereby playing a pivotal role in the host-pathogen interaction network.Nevertheless, our increasing knowledge of the host-virus interaction at the molecular level should lead us toward possible explanations to viral tropism, latency and oncogenesis along with the development of an effective, durable and nontoxic antiviral therapy.Here, we summarize the recent updates on miRNA-induced gene-silencing mechanism, modulating host-virus interactions with a glimpse of the miRNA-based antiviral therapy for near future.

View Article: PubMed Central - PubMed

Affiliation: Computational Biology Group, Indian Association for the Cultivation of Science, Jadavpur, Calcutta 700 032, India. ghosh.jhumur@gmail.com

ABSTRACT
MicroRNAs (miRNAs) mark a new paradigm of RNA-directed gene expression regulation in a wide spectrum of biological systems. These small non-coding RNAs can contribute to the repertoire of host-pathogen interactions during viral infection. This interplay has important consequences, both for the virus and the host. There have been reported evidences of host-cellular miRNAs modulating the expression of various viral genes, thereby playing a pivotal role in the host-pathogen interaction network. In the hide-and-seek game between the pathogens and the infected host, viruses have evolved highly sophisticated gene-silencing mechanisms to evade host-immune response. Recent reports indicate that virus too encode miRNAs that protect them against cellular antiviral response. Furthermore, they may exploit the cellular miRNA pathway to their own advantage. Nevertheless, our increasing knowledge of the host-virus interaction at the molecular level should lead us toward possible explanations to viral tropism, latency and oncogenesis along with the development of an effective, durable and nontoxic antiviral therapy. Here, we summarize the recent updates on miRNA-induced gene-silencing mechanism, modulating host-virus interactions with a glimpse of the miRNA-based antiviral therapy for near future.

Show MeSH

Related in: MedlinePlus

Virus-encoded microRNAs as orthologs of cellular microRNAs. Encircled boxes show sequence homology of viral miRNAs to human/mouse miRNAs. The homologous bases are shown in blue. (a) Orthologs of cellular miR-155; (b) orthologs of cellular miR-151; (c) orthologs of cellular miR-18a and miR-18b.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC2651794&req=5

Figure 2: Virus-encoded microRNAs as orthologs of cellular microRNAs. Encircled boxes show sequence homology of viral miRNAs to human/mouse miRNAs. The homologous bases are shown in blue. (a) Orthologs of cellular miR-155; (b) orthologs of cellular miR-151; (c) orthologs of cellular miR-18a and miR-18b.

Mentions: In general, viral miRNAs and cellular miRNAs do not bear seed homology. But presumably, due to the presence of highly evolved gene-regulatory networks, some viral miRNAs have seed homology with cellular miRNAs. Recent report suggests that miR-K12-11 encoded by KSHV shares the first eight nts with hsa-miR-155 (27,73) (refer Figure 2). MiR-155 is processed from a primary transcript, termed as BIC gene (B-cell Integration Cluster), whose upstream region was identified as a common site of integration of the avian leucosis virus (ALV) (74) in lymphomas. miRNA-profiling studies have shown increased expression of miR-155 in a wide range of cancers including lymphomas (75). Gottwein et al. (73) reported that miR-155 and miR-K12-11 regulate similar set of targets including genes with known roles in cell-growth regulation. It has been shown that BACH-1 is one of the predicted mRNAs, targeted by both miR-155 and miR-K12-11 (27). Transient expression of miR-155 occurs in macrophages, T and B lymphocytes and miR-155 knockout mice revealed defects in adaptive immune responses. Furthermore, overexpression of miR-155 in B-cells is associated with the development of B-cell lymphomas in humans, mice and chickens (74) although the mechanism is unknown. Given the apparent role of miR-155 in tumorigenesis and miR-K12-11 being an ortholog of miR-155, it is tempting to speculate that miR-K12-11 may contribute to the development of B-cell tumors seen in KSHV-infected individuals. Inspite of being a distantly related γ-herpesvirus, EBV miRNAs do not bear homology to miR-155 (76). However, previous reports have shown the expression of BIC during EBV infection expressing the full repertoire of EBV latency genes, which implies the role of EBV latency genes in inducing BIC gene (77).Figure 2.


Cellular versus viral microRNAs in host-virus interaction.

