Amplification of a tandem direct repeat within inverted repeats of Marek's disease virus DNA during serial in vitro passage

Maotani, Kumiko; Kanamori, A; Ikuta, Kazuyoshi; Ueda, Seinosuke; Kato, Shiro; Hirai, Kanji

doi:10.1128/jvi.58.2.657-660.1986

Cited by 88 publications

(26 citation statements)

References 16 publications

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“…We have examined the 132-bp repeat regions of the RB1Bp9, RB1Bp24, and RB1B⌬4.5lac genomes. This repeated region is amplified during attenuation and has been correlated with a loss of oncogenicity (13,21,41). RB1Bp9, RB1Bp24, and RB1B⌬4.5lac, as well as these strains reisolated from chickens and RB1Bp9 and RB1B⌬4.5lac reactivated from lymphoblastoid cell lines, had predominantly two copies of the 132-bp repeat as determined by PCR analysis (18a).…”

Section: Discussionmentioning

confidence: 99%

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Retention of oncogenicity by a Marek's disease virus mutant lacking six unique short region genes

Parcells

Anderson

Morgan

1995

J Virol

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We previously reported the construction of Marek's disease virus (MDV) strains having mutations in various genes that map to the unique short (US) region of the viral genome (These strains were constructed by using a high-passage-level serotype 1 MDV strain which grew well in chicken embryo fibroblasts. Despite the growth of the parent and mutant viruses in cell culture, in vivo studies were limited by poor growth of these strains in chickens. One of the mutants studied lacked 4.5 kbp of US region DNA and contained the lacZ gene of Escherichia coli inserted at the site of the deletion. The deletion removed MDV homologs to the US1, US2, and US10 genes of herpes simplex virus type 1 as well as three MDV-specific open reading frames. We now report the construction of a mutant MDV containing a similar deletion in the US region of the highly oncogenic RB1B strain. This mutant, RB1B⌬4.5lac, had a growth impairment in established chicken embryo fibroblasts similar to that described previously for MDVs lacking a functional US1 gene. In chickens, RB1B⌬4.5lac showed decreased early cytolytic infection, mortality, tumor incidence, and horizontal transmission. Several lymphoblastoid cell lines were established from RB1B⌬4.5lacinduced tumors, and virus reactivated from these cell lines was LacZ ؉ . These results indicate that the deleted genes are nonessential for the transformation of chicken T cells or for the establishment and maintenance of latency. On the basis of the growth impairment observed for RB1B⌬4.5lac in cell culture and in vivo, we conclude that deletion of these genes affects the lytic replication of MDV. This is the first MDV mutant constructed in the RB1B oncogenic strain, and the methodology described herein provides for the direct examination of MDV-encoded determinants of oncogenicity.

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Section: Discussionmentioning

confidence: 99%

“…Oncogenic MDV strains do not replicate well in cell culture and become attenuated rapidly during serial passage (10). Attenuation is accompanied by alterations in the sequence and expression of the MDV genome (3,4,13,21,41,44), loss of horizontal transmission (10), and a decreased ability to infect lymphocytes in vivo and in vitro (39).…”

mentioning

confidence: 99%

Retention of oncogenicity by a Marek's disease virus mutant lacking six unique short region genes

Parcells

Anderson

Morgan

1995

J Virol

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“…Alterations in MDV genome structure have been previously shown to correlate with attenuation of in vivo MDV pathogenicity. The best established correlate involves expansion of a 132-bp reiterated sequence adjacent to the origin of replication in R L (8,21,36). This expansion appears to alter the transcriptional pattern characteristic of the BamH gene family (for a review, see reference 20).…”

Section: Fig 4 In Vitro Growth Rate Of Rm1 Rm1-and Jm-infected Celmentioning

confidence: 99%

Retroviral insertional activation in a herpesvirus: transcriptional activation of US genes by an integrated long terminal repeat in a Marek's disease virus clone

