@article{mbs:/content/journal/jgv/10.1099/vir.0.79778-0, author = "Tomioka, Y. and Ochiai, K. and Ohashi, K. and Ono, E. and Toyoda, T. and Kimura, T. and Umemura, T.", title = "Genome sequence analysis of the avian retrovirus causing so-called fowl glioma and the promoter activity of the long terminal repeat", journal= "Journal of General Virology", year = "2004", volume = "85", number = "3", pages = "647-652", doi = "https://doi.org/10.1099/vir.0.79778-0", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.79778-0", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", abstract = "So-called fowl glioma is a retroviral infectious disease caused by avian leukosis virus subgroup A (ALV-A). We determined the complete nucleotide sequence of the virus genome. The full-length sequence was consistent with a genetic organization typical of a replication-competent type C retrovirus lacking viral oncogenes. The coding sequences were well conserved with those of replication-competent viruses, but the 3′ noncoding regions including LTR were most related to those of replication-defective sarcoma viruses. The U3 region of the LTR had a few deletions and several point mutations compared to that of other ALVs. The promoter activities of the LTRs of glioma-inducing ALV and ALV-A standard strain, RAV-1, were equivalent in chick embryo fibroblasts (CEF), while that of glioma-inducing ALV was significantly lower than that of RAV-1 in human astrocytic cells. These subtle differences of the promoter activity of the LTR may be related to the induction of glial neoplasm.", }