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Retroviral vector-based RNA interference against Marek's disease virus and avian leukosis virusChen, Mo. January 2008 (has links)
Thesis (Ph. D.)--Michigan State University. Microbiology and Molecular Genetics, 2008. / Title from PDF t.p. (Proquest, viewed on Aug. 20, 2009) Includes bibliographical references. Also issued in print.
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Nuclear Factor kappa B is central to Marek's Disease herpesvirus induced neoplastic transformation of CD30 expressing lymphocytes in-vivoKumar, Shyamesh, Kunec, Dusan, Buza, Joram, Chiang, Hsin-I, Zhou, Huaijun, Subramaniam, Sugalesini, Pendarvis, Ken, Cheng, Hans, Burgess, Shane January 2012 (has links)
BACKGROUND:Marek's Disease (MD) is a hyperproliferative, lymphomatous, neoplastic disease of chickens caused by the oncogenic Gallid herpesvirus type 2 (GaHV-2 / MDV). Like several human lymphomas the neoplastic MD lymphoma cells overexpress the CD30 antigen (CD30hi) and are in minority, while the non-neoplastic cells (CD30lo) form the majority of population. MD is a unique natural in-vivo model of human CD30hi lymphomas with both natural CD30hi lymphomagenesis and spontaneous regression. The exact mechanism of neoplastic transformation from CD30lo expressing phenotype to CD30hi expressing neoplastic phenotype is unknown. Here, using microarray, proteomics and Systems Biology modeling / we compare the global gene expression of CD30lo and CD30hi cells to identify key pathways of neoplastic transformation. We propose and test a specific mechanism of neoplastic transformation, and genetic resistance, involving the MDV oncogene Meq, host gene products of the Nuclear Factor Kappa B (NF-kappaB) family and CD30 / we also identify a novel Meq protein interactome.RESULTS:Our results show that a) CD30lo lymphocytes are pre-neoplastic precursors and not merely reactive lymphocytes / b) multiple transformation mechanisms exist and are potentially controlled by Meq / c) Meq can drive a feed-forward cycle that induces CD30 transcription, increases CD30 signaling which activates NF-kappaB, and, in turn, increases Meq transcription / d) Meq transcriptional repression or activation of the CD30 promoter generally correlates with polymorphisms in the CD30 promoter distinguishing MD-lymphoma resistant and susceptible chicken genotypes e) MDV oncoprotein Meq interacts with proteins involved in physiological processes central to lymphomagenesis.CONCLUSIONS:In the context of the MD lymphoma microenvironment (and potentially in other CD30hi lymphomas as well), our results show that the neoplastic transformation is a continuum and the non-neoplastic cells are actually pre-neoplastic precursor cells and not merely immune bystanders. We also show that NF-kappaB is a central player in MDV induced neoplastic transformation of CD30-expressing lymphocytes in vivo. Our results provide insights into molecular mechanisms of neoplastic transformation in MD specifically and also herpesvirus induced lymphoma in general.
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Characterization of the Meq oncoproteins of Marek's disease virus vaccine strain CVI988/RispensAjithdoss, Dharani K. 2009 May 1900 (has links)
Marek?s disease virus serotype-1 (MDV-1) causes T cell lymphomas in chickens.
Vaccines prepared from attenuated CVI988/Rispens MDV-1 strain currently offer the
best protection. Although attenuated CVI988 is non-oncogenic, it codes for two forms of
the MDV-1 oncoprotein Meq (CVI-Meq and CVI-L Meq). In this study, both CVI-Meq
proteins, like the Meq protein of Md5 (a very virulent oncogenic strain), transformed
Rat-2 and NIH3T3 cells. Both CVI-Meq and CVI-L Meq proteins activated the meq
promoter only in the presence of chicken c-Jun (CK-Jun) whereas Md5-Meq activated
the same promoter irrespective of CK-Jun co-expression. However, all three Meq
proteins bound the meq promoter regardless of whether CK-Jun was co-expressed. We
constructed three chimeric Meq proteins, namely, Md5-CVI-Meq, CVI-Md5-Meq, and
Md5-CVI-L by exchanging domains between Md5 meq and CVI meq genes. Although
these chimeric Meq proteins transactivated the meq promoter, the activation was
significantly less than Md5-Meq. The current study indicated amino acid residues at
positions 71 and 320 were important for Md5-Meq increase transcription of its own promoter. All three Meq proteins activated the MDV gB, MMP-3 and Bcl-2 promoters
and suppressed transcription from the MDV pp38/pp14 bidirectional promoter.
