Role of Virus-Encoded microRNAs in Avian Viral Diseases

Yao, Yongxiu; Nair, Venugopal

doi:10.3390/v6031379

Cited by 48 publications

(49 citation statements)

References 69 publications

(125 reference statements)

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“…These include chicken sarcomas associated with Marek's disease virus (MDV) and various human lymphocyte and solid tumors associated with Epstein Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) (63-70). Additionally, we have identified a miRNA encoded by the bovine leukemia retrovirus (BLV) that mimics a known host oncogenic miRNA (56), and this miRNA was later identified in BLV-associated tumors (71).…”

Section: Discussionmentioning

confidence: 99%

Identification of a polyomavirus microRNA highly expressed in tumors

et al. 2015

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Polyomaviruses (PyVs) are associated with tumors including Merkel cell carcinoma (MCC). Several PyVs encode microRNAs (miRNAs) but to date no abundant PyV miRNAs have been reported in tumors. To better understand the function of the Merkel cell PyV (MCPyV) miRNA, we examined phylogenetically-related viruses for miRNA expression. We show that two primate PyVs and the more distantly-related raccoon PyV (RacPyV) encode miRNAs that share genomic position and partial sequence identity with MCPyV miRNAs. Unlike MCPyV miRNA in MCC, RacPyV miRNA is highly abundant in raccoon tumors. RacPyV miRNA negatively regulates reporters of early viral (T antigen) transcripts, yet robust viral miRNA expression is tolerated in tumors. We also identify raccoon miRNAs expressed in RacPyV-associated neuroglial brain tumors, including several likely oncogenic miRNAs (oncomiRs). This work describes the first PyV miRNA abundantly expressed in tumors and is consistent with a possible role for both host and viral miRNAs in RacPyV-associated tumors.

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Section: Discussionmentioning

confidence: 99%

Identification of a polyomavirus microRNA highly expressed in tumors

et al. 2015

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“…To know more regarding pathogenesis of DEV after infecting the duck embryonic fibroblast cells under in vitro conditions either after antiviral therapy, immunization or through biomarker response, a cDNA library has been framed with the use of switching mechanism at 5' end of the RNA transcript technique for proteomic analysis of DEV infected duck embryonic fibroblast cells . Micro (mi) RNAs were found recently which could provide insights into the pathogenesis of DEV (Yao et al 2012;Yao & Nair 2014).…”

Section: Pathogenesismentioning

confidence: 99%

Duck virus enteritis (duck plague) – a comprehensive update

Dhama

Kumar

Saminathan

et al. 2017

Veterinary Quarterly

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Duck virus enteritis (DVE), also called duck plague, is one of the major contagious and fatal diseases of ducks, geese and swan. It is caused by duck enteritis virus (DEV)/Anatid herpesvirus-1 of the genus Mardivirus, family Herpesviridae, and subfamily Alpha-herpesvirinae. Of note, DVE has worldwide distribution, wherein migratory waterfowl plays a crucial role in its transmission within and between continents. Furthermore, horizontal and/ or vertical transmission plays a significant role in disease spread through oral-fecal discharges. Either of sexes from varying age groups of ducks is vulnerable to DVE. The disease is characterized by sudden death, vascular damage and subsequent internal hemorrhage, lesions in lymphoid organs, digestive mucosal eruptions, severe diarrhea and degenerative lesions in parenchymatous organs. Huge economic losses are connected with acute nature of the disease, increased morbidity and mortality (5%-100%), condemnations of carcasses, decreased egg production and hatchability. Although clinical manifestations and histopathology can provide preliminary diagnosis, the confirmatory diagnosis involves virus isolation and detection using serological and molecular tests. For prophylaxis, both live-attenuated and killed vaccines are being used in broiler and breeder ducks above 2 weeks of age. Since DEV is capable of becoming latent as well as shed intermittently, recombinant subunit and DNA vaccines either alone or in combination (polyvalent) are being targeted for its benign prevention. This review describes DEV, epidemiology, transmission, the disease (DVE), pathogenesis, and advances in diagnosis, vaccination and antiviral agents/therapies along with appropriate prevention and control strategies.

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“…For example, both host and viral miRNAs have been implicated in the adaptive and innate immune responses, cell death, and tumorigenesis (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14). miRNAs are generally derived from primary transcripts that are processed by the Microprocessor complex (comprised of the endonuclease Drosha and its binding partner, DGCR8) that give rise to the ϳ65-nucleotide hairpin precursor miRNA (pre-miRNA) (15)(16)(17)(18).…”

mentioning

confidence: 99%

Naturally Arising Strains of Polyomaviruses with Severely Attenuated MicroRNA Expression

Chen¹,

Kincaid²,

Azarm³

et al. 2014

J Virol

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Several different polyomaviruses (PyVs) encode microRNAs (miRNAs) that regulate viral as well as host gene expression. However, the functions of polyomaviral miRNAs, particularly during in vivo infection, remain poorly understood. Here we identify rare naturally arising PyVs that are severely attenuated or null for miRNA expression. We identify hypomorphic or null strains for miRNA expression from rhesus macaque simian virus 40 (SV40) and human JC virus. These strains were isolated from immunocompromised hosts and derive from insertions or deletions in the viral DNA that preserve the amino acid reading frame of opposing-strand large T antigen gene. Characterization of the SV40 miRNA hypomorph, K661, shows that it is inhibited at the early miRNA biogenesis step of Drosha-mediated processing. Despite having a nonrearranged enhancer, which a previous study has shown renders some PyVs more susceptible to the autoregulatory activities of the miRNA, restoring miRNA expression to K661 has little effect on virus growth in either immortalized or primary monkey kidney cells. Thus, in addition to any effect of accompanying genomic elements, these results suggest that the cellular context also determines susceptibility to PyV miRNAmediated effects. Combined, these results demonstrate that polyomaviruses lacking miRNAs can arise infrequently and that the functional importance of polyomaviral miRNAs is context dependent, consistent with an activity connected to the immune status of the host. IMPORTANCEDiverse virus families encode miRNAs, yet much remains unknown about viral miRNA function and contribution to the infectious cycle. Polyomaviruses (PyVs) are small DNA viruses, long known to be important as etiological agents of rare diseases and valuable models of DNA virus infection. Here, in immunosuppressed hosts, we uncover rare naturally arising variants of different PyVs that have lost the ability to express miRNAs. This represents some of the only known natural viruses to have lost miRNA expression. By probing the biogenesis pathways of these variants, we uncover that miRNA expression is lost via small insertions or deletions that render the transcripts resistant to early steps of miRNA biogenesis while preserving the reading frame of the opposing T antigen transcripts. Overall, our study informs how miRNA genes evolve/devolve in viruses and suggests that miRNA function is exquisitely dependent not only on viral genomic context but also on the cellular and host environment.

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Role of Virus-Encoded microRNAs in Avian Viral Diseases

Cited by 48 publications

References 69 publications

Identification of a polyomavirus microRNA highly expressed in tumors

Identification of a polyomavirus microRNA highly expressed in tumors

Duck virus enteritis (duck plague) – a comprehensive update

Naturally Arising Strains of Polyomaviruses with Severely Attenuated MicroRNA Expression

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