Open reading frame L1 of Marek's disease herpesvirus is not essential for in vitro and in vivo virus replication and establishment of latency.

Schat, Karel A.; Iddekinge, B.J.L. Hooft van; Boerrigter, H. M.; O'Connell, Priscilla H.; Koch, G.

doi:10.1099/0022-1317-79-4-841

Cited by 18 publications

(12 citation statements)

References 20 publications

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“…2). One of the previously identified miRNAs, miR-M1, mapped downstream of Meq embedded in the ORF of the L1/ RLORF5a transcript, although it is not clear whether it affects the expression of this transcript (33,46,59). We have identified a new miRNA, mdv-miR-M11, located just downstream of the Meq ORF (Fig.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Profile of Marek's Disease Virus-Transformed T-Cell Line MSB-1: Predominance of Virus-Encoded MicroRNAs

Yao

Zhao

et al. 2008

J Virol

126

141

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Section: Discussionmentioning

confidence: 99%

MicroRNA Profile of Marek's Disease Virus-Transformed T-Cell Line MSB-1: Predominance of Virus-Encoded MicroRNAs

Yao

Zhao

et al. 2008

J Virol

126

141

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“…ORF L1 deletion mutants were generated using the CVI988 strain of MDV. These mutants were able to establish latency, and virus could be rescued from latent infections, suggesting that ORF L1 is not important for these functions (57).…”

Section: Marek's Disease (Md) Is a Highly Contagious Lymphoproliferatmentioning

confidence: 96%

Transactivation of Latent Marek's Disease Herpesvirus Genes in QT35, a Quail Fibroblast Cell Line, by Herpesvirus of Turkeys

Yamaguchi

Kaplan

Wakenell

et al. 2000

J Virol

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(62) showed that MDV and HVT can transactivate the promoter region in the long terminal repeat (LTR) of Rous sarcoma virus. Furthermore, they reported that HVT can efficiently transactivate the ICP4 and beta-thymidine kinase gene promoters of HSV as well as the promoter of the IE gene of human cytomegalovirus.More than 200 lymphoblastoid cell lines have been established from MD tumors (1, 7-9, 32, 35, 39). Most of these cell lines are CD4 ϩ CD8 Ϫ T cells (56). These lymphoblastoid cell lines are often considered the equivalent of latently infected cells, based on the limited expression of viral genes. In addition to the lymphoblastoid cell lines, an MDV-transformed chicken embryo fibroblast (CEF) cell line has been established, but this cell line also expresses late MDV genes, such as that for glycoprotein B (gB) (5).Three groups of transcripts located in the repeat regions of MDV in MD lymphoblastoid cell lines have been described. The first group consists of the latency-associated transcripts (LATs), which are antisense to ICP4 (see Fig. 1). Several groups have reported the presence of LATs in MD lymphomas and MD-derived lymphoblastoid cell lines (10,11,21,22,27,33); some of these (the MD small RNAs [MSRs]) are poly(A) negative and are retained in the nuclei (11), similar to the 1.5-and 2.0-kb LATs described for HSV (64). Interestingly, the MSRs are also found in nuclei of CEF productively infected with MDV.The second and third group of transcripts described for MD lymphomas and lymphoblastoid cell lines are located in the I 2 ,

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“…RLORF5a transcripts are expressed more abundantly in MDCC lines than in infected chick kidney cell (CKC) cultures (20). Deletion of this ORF in attenuated CVI988 indicated that it is not essential for virus replication and the establishment of latency (31). RLORF4 transcripts were recently shown to be expressed in MDCC lines and MDV-infected CKC cultures.…”

mentioning

confidence: 99%

“…(19). Deletion of RLORF5a in the attenuated vaccine strain CVI988 indicated that it is not essential for virus replication and the establishment of latency; however, the effect on oncogenesis could not be determined using this strain of MDV (31).…”

mentioning

confidence: 99%

Attenuation of Marek's Disease Virus by Deletion of Open Reading Frame RLORF4 but Not RLORF5a

