scholarly journals Diversity (Polymorphism) of the meq Gene in the Attenuated Marek's Disease Virus (MDV) Serotype 1 and MDV-Transformed Cell Lines

2002 ◽  
Vol 64 (12) ◽  
pp. 1097-1101 ◽  
Author(s):  
Kyung-Soo CHANG ◽  
Kazuhiko OHASHI ◽  
Misao ONUMA
Viruses ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 391 ◽  
Author(s):  
Yaoyao Zhang ◽  
Jun Luo ◽  
Na Tang ◽  
Man Teng ◽  
Vishwanatha R.A.P. Reddy ◽  
...  

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.


2000 ◽  
Vol 62 (3) ◽  
pp. 287-292 ◽  
Author(s):  
Sung-Il LEE ◽  
Michihiro TAKAGI ◽  
Kazuhiko OHASHI ◽  
Chihiro SUGIMOTO ◽  
Misao ONUMA

2002 ◽  
Vol 64 (5) ◽  
pp. 413-417 ◽  
Author(s):  
Kyung-Soo CHANG ◽  
Sung-Il LEE ◽  
Kazuhiko OHASHI ◽  
Ahmed IBRAHIM ◽  
Misao ONUMA

2021 ◽  
Vol 9 (8) ◽  
pp. 1681
Author(s):  
Poornima Roy ◽  
Katy Moffat ◽  
Venugopal Nair ◽  
Yongxiu Yao

Marek’s disease (MD) is an immunosuppressive and highly contagious lymphoproliferative disease caused by Marek’s disease virus (MDV) in poultry. Lymphoblastoid cell lines (LCLs) generated ex vivo from MD lymphomas are considered excellent models to study virus-host molecular interactions. LCLs mostly have latently infected MDV genome, but many of them also have varying populations of lytically-infected cells, thus making them very suitable to examine the molecular events associated with the switch from latent to lytic infection. MDV-encoded phosphoprotein 38 (pp38) is readily detectable in lytically-infected LCLs and hence considered as a biomarker for lytic infection. Whilst previous studies have suggested that pp38 is essential for the early cytolytic infection of B-cells, its role in the switch from latent to lytic infection of LCLs is still unclear. pp24, another phosphorylated protein in the same protein complex, shares the same promoter and N-terminal 65 amino acids as pp38. In this study we employed CRISPR activation (CRISPRa) technology for targeted activation of pp38/pp24 in LCLs to investigate their role in inducing lytic infection. Our results show that enforced expression of pp38/pp24 through CRISPRa induces orchestrated upregulation of other MDV genes including ICP4, gB, Meq and pp14 as well as differential expression of host genes thereby facilitating lytic infection. Our results also show that pp38/pp24 expression induces the lytic switch through inhibiting apoptosis.


1987 ◽  
Vol 68 (5) ◽  
pp. 1485-1490 ◽  
Author(s):  
A. Kanamori ◽  
K. Ikuta ◽  
S. Ueda ◽  
S. Kato ◽  
K. Hirai

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