Jones

Brunovskis

Witter

et al. 1996

J Virol

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Insertional activation of host proto-oncogenes has been recognized as a basic mechanism by which nonacute retroviruses induce cancer. Our previous work has demonstrated that retroviruses can efficiently integrate into DNA virus genomes. Specifically, coinfection of cultured fibroblasts with a chicken herpesvirus, Marek's disease virus (MDV), and a chicken retrovirus results in frequent stable retroviral insertions into the herpesvirus genome. Such insertions could alter the expression of herpesvirus genes, possibly resulting in novel phenotypic properties. In this article, we report the characterization of a replication-competent clone of MDV with integrated retroviral sequences. This virus was isolated from a chicken following injection of fibroblasts coinfected with MDV and the retrovirus, reticuloendotheliosis virus. Transcripts originating from the reticuloendotheliosis virus long terminal repeat promoters were found to encode the adjoining MDV genes, SORF2, US1, and US10. This virus replicates well in culture but has an unusual phenotype in chickens, characterized by an attenuated virulence which produces no nerve lesions but, rather, severe thymic atrophy. While the causal relationship between the insertion and the observed phenotypes remains to be established, our data provide the first evidence of retroviral insertional activation of herpesvirus genes.

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“…The nonprotective variants of HVT did not replicate in vivo in chickens, but replicated well in cultured cells. Since serial passages of the oncogenic MDV 1 in cultured cells resulted in a structural change of the viral DNA with simultaneous loss of oncogenicity (2,4,5,7,15,16), the structure of HVT DNA may also change during its serial passages of HVT in cultured cells. However, very little is known about the variable regions on the genomes of various HVT isolates.…”

Section: Herpesvirus Of Turkeys (Hvt) Ormentioning

confidence: 99%

Genomic Difference of Herpesvirus of Turkeys at Low and High Passage Levels in Culture of O1 and FC126 Strains

Hirai

Ikuta

Mikami

et al. 1989

Microbiology and Immunology

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Serial passages in culture of herpesvirus of turkeys resulted in structural genomic changes at the regions common to two virus strains with loss of their protective ability against Marek's disease.Herpesvirus of turkeys (HVT) or Marek's disease virus (MDV) serotype 3 have been used for vaccination against Marek's disease (MD), a highly contagious lymphoproliferative disease, caused by MDV serotype 1 (MDV1). Although most of the virus-specific polypeptides of MDVl and HVT have cross-reactive epitopes (10,11,17), the two viruses have no significant DNA homology except in a restricted portion of their genomes (4,12,14). However, Southern blot hybridization under less stringent conditions indicated that regions with weak homology were distributed over most of these two viral genomes (3, 6). A similar relationship exists between the DNAs of MDV type 2 and MDV 1 or HVT (8). The homologous DNA regions found by low-stringency hybridization were located at the corresponding positions on the restriction enzyme maps of MDV1 and HVT DNAs, indicating the collinear relationship between these two virus genomes (9). The genome structure of both MDVl and HVT consists of a long unique region (UL) and a short unique region (Us) bounded by inverted repeats (1).Serial passages of HVT over 70 times in cultured cells resulted in a loss of their ability to protect chickens from MD (13,18,19). The nonprotective variants of HVT did not replicate in vivo in chickens, but replicated well in cultured cells. Since serial passages of the oncogenic MDV 1 in cultured cells resulted in a structural change of the viral DNA with simultaneous loss of oncogenicity (2,4,5,7,15,16), the structure of HVT DNA may also change during its serial passages of HVT in cultured cells. However, very little is known about the variable regions on the genomes of various HVT isolates. In this study, we attempted to locate the common regions on the HVT genome which differed in structure between low-passaged, 871

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Amplification of a tandem direct repeat within inverted repeats of Marek's disease virus DNA during serial in vitro passage

Cited by 88 publications

References 16 publications

Retention of oncogenicity by a Marek's disease virus mutant lacking six unique short region genes

Retention of oncogenicity by a Marek's disease virus mutant lacking six unique short region genes

Retroviral insertional activation in a herpesvirus: transcriptional activation of US genes by an integrated long terminal repeat in a Marek's disease virus clone

Genomic Difference of Herpesvirus of Turkeys at Low and High Passage Levels in Culture of O1 and FC126 Strains

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