Immunization against Marek's Disease Transplantable Cell Lines

1984 ◽  
Vol 28 (1) ◽  
pp. 160 ◽  
Author(s):  
K. Nazerian ◽  
R. L. Witter
Keyword(s):  
Cell Lines ◽  
Marek's Disease ◽  
Marek’S Disease ◽  
Transplantable Cell

scholarly journals Marek's Disease Virus-Encoded MicroRNA 155 Ortholog Critical for the Induction of Lymphomas Is Not Essential for the Proliferation of Transformed Cell Lines

2019 ◽  
Vol 93 (17) ◽  
Author(s):  
Yaoyao Zhang ◽  
Na Tang ◽  
Jun Luo ◽  
Man Teng ◽  
Katy Moffat ◽  
...  
Keyword(s):  
T Cell ◽  
Disease Virus ◽  
Cell Lines ◽  
Critical Role ◽  
Marek's Disease Virus ◽  
Marek's Disease ◽  
Marek’S Disease Virus ◽  
Marek’S Disease ◽  
T Cell Lymphomas

ABSTRACT MicroRNAs (miRNAs) are small noncoding RNAs with profound regulatory roles in many areas of biology, including cancer. MicroRNA 155 (miR-155), one of the extensively studied multifunctional miRNAs, is important in several human malignancies such as diffuse large B cell lymphoma and chronic lymphocytic leukemia. Moreover, miR-155 orthologs KSHV-miR-K12-11 and MDV-miR-M4, encoded by Kaposi’s sarcoma-associated herpesvirus (KSHV) and Marek’s disease virus (MDV), respectively, are also involved in oncogenesis. In MDV-induced T-cell lymphomas and in lymphoblastoid cell lines derived from them, MDV-miR-M4 is highly expressed. Using excellent disease models of infection in natural avian hosts, we showed previously that MDV-miR-M4 is critical for the induction of T-cell lymphomas as mutant viruses with precise deletions were significantly compromised in their oncogenicity. However, those studies did not elucidate whether continued expression of MDV-miR-M4 is essential for maintaining the transformed phenotype of tumor cells. Here using an in situ CRISPR/Cas9 editing approach, we deleted MDV-miR-M4 from the MDV-induced lymphoma-derived lymphoblastoid cell line MDCC-HP8. Precise deletion of MDV-miR-M4 was confirmed by PCR, sequencing, quantitative reverse transcription-PCR (qRT-PCR), and functional analysis. Continued proliferation of the MDV-miR-M4-deleted cell lines demonstrated that MDV-miR-M4 expression is not essential for maintaining the transformed phenotype, despite its initial critical role in the induction of lymphomas. Ability to examine the direct role of oncogenic miRNAs in situ in tumor cell lines is valuable in delineating distinct determinants and pathways associated with the induction or maintenance of transformation in cancer cells and will also contribute significantly to gaining further insights into the biology of oncogenic herpesviruses. IMPORTANCE Marek’s disease virus (MDV) is an alphaherpesvirus associated with Marek’s disease (MD), a highly contagious neoplastic disease of chickens. MD serves as an excellent model for studying virus-induced T-cell lymphomas in the natural chicken hosts. Among the limited set of genes associated with MD oncogenicity, MDV-miR-M4, a highly expressed viral ortholog of the oncogenic miR-155, has received extensive attention due to its direct role in the induction of lymphomas. Using a targeted CRISPR-Cas9-based gene editing approach in MDV-transformed lymphoblastoid cell lines, we show that MDV-miR-M4, despite its critical role in the induction of tumors, is not essential for maintaining the transformed phenotype and continuous proliferation. As far as we know, this was the first study in which precise editing of an oncogenic miRNA was carried out in situ in MD lymphoma-derived cell lines to demonstrate that it is not essential in maintaining the transformed phenotype.