CVI-Meq protein in the context of other Md5 genes caused tumors only in 6% of
chickens when compared to parental rMd5 (a very virulent strain), which induced
lymphomas in 100% of chickens, (Reddy and Lupiani, unpublished data). Taking
advantage of these two different phenotypes, we constructed two chimeric Meq proteins,
Md5/CVI-Meq and CVI/Md5-Meq, by exchanging DNA binding and transactivation
domains between Md5-Meq and CVI-Meq to understand the role of the DNA binding
and the transactivation domains of Meq in transformation. rMd5-Md5/CVI-Meq virus
caused 100% mortality in chickens and T lymphomas were found at high frequency in
the peripheral nerves and various organs such as the heart, spleen, kidney, and gonads.
On the other hand, rMd5-CVI/Md5-Meq induced disease in 36% of chickens on average
and lesions were primarily in the nerves. Very rarely, lesions were present in the spleen
and heart and no tumors were present in the kidney or gonads. Our results suggest that
both the DNA binding domain and transactivation domain of Meq could cooperatively
determine the nature of lymphomas in chickens.
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Characterization of a bacterial artificial chromosome (BAC)-based infectious clone of a low passage Marek's disease virus (MDV) vaccine strain, CVI988McDowell, Erin. January 2009 (has links)
Thesis (M.S.)--University of Delaware, 2009. / Principal faculty advisor: Mark Parcells, Dept. of Animal & Food Sciences. Includes bibliographical references.
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Association of markers in genes of the growth hormone axis with the viral load in lymphoid tissues of chickens infected with Marek's disease virusLinher, Katja. January 2000 (has links)
Vaccination against Marek's disease (MD) is greatly enhanced by host genetic resistance. Genes of the growth hormone (GH) axis have been reported to affect the ontogeny and effector functions of cells of the immune system. Two strains of White Leghorn chickens bred for contrasting homozygous markers in the GH and GH receptor (GHR) genes were challenged with MDV. Contrasts for the significant interaction between marker genotype and tissue indicated that the GH/GHR marker genotype caused a shift in the distribution of the viral load in lymphoid tissues in the two strains. The analysis suggests that genetic variations in genes of the GH axis may differentially affect the host response to MDV replication in lymphoid tissues. Regarding the early time course of infection, at day 6 the viral load was highest in the thymus, while at day 10, it was highest in the spleen, indicating that the virus may have accumulated in the spleen or was continuing to replicate in this tissue. (Abstract shortened by UMI.)
