GENETIC AND BIOLOGICAL DETERMINANTS OF AVIAN TUMOR VIRUS PATHOGENICITY, TRANSMISSION, AND EVOLUTION
Location: Avian Disease and Oncology Laboratory
Title: Some observations on the pathogenicity of a molecular clone of a very virulent strain of Marek’s disease virus containing an insert of long terminal repeat of reticuloendotheliosis virus
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: May 22, 2012
Publication Date: June 24, 2012
Citation: Fadly, A.M., Mays, J.K., Silva, R.F., Kim, T. 2012. Some observations on the pathogenicity of a molecular clone of a very virulent strain of Marek’s disease virus containing an insert of long terminal repeat of reticuloendotheliosis virus [abstract]. 9th International Symposium on Marek's Disease and Avian Herpesviruses, June 24-28, 2012, Freie Universitat Berlin. p. 43.
We recently artificially inserted REV LTR into a bacterial artificial chromosome (BAC) clone of a very virulent strain of Marek’s disease (MD) virus (MDV), Md5; the virus was designated rMd5-RM1-LTR (Kim et al., 2011). In the present study, susceptible chickens of ADOL line 15I5 X 71 with and without MD maternal antibody were used to study the influence of REV LTR insert on the pathogenicity of strain Md5 of MDV. Chickens were intra-abdominally inoculated at hatch with rMd5-RM1-LTR, rMd5 BAC parental virus, wild type of strain Md5, or strain RM1 (Witter et al., 1997) of MDV viruses. Chickens were observed for MDV-induced tumors, and bursal and thymus atrophy (BTA) for 8 weeks of age. The rMd5-RM1-LTR virus induced BTA and tumors at passage 10; however was highly attenuated at passage 40 and caused no BTA and tumors. Using PCR analysis, REV LTR insert was detected in MDV isolated from Buffy coat cells collected from chickens inoculated with rMd5-RM1-LTR, but only at 1 week post-inoculation (PI). The data suggest that the presence of REV LTR insert within MDV genome for one week PI with virus at hatch is sufficient to cause reduction in pathogenicity of strain Md5 of MDV.