DNA vaccination against v-src oncogene-induced tumours in congenic chickens

Plachý, Jiřı́; Hejnar, Jiřı́; Trtková, Kateřina Smešný; Trejbalová, Kateřina; Svoboda, Jan; Hála, K

doi:10.1016/s0264-410x(01)00181-5

Cited by 12 publications

(4 citation statements)

References 32 publications

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“…The Prague congenic chickens are among the best genetically defined model systems for immunological studies [91] – [93] . We introduced modifications in the genome of syngeneic CB (B 12 /B 12 ) chickens through the inoculation of T. cruzi trypomastigotes into fertilized eggs prior to incubation.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Autoimmune Chagas-Like Heart Disease by Bone Marrow Transplantation

et al. 2014

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BackgroundInfection with the protozoan Trypanosoma cruzi manifests in mammals as Chagas heart disease. The treatment available for chagasic cardiomyopathy is unsatisfactory.Methods/Principal FindingsTo study the disease pathology and its inhibition, we employed a syngeneic chicken model refractory to T. cruzi in which chickens hatched from T. cruzi inoculated eggs retained parasite kDNA (1.4 kb) minicircles. Southern blotting with EcoRI genomic DNA digests revealed main 18 and 20 kb bands by hybridization with a radiolabeled minicircle sequence. Breeding these chickens generated kDNA-mutated F1, F2, and F3 progeny. A targeted-primer TAIL-PCR (tpTAIL-PCR) technique was employed to detect the kDNA integrations. Histocompatible reporter heart grafts were used to detect ongoing inflammatory cardiomyopathy in kDNA-mutated chickens. Fluorochromes were used to label bone marrow CD3+, CD28+, and CD45+ precursors of the thymus-dependent CD8α+ and CD8β+ effector cells that expressed TCRγδ, vβ1 and vβ2 receptors, which infiltrated the adult hearts and the reporter heart grafts.Conclusions/SignificanceGenome modifications in kDNA-mutated chickens can be associated with disruption of immune tolerance to compatible heart grafts and with rejection of the adult host's heart and reporter graft, as well as tissue destruction by effector lymphocytes. Autoimmune heart rejection was largely observed in chickens with kDNA mutations in retrotransposons and in coding genes with roles in cell structure, metabolism, growth, and differentiation. Moreover, killing the sick kDNA-mutated bone marrow cells with cytostatic and anti-folate drugs and transplanting healthy marrow cells inhibited heart rejection. We report here for the first time that healthy bone marrow cells inhibited heart pathology in kDNA+ chickens and thus prevented the genetically driven clinical manifestations of the disease.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Autoimmune Chagas-Like Heart Disease by Bone Marrow Transplantation

et al. 2014

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“…TSTA is encoded by the transforming v-src gene, and its formation triggers an 11 amino-acid insertion into v-src. The tumorigenic activity of retroviruses is connected to the expression of the v-src oncogene [[62], [63], [64], [65]]. c-Src is the cellular homologue of the v-src viral oncogene.…”

Section: Discussionmentioning

confidence: 99%

The full recovery of mice (Mus Musculus C57BL/6 strain) from virus–induced sarcoma after treatment with a complex of DDMC delivery system and sncRNAs

Klimenko¹,

Сидоров²

2019

Non-coding RNA Research

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Background Virus-induced cellular genetic modifications result in the development of many human cancers. Methods In our experiments, we used the RVP3 cell line, which produce primary mouse virus-induced sarcoma in 100% of cases. Inbreed 4-week-old female C57BL/6 mice were injected subcutaneously in the interscapular region with RVP3 cells. Three groups of mice were used. For treatment, one and/or two intravenous injections of a complex of small non-coding RNAs (sncRNAs) a-miR-155, piR-30074, and miR-125b with a 2-diethylaminoethyl-dextran methyl methacrylate copolymer (DDMC) delivery system were used. The first group consisted of untreated animals (control). The second group was treated with one injection of complex DDMC/sncRNAs (1st group). The third group was treated with two injections of complex DDMC/sncRNAs (2nd group). The tumors were removed aseptically, freed of necrotic material, and used with spleen and lungs for subsequent RT-PCR and immunofluorescence experiments, or stained with Leishman-Romanowski dye. Results As a result, the mice fully recovered from virus-induced sarcoma after two treatments with a complex including the DDMC vector and a-miR-155, piR-30074, and miR-125b. In vitro studies showed genetic and morphological transformations of murine cancer cells after the injections. Conclusions Treatment of virus-induced sarcoma of mice with a-miR-155, piR-30074, and miR-125b as active component of anti-cancer complex and DDMC vector as delivery system due to epigenetic-regulated transformation of cancer cells into cells with non-cancerous physiology and morphology and full recovery of disease.

