Whole-genome transcriptional profiles of a novel marine fish iridovirus, Singapore grouper iridovirus (SGIV) in virus-infected grouper spleen cell cultures and in orange-spotted grouper, Epinephulus coioides

Teng, Yong; Hou, Zhuoni; Gong, Jie; Hong, Liu; Xie, Xiayang; Zhang, Liang; Chen, Xiaohong; Qi, Qin

doi:10.1016/j.virol.2008.04.011

Cited by 52 publications

(37 citation statements)

References 27 publications

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“…In the present study, MyD88 transcripts in the grouper spleen were markedly up-regulated after SGIV stimulation, indicating that MyD88 is potentially involved in grouper response to SGIV infection. Up-regulation of Og-MyD88 may be due to proliferation or recruitment of MyD88-expressing immune cells in the grouper spleen, which is reported to be the most susceptible target organ for SGIV infection [45,46]. Our results are in agreement with those observed in the Japanese flounder and rock bream [28,31].…”

Section: Discussionsupporting

confidence: 91%

Functional genomic studies on an immune- and antiviral-related gene of MyD88 in orange-spotted grouper, Epinephelus coioides

et al. 2012

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Myeloid differentiation factor 88 (MyD88) is a universal adaptor protein involved in Toll-like receptors and in interleukin-1 receptor-induced nuclear factor-kappaB (NF-κB) activation. In this study, a new MyD88 gene (designated as Og-MyD88) was cloned from orange-spotted grouper, Epinephelus coioides, based on the expressed sequence tag (EST) obtained following Roche 454 GS-FLX™ sequencing. The full-length Og-MyD88 cDNA is composed of 1682 bp and encodes a deduced polypeptide of 289 amino acids with 86% homology to MyD88 of Siniperca chuatsi. The deduced amino acid sequence of Og-MyD88 contains a typical death domain at the amino terminus and a conserved Toll/IL-1R (TIR) domain at the carboxyl terminus, as well as three highly conserved motifs (Box1, Box2 and Box3) within the C-terminal TIR domain. In healthy fish, Og-MyD88 was found to be strongly expressed in immune-related tissues, including the spleen, head kidney, kidney, liver, skin and intestine, with lower expression in heart, stomach, brain and muscle. Transcripts of Og-MyD88 were found to be markedly up-regulated in fish spleen after challenge with Singapore grouper iridovirus (SGIV), a highly lethal viral pathogen to grouper fish. Furthermore, the full length Og-MyD88 and its N-terminal death domain were capable of inducing NF-κB activity in HEK-293 cells. Overexpressed Og-MyD88 showed the ability to inhibit replication of SGIV in grouper spleen (GS) cells. These results suggest that Og-MyD88 is involved in the grouper immune response to invasion of viral pathogens and may share similar functions to those observed in higher vertebrates.

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Section: Discussionsupporting

confidence: 91%

Functional genomic studies on an immune- and antiviral-related gene of MyD88 in orange-spotted grouper, Epinephelus coioides

et al. 2012

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“…Similar results were obtained for other large DNA viruses such as vaccinia virus and monkeypox viruses in which ϳ95% of their CDSs are expressed in cell cultures (3,27). Transcription analysis using microarrays was also performed with two marine fish iridoviruses: (i) Singapore grouper iridovirus expressed 97% of its CDSs in cell culture (31), and (ii) Red Sea bream iridovirus expressed 96% of its CDSs during in vitro infection (17). Therefore, it appears that most CDSs are expressed in these large dsDNA viruses, even in laboratory conditions.…”

Section: Resultssupporting

confidence: 61%

Microarray Analysis of Paramecium bursaria Chlorella Virus 1 Transcription

Yanai-Balser

Duncan

Eudy

et al. 2010

J Virol

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Paramecium bursaria chlorella virus 1 (PBCV-1), the prototype of the genus Chlorovirus (family Phycodnaviridae), is a large, icosahedral (190 nm in diameter), plaque-forming virus that infects the unicellular, eukaryotic green alga Chlorella sp. strain NC64A. The PBCV-1 virion has a lipid membrane located inside an outer glycoprotein capsid. The 330-kb genome is a linear, nonpermutated, double-stranded DNA (dsDNA) molecule with covalently closed hairpin ends that has approximately 365 protein encoding genes (CDSs), as well as 11 tRNA encoding genes (reviewed in references 34, 39, and 40). The CDSs are evenly distributed on both strands and intergenic space is minimal (typically fewer than 100 nucleotides); the exception is a 1,788-bp sequence in the middle of the genome that encodes the tRNA genes. Approximately 35% of the 365 PBCV-1 gene products resemble proteins in the public databases.PBCV-1 initiates infection by attaching rapidly and specifically to the cell wall of its host (22), probably at a unique virus vertex (4, 26). Attachment is immediately followed by host cell wall degradation by a virus-packaged enzyme(s) at the point of contact. After wall degradation, the viral internal membrane presumably fuses with the host membrane, causing host membrane depolarization (9), potassium ion efflux (25), and an increase in the cytoplasm pH (2). These events are predicted to facilitate entry of the viral DNA and virion-associated proteins into the cell. PBCV-1 lacks a gene encoding a recognizable RNA polymerase or a subunit of it, and RNA polymerase activity is not detected in PBCV-1 virions. Therefore, viral DNA and virion-associated proteins are predicted to migrate to the nucleus, and early viral transcription is detected 5 to 10 min postinfection (p.i.), presumably by commandeering a host RNA polymerase(s) (possibly RNA polymerase II) (14, 29). Virus DNA synthesis begins 60 to 90 min p.i., followed by virus assembly at 3 to 5 h p.i. in localized regions of the cytoplasm, called virus assembly centers (21). At 6 to 8 h p.i., virusinduced host cell lysis occurs resulting in release of progeny virions (ϳ1,000 viruses/cell, ϳ25% of which are infectious). These events are depicted in Fig. 1.To initiate PBCV-1 transcription, the host RNA polymerase(s), possibly in combination with a virus transcription factor(s), must recognize virus DNA promoter sequences. Recently, three short nucleotide sequences were identified in putative virus promoter regions (150 bp upstream and 50 bp downstream of the ATG translation site) that are conserved in PBCV-1 and other Chlorovirus members (7). PBCV-1 CDSs are not spatially clustered on the genome by either temporal or functional class, suggesting that transcription regulation must occur via cis-and possible trans-acting regulatory elements.To understand the dynamics of PBCV-1 global gene expression during virus replication, we constructed a microarray containing 50-mer probes to each of the 365 PBCV-1 CDSs.

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“…Following microarray analysis of FV3 gene expression, 33 IE and 22 DE transcripts, corresponding to approximately half of the FV3 coding potential, were identifi ed (Majji et al 2009 ). Similar levels of IE and DE gene products were seen with other ranaviruses Teng et al 2008 ). Host POL-II is responsible for the transcription of IE (and perhaps DE) viral mRNAs, whereas, as described below, vPOL-II directs transcription of late viral messages.…”

Section: Nuclear Eventsmentioning

confidence: 60%