Jarosinski

Osterrieder

Nair

et al. 2005

J Virol

116

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Marek's disease (MD) in chickens is caused by the alphaherpesvirus MD virus (MDV) and is characterizedby the development of lymphoblastoid tumors in multiple organs. The recent identification and cloning of RLORF4 and the finding that four of six attenuated strains of MDV contained deletions within RLORF4 suggested that it is involved in the attenuation process of MDV. To assess the role of RLORF4 in MD pathogenesis, its coding sequence was deleted in the pRB-1B bacterial artificial chromosome clone. Additionally, RLORF5a was deleted separately to examine its importance for oncogenesis. The sizes of plaques produced by MDV reconstituted from pRB-1B⌬RLORF5a (rRB-1B⌬RLORF5a) were similar to those produced by the parental pRB-1B virus (rRB-1B). In contrast, virus reconstituted from pRB-1B⌬RLORF4 (rRB-1B⌬RLORF4) produced significantly larger plaques. Replication of the latter virus in cultured cells was higher than that of rRB-1B or rRB-1B⌬RLORF5a using quantitative PCR (qPCR) assays. In vivo, both deletion mutants and rRB-1B replicated at comparable levels at 4, 7, and 10 days postinoculation (p.i.), as determined by virus isolation and qPCR assays. At 14 days p.i., the number of PFU of virus isolated from chickens infected with rRB-1B⌬RLORF4 was comparable to that from chickens infected with highly attenuated RB-1B and significantly lower than that from rRB-1B-infected birds. The number of tumors and kinetics of tumor production in chickens infected with rRB-1B⌬RLORF5a were similar to those of P2a chickens infected with rRB-1B. In stark contrast, none of the chickens inoculated with rRB-1B⌬RLORF4 died up to 13 weeks p.i.; however, two chickens had tumors at the termination of the experiment. The data indicate that RLORF4 is involved in attenuation of MDV, although the function of RLORF4 is still unknown.Marek's disease (MD) is a lymphoproliferative disease in chickens caused by a member of the Alphaherpesvirinae subfamily, MD virus (MDV). The pathogenesis of infection with MDV can be divided into four phases (3). Bursa-derived (B) lymphocytes are infected between 3 and 6 days postinfection (p.i.) and are the primary target cells for the first phase of lytic infection, which is followed by infection of activated CD4 ϩ thymus-derived (T) lymphocytes in the second phase. During the second phase, viral replication typically decreases and a latent infection is established between 5 and 10 days p.i. in activated CD4ϩ T lymphocytes. The third phase is characterized by reactivation of MDV replication between 14 and 21 days p.i. After the third phase, lymphomas may develop depending on the genetic susceptibility of the chickens and the virulence of the virus strain.The MDV genome consists of two unique regions, the unique short region (U S ) and the unique long region (U L ), flanked by inverted repeats known as the inverted repeat long (IR L ) and short (IR S ), and the terminal repeat long (TR L ) and short (TR S ). The MDV Eco Q (Meq or RLORF7) and viral interleukin-8 (IL-8) homologue genes and the open reading frames ...

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Open reading frame L1 of Marek's disease herpesvirus is not essential for in vitro and in vivo virus replication and establishment of latency.

Cited by 18 publications

References 20 publications

MicroRNA Profile of Marek's Disease Virus-Transformed T-Cell Line MSB-1: Predominance of Virus-Encoded MicroRNAs

MicroRNA Profile of Marek's Disease Virus-Transformed T-Cell Line MSB-1: Predominance of Virus-Encoded MicroRNAs

Transactivation of Latent Marek's Disease Herpesvirus Genes in QT35, a Quail Fibroblast Cell Line, by Herpesvirus of Turkeys

Attenuation of Marek's Disease Virus by Deletion of Open Reading Frame RLORF4 but Not RLORF5a

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