Ghosh Z, Mallick B, Chakrabarti J - Nucleic Acids Res. (2008)

Virus-encoded microRNAs as orthologs of cellular microRNAs. Encircled boxes show sequence homology of viral miRNAs to human/mouse miRNAs. The homologous bases are shown in blue. (a) Orthologs of cellular miR-155; (b) orthologs of cellular miR-151; (c) orthologs of cellular miR-18a and miR-18b.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2651794&req=5

Figure 2: Virus-encoded microRNAs as orthologs of cellular microRNAs. Encircled boxes show sequence homology of viral miRNAs to human/mouse miRNAs. The homologous bases are shown in blue. (a) Orthologs of cellular miR-155; (b) orthologs of cellular miR-151; (c) orthologs of cellular miR-18a and miR-18b.
Mentions: In general, viral miRNAs and cellular miRNAs do not bear seed homology. But presumably, due to the presence of highly evolved gene-regulatory networks, some viral miRNAs have seed homology with cellular miRNAs. Recent report suggests that miR-K12-11 encoded by KSHV shares the first eight nts with hsa-miR-155 (27,73) (refer Figure 2). MiR-155 is processed from a primary transcript, termed as BIC gene (B-cell Integration Cluster), whose upstream region was identified as a common site of integration of the avian leucosis virus (ALV) (74) in lymphomas. miRNA-profiling studies have shown increased expression of miR-155 in a wide range of cancers including lymphomas (75). Gottwein et al. (73) reported that miR-155 and miR-K12-11 regulate similar set of targets including genes with known roles in cell-growth regulation. It has been shown that BACH-1 is one of the predicted mRNAs, targeted by both miR-155 and miR-K12-11 (27). Transient expression of miR-155 occurs in macrophages, T and B lymphocytes and miR-155 knockout mice revealed defects in adaptive immune responses. Furthermore, overexpression of miR-155 in B-cells is associated with the development of B-cell lymphomas in humans, mice and chickens (74) although the mechanism is unknown. Given the apparent role of miR-155 in tumorigenesis and miR-K12-11 being an ortholog of miR-155, it is tempting to speculate that miR-K12-11 may contribute to the development of B-cell tumors seen in KSHV-infected individuals. Inspite of being a distantly related γ-herpesvirus, EBV miRNAs do not bear homology to miR-155 (76). However, previous reports have shown the expression of BIC during EBV infection expressing the full repertoire of EBV latency genes, which implies the role of EBV latency genes in inducing BIC gene (77).Figure 2.

Bottom Line: There have been reported evidences of host-cellular miRNAs modulating the expression of various viral genes, thereby playing a pivotal role in the host-pathogen interaction network.Nevertheless, our increasing knowledge of the host-virus interaction at the molecular level should lead us toward possible explanations to viral tropism, latency and oncogenesis along with the development of an effective, durable and nontoxic antiviral therapy.Here, we summarize the recent updates on miRNA-induced gene-silencing mechanism, modulating host-virus interactions with a glimpse of the miRNA-based antiviral therapy for near future.

View Article: PubMed Central - PubMed

Affiliation: Computational Biology Group, Indian Association for the Cultivation of Science, Jadavpur, Calcutta 700 032, India. ghosh.jhumur@gmail.com

ABSTRACT
MicroRNAs (miRNAs) mark a new paradigm of RNA-directed gene expression regulation in a wide spectrum of biological systems. These small non-coding RNAs can contribute to the repertoire of host-pathogen interactions during viral infection. This interplay has important consequences, both for the virus and the host. There have been reported evidences of host-cellular miRNAs modulating the expression of various viral genes, thereby playing a pivotal role in the host-pathogen interaction network. In the hide-and-seek game between the pathogens and the infected host, viruses have evolved highly sophisticated gene-silencing mechanisms to evade host-immune response. Recent reports indicate that virus too encode miRNAs that protect them against cellular antiviral response. Furthermore, they may exploit the cellular miRNA pathway to their own advantage. Nevertheless, our increasing knowledge of the host-virus interaction at the molecular level should lead us toward possible explanations to viral tropism, latency and oncogenesis along with the development of an effective, durable and nontoxic antiviral therapy. Here, we summarize the recent updates on miRNA-induced gene-silencing mechanism, modulating host-virus interactions with a glimpse of the miRNA-based antiviral therapy for near future.

Show MeSH
Related in: MedlinePlus