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Identification of genetic markers associated with Marek's disease resistance in chickensMasilamani, Twinkle Jasmine January 2003 (has links)
Marek's disease (MD) is a highly contagious and economically important disease in the poultry industry. It is caused by an oncogenic avian herpes virus. The ability of the virus to evolve into new strains is a continual threat. Vaccination, proper management and genetic resistance are required to completely eliminate the pathogen. The discovery of several markers associated with MD resistance shows that genetic selection for resistance is feasible. Our objective was to identify markers in QTL regions that are associated with MD viraemia. The markers analysed were in the ODC gene, the GH gene and two chemokine genes, all of which are candidate genes for immune responsiveness. A database in a commercial strain of White Leghorn chickens was created. Heterozygous males and homozygous females were identified. The offspring were challenged with MD virus and spleen and thymus samples were collected six days after infection. The viral titre was quantified using competitive PCR. The data was analysed using non-parametric statistics. We found that the paternal alleles of a Hindlll RFLP in the ODC gene were associated with differences in MD viraemia in one of the six sire families analysed. In addition, a Sacl RFLP located in the GH gene also segregated for alleles, which affected MD viraemia. The analysis of the ODC gene was extended to include a second RFLP at a Msp\ site. Together with the Hindlll RFLP it defines three different haplotypes. One genotypic class AB (Hindlll (+/-), Mspl (+/+)) was associated with low vireamia in the thymus and the genotype BB (Hindlll (-/-), Mspl (+/+)) with high viraemia in the spleen. The result suggests that genetic variations in the ODC and GH gene affect MD viraemia. However, we cannot exclude that the observed effects might be due to linkage disequilibrium with adjacent genes. In the latter case, chromosome 3 and chromosome 1, which harbour the ODC and GH gene respectively, must segregate for regions that affect viraemia. The markers identified in this analysis can be used in marker assisted selection.
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Association of markers in genes of the growth hormone axis with the viral load in lymphoid tissues of chickens infected with Marek's disease virusLinher, Katja. January 2000 (has links)
No description available.
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Identification of genetic markers associated with Marek's disease resistance in chickensMasilamani, Twinkle Jasmine January 2003 (has links)
No description available.
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Mechanisms of Genetic Resistance and Neoplastic Transformation in Marek's DiseaseKumar, Shyamesh 09 December 2011 (has links)
Marek’s disease (MD) of chickens is an economically important, contagious, neoplastic disease caused by Gallid herpesvirus type 2. All chicken are susceptible to MDV infection and neoplastic transformation, but, only susceptible genotypes develop gross lymphomas. Lymphomas regress in resistant genotypes from 21 days post infection (dpi). The central aims of this study were to understand the mechanisms of non-MHC associated genetic resistance and the molecular pathways of neoplastic transformation. We hypothesized that, a) in resistant chickens at 21 dpi the tissue microenvironment is compatible with cell mediated immunity but in susceptible lines antagonistic to cell mediated immunity, b) resistant genotypes present immunogenic peptides on their MHC class I which while the peptides presented by susceptible genotypes do not induce CTL immunity resulting in tumor progression. We used inbred, MHC homozygous MD resistant (L6) and susceptible (L7) chickens and reductionist methods to test our hypotheses. Our results indicated that the tumor microenvironment is pro T-regulatory in both resistant and susceptible genotypes, and, the host immune response (pro Th-1 in resistant and pro Th-2/T-reg in susceptible) influences the tumor regression or progression. Statistical analysis of MHC class I bound peptides from resistant and susceptible genotypes confirmed that they present the same peptides and perhaps genes outside the MHC locus play an important role in determining resistance. Next, using Systems Biology tools like genomics, proteomics, Gene Ontology modeling and pathway analysis we compared the transcriptome and proteome of neoplastically transformed cells (CD30hi) and non-neoplastically transformed cells (CD30lo) which are the two components of tumor microenvironment. We demonstrated that: a) in situ, CD30lo cells are pre-neoplastic and the proteome involved in transformation and potential mechanisms that may be controlled by MDV oncogene Meq; b) Meq can drive a feed forward loop that induces CD30 transcription and overexpression, increased CD30 signaling, which then activates NFêB and, in turn, increases Meq transcription; c) Meq transcriptional repression or activation from the CD30 promoter generally correlates with a polymorphism in the CD30 promoter between MD-resistant and -susceptible chicken genotypes and so a herpesvirus has evolved to utilize NFêB as a direct transcriptional activator for its oncogene.
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Functional analysis of Meq, a Marek's disease virus (MDV)bZIP protein associated with T cell transformationQian, Zheng January 1996 (has links)
No description available.
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