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“…The growth of sarcomas at the site of inoculation was monitored by calculating the area of prominent tumor. Transparent foil was placed on the tumor, the contours of the tumor were traced, and the area of the tumor was calculated in mm 2 (21). Birds bearing vast nonregressing tumors were sacrificed before they reached the terminal stage.…”

Section: Methodsmentioning

confidence: 99%

A Single-Amino-Acid Substitution in the Tvb ^S1 Receptor Results in Decreased Susceptibility to Infection by Avian Sarcoma and Leukosis Virus Subgroups B and D and Resistance to Infection by Subgroup E In Vitro and In Vivo

Reinišová

Šenigl

Yin

et al. 2008

J Virol

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The avian sarcoma and leukosis virus (ASLV) family of retroviruses contains five highly related envelope subgroups (A to E) thought to have evolved from a common viral ancestor in the chicken population. Three genetic loci in chickens determine the susceptibility or resistance of cells to infection by the subgroup A to E ASLVs. Some inbred lines of chickens display phenotypes that are somewhere in between either efficiently susceptible or resistant to infection by specific subgroups of ASLV. The tvb gene encodes the receptor for subgroups B, D, and E ASLVs. The wild-type Tvb S1 receptor confers susceptibility to subgroups B, D, and E ASLVs. In this study, the genetic defect that accounts for the altered susceptibility of an inbred chicken Retroviruses cause serious diseases in animals and humans. The disease process begins with the virus infecting a cell(s), a process mediated by the interaction of the retroviral envelope glycoproteins with specific cell surface proteins that act as receptors (14,24). A proper viral-glycoprotein-receptor interaction initiates conformational changes in the viral glycoproteins that ultimately result in the fusion of the viral and cellular membranes and entry of viral components (9). Despite the complexity and specificity of the viral-glycoprotein-receptor interaction required for virus entry, families of closely related retroviruses have evolved their glycoproteins to use different cellular proteins as receptors. Presumably, the presence of multiple viral subgroups that utilize different receptors is an advantage for viruses in overcoming host resistance. Resistance to retroviral infection occurs when the specific receptor protein is not available. Genetic alteration(s) can account for resistance, resulting in the complete lack of receptor protein expression or the expression of an aberrant protein not suitable as a viral receptor. In addition, receptors can be saturated with viral glycoproteins expressed by the cell, physically blocking receptor accessibility, a phenomenon known as receptor interference (14, 24).The avian sarcoma and leukosis virus (ASLV) family of retroviruses contains five highly related envelope subgroups (A to E) thought to have evolved in the chicken population from a common viral ancestor (4,5,24). Three genetic loci in chickens determine the susceptibility or resistance of cells to infection by the subgroup A to E ASLVs. Susceptibility to subgroup A ASLVs is determined by the tva locus; susceptibility to subgroup C ASLVs by the tvc locus; and susceptibility to the subgroup B, D, and E ASLVs by the tvb locus. The Tva proteins are related to the low-density lipoprotein receptor family (6, 25). The Tvb proteins are related to the tumor necrosis factor receptor (TNFR) family (2, 3, 7). The Tvc proteins are most closely related to mammalian butyrophilins of the immunoglobulin superfamily (11). The normal functions and ligands of the Tva, Tvb, and Tvc proteins in birds are unknown.The genetic defects that account for resistance to infection by specific ASLVs, tv...

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DNA vaccination against v-src oncogene-induced tumours in congenic chickens

Cited by 12 publications

References 32 publications

Inhibition of Autoimmune Chagas-Like Heart Disease by Bone Marrow Transplantation

Inhibition of Autoimmune Chagas-Like Heart Disease by Bone Marrow Transplantation

The full recovery of mice (Mus Musculus C57BL/6 strain) from virus–induced sarcoma after treatment with a complex of DDMC delivery system and sncRNAs

A Single-Amino-Acid Substitution in the Tvb ^S1 Receptor Results in Decreased Susceptibility to Infection by Avian Sarcoma and Leukosis Virus Subgroups B and D and Resistance to Infection by Subgroup E In Vitro and In Vivo

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DNA vaccination against v-src oncogene-induced tumours in congenic chickens

Cited by 12 publications

References 32 publications

Inhibition of Autoimmune Chagas-Like Heart Disease by Bone Marrow Transplantation

Inhibition of Autoimmune Chagas-Like Heart Disease by Bone Marrow Transplantation

The full recovery of mice (Mus Musculus C57BL/6 strain) from virus–induced sarcoma after treatment with a complex of DDMC delivery system and sncRNAs

A Single-Amino-Acid Substitution in the Tvb S1 Receptor Results in Decreased Susceptibility to Infection by Avian Sarcoma and Leukosis Virus Subgroups B and D and Resistance to Infection by Subgroup E In Vitro and In Vivo

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A Single-Amino-Acid Substitution in the Tvb ^S1 Receptor Results in Decreased Susceptibility to Infection by Avian Sarcoma and Leukosis Virus Subgroups B and D and Resistance to Infection by Subgroup E In Vitro and In Vivo