Submitted to: Meeting Abstract
Publication Type: Abstract only
Publication Acceptance Date: 9/1/2010
Publication Date: 10/18/2010
Citation: Fadly, A.M., Mays, J.K., Kim, T., Silva, R.F. 2010. Further studies of a molecular clone of Marek's disease virus with an insert of long terminal repeat of reticuloendotheliosis virus [abstract]. In: 5th International Workshop on the Molