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to an E box motif in the R region of the bovine leukemia virus long terminal repeat stimulates viral gene expression. J Biol Chem 2002, 277, 8775-8789. 4. Dekoninck A., Calomme C., Nizet S., de Launoit Y., Burny A., Ghysdael J., Van Lint C.: Identification and characterization of a PU.1/Spi-B binding site in the bovine leukemia virus long terminal repeat. Oncogene 2003, 22, 2882-2896. 5. Derse D., Casey J.W.: Two elements in the bovine leukemia virus long terminal repeat that regulate gene expression. Science 1986, 231, 1437-1440. 6. Dube S., Abbott L., Dube D

differentiation of presumed clones of the apricot cultivar Velkopavlovická. Sci. Horticult ., 143 , 1–6. Bayram, E., Yilmaz, S., Hamat-Mecbur, H., Kartal-Alacam, G., Gozukirmizi, N. (2012). Nikita retrotransposon movements in callus cultures of barley ( Hordeum vulgare L.). Plant Omics Journal (POJ) , 5 (3), 211–215. Benachenhou, F., Sperber, G. O., Bongcam-Rudloff, E., Andersson, G., Boeke, J. D., Blomberg, J. (2013). Conserved structure and inferred evolutionary history of long terminal repeats (LTRs). Mobile DNA , doi: 10.1186/1759-8753-4-5. Berg, D. E., Howe, M. H

terminal repeat into a bacterial artificial chromosome clone of Marek's disease virus (MDV) alters expression of nearby MDV genes. Virus Genes 2011, 42 , 369 - 376. 9. Messerle M., Crnkovic I., Hammerschmidt W., Ziegler H., Koszinowski U.H.: Cloning and mutagenesis of a herpesvirus genome as an infectious bacterial artificial chromosome. Proc Nat Acad Sci USA 1997, 94 , 14759 - 14763. 10. Mays J.K., Silva R.F., Kim T., Fadly A.: Insertion of reticuloendotheliosis virus long terminal repeat into a bacterial artificial chromosome clone of a very virulent Marek's disease

59 v-rel oncoprotein. This gene belongs to the rel/dorsal protein family related to nuclear factor kappa B involved in binding of DNA transcription factors. REV-T is responsible for an acute form of neoplasia in infected cells. The regions of long terminal repeats (LTRs) are 569 bp long and harbour promoter sites for cell machinery in a number of cell lines ( 22 ). These LTR sequences act as a promoter and enhancer for viral RNA translation. So far, at least two complete field strain sequences of the REV genome originating from the United States and China have

chain reaction. J Virol Methods 1999, 78, 199-208. 24. Renshaw R.W., Casey J.W.: Analysis of the 5’long terminal repeat of bovine syncytia virus. Gene 1994, 141, 221-224. 25. Romen F., Backes P., Materniak M., Sting R., Vahlenkamp T.W., Riebe R., Pawlita M., Kuzmak J., Löchelt M.: Serological detection systems for identification of cows shedding bovine foamy virus via milk. Virology 2007, 364, 123-131. 26. Winkler I.G., Löchelt M., Levesque J-P., Bodem J., Flügel R.M., Flower R.L.P.: A rapid streptavidin-capture ELISA specific for the detection of antibodies to feline

Virol 1998, 79, 101–106. 4. Chen H., Wilcox G., Kertayadnya G., Wood C.: Characterization of the Jembrana disease virus tat gene and the cis- and trans-regulatory elements in its long terminal repeats. J Virol 1999, 73, 658–666. 5. Craigo J.K., Montelaro R.C.: Lessons in AIDS vaccine development learned from studies of equine infectious anemia virus infection and immunity. Viruses 2013, 5, 2963–2976. 6. Ditcham W.G.F.: The development of recombinant vaccines against Jembrana disease, Murdoch University 2007, http://researchrepository.murdoch.edu.au/id/eprint/438 . 7

long terminal repeat and leadergag regions using real-time polymerase chain reaction. J Virol. Methods 2008, 147, 338-344. 6. Brodie S.J., de la Concha-Bermejillo A., Koenig G., Snowder G.D., DeMartini J.C.: Maternal factors associated with prenatal transmission of ovine lentivirus. J Infect Dis 1994, 169, 653-657. 7. Broughton-Neiswanger L.E., White S.N., Knowles D.P., Mousel M.R., Lewis G.S., Herndon D.R., Hermann-Hoesing L.M.: Non-maternal transmission is the major mode of ovine lentivirus transmission in a ewe flock: A molecular epidemiology study. Infect. Genet

many generations. At present, about 8.0% of the human genome is occupied by endogenous retrovirus elements [ 9 ]. The HERVs are composed of two long terminal repeats (LTRs) and four genes, gag, pol, pro and env The gag gene encodes a group-specific antigen that serves as a retroviral capsid protein. Another gene, pro , codes for the viral protease, while pol contains a reverse transcriptase coding region. A HERV element differs from other LTR retrotransposons by the presence of the env gene encoding viral membrane proteins. Long terminal repeats contain

., Liu W., Li F., Zhang Q., Lu Y., Cao D. (2015). Association between BMP15 gene polymorphism and reproduction traits and its tissues expression characteristics in chicken. PLo S One., 10 e0143298. Han J.S. (2010). Non-long terminal repeat (non-LTR) retrotransposons: mechanisms, recent developments and unanswered questions. Mob. DNA, 1: 15. Hanrahan J.P., Gregan S.M., Mulsant P., Mullen M., Davis G.H., Powell R., Gal- loway S.M. (2004). Mutations in the genes for oocyte-derived growth factors GDF9 and BMP15 are associated with both increased ovulation rate and

-J and REV) which induced immunosuppressive and tumourigenic diseases in poultry in infected CEF cells. This may indicate a direct role for MIF in MDV replication or pathogenesis. Induction of MIF expression was also found in herpes simplex virus type 1 (HSV-1) ( 18 ), human cytomegalovirus (HCMV), ( 6 ) and dengue virus ( 5 ). HCMV paralyses macrophage motility through release of MIF ( 6 ), and MIF promotes HIV-1 replication through the activation of HIV-1 long terminal repeats (LTR) ( 22 ). However, the reduction of MIF in skin, spleen, and thymus during early and