Use of an agar culture technique for establishing lymphoid cell lines from Marek's disease lymphomas

1981 ◽  
Vol 28 (6) ◽  
pp. 757-766 ◽  
Author(s):  
L. N. Payne ◽  
K. Howes ◽  
M. Rennie ◽  
Janene M. Bumstead ◽  
A. W. Kidd
Keyword(s):  
Cell Lines ◽  
Lymphoid Cell ◽  
Culture Technique ◽  
Marek's Disease ◽  
Marek’S Disease ◽  
Agar Culture ◽  
Lymphoid Cell Lines

scholarly journals Identification and characterization of a novel spliced form of the meq transcript in lymphoblastoid cell lines derived from Marek's disease tumours

2007 ◽  
Vol 88 (8) ◽  
pp. 2111-2120 ◽  
Author(s):  
Tsukasa Okada ◽  
Michihiro Takagi ◽  
Shiro Murata ◽  
Misao Onuma ◽  
Kazuhiko Ohashi
Keyword(s):  
Cell Lines ◽  
Leucine Zipper ◽  
Interleukin 2 ◽  
Direct Interaction ◽  
Marek's Disease ◽  
Negative Regulator ◽  
Lymphoblastoid Cell Lines ◽  
Dependent Manner ◽  
Marek’S Disease ◽  
Basic Leucine Zipper

In tumour cell lines established from Marek's disease (MD) lymphomas L-meq is consistently expressed. It contains a 180 bp insertion encoding additional copies of the proline-rich repeat in the meq open reading frame and its product may contribute to the maintenance of MD virus (MDV) latency. In this study, we identified a novel spliced form of the meq transcript in MD-derived lymphoblastoid cell lines and in MDV-infected cells. This transcript, termed Δmeq, encodes an N-terminal 98 aa of the Meq protein and lacks part of the basic leucine zipper (bZIP) and transactivation domains. In MD cell lines, transcription of L-meq was significantly downregulated, while that of the Δmeq transcript was upregulated during apoptosis. These observations were also confirmed at the protein expression level. Reporter assays using meq- and interleukin-2 (IL-2)-promoter-driven luciferase vectors revealed that ΔMeq suppressed transactivation by L-Meq or Meq in a dose-dependent manner. Immunoprecipitation confirmed that ΔMeq was associated with L-Meq or Meq physically. These results suggest that ΔMeq could be involved in apoptosis in MD cell lines as it works as a negative regulator of L-Meq and Meq by direct interaction.

scholarly journals Expression of major histocompatibility antigens on Marek's disease lymphoma-derived cell lines.

1984 ◽  
Vol 46 (1) ◽  
pp. 105-113 ◽  
Author(s):  
Tomoko HIGASHIHARA ◽  
Takeshi MIKAMI ◽  
Misao ONUMA ◽  
Hisao IZAWA ◽  
Haruo MATSUDA ◽  
...  
Keyword(s):  
Cell Lines ◽  
Marek's Disease ◽  
Marek’S Disease ◽  
Major Histocompatibility ◽  
Histocompatibility Antigens ◽  
Major Histocompatibility Antigens

scholarly journals Targeted Editing of the pp38 Gene in Marek’s Disease Virus-Transformed Cell Lines Using CRISPR/Cas9 System

Viruses ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 391 ◽  
Author(s):  
Yaoyao Zhang ◽  
Jun Luo ◽  
Na Tang ◽  
Man Teng ◽  
Vishwanatha R.A.P. Reddy ◽  
...  
Keyword(s):  
Disease Virus ◽  
Cell Lines ◽  
Marek's Disease Virus ◽  
Marek's Disease ◽  
Viral Gene ◽  
Marek’S Disease Virus ◽  
Marek’S Disease ◽  
Transformed Cell ◽  
Transformed Cell Lines

Marek’s disease virus (MDV), a lymphotropic α-herpesvirus associated with T-cell lymphomas in chickens, is an excellent model for herpesvirus biology and virus-induced oncogenesis. Marek’s disease (MD) is also one of the cancers against which a vaccine was first used. In the lymphomas and lymphoblastoid cell lines (LCLs) derived from them, MDV establishes latent infection with limited gene expression. Although LCLs are valuable for interrogating viral and host gene functions, molecular determinants associated with the maintenance of MDV latency and lytic switch remain largely unknown, mainly due to the lack of tools for in situ manipulation of the genomes in these cell lines. Here we describe the first application of CRISPR/Cas9 editing approach for precise editing of the viral gene phosphoprotein 38 (pp38), a biomarker for latent/lytic switch in MDV-transformed LCLs MDCC-MSB-1 (Marek’s disease cell line MSB-1) and MDCC-HP8. Contradictory to the previous reports suggesting that pp38 is involved in the maintenance of transformation of LCL MSB-1 cells, we show that pp38-deleted cells proliferated at a significant higher rate, suggesting that pp38 is dispensable for the transformed state of these cell lines. Application of CRISPR/Cas9-based gene editing of MDV-transformed cell lines in situ opens up further opportunities towards a better understanding of MDV pathogenesis and virus-host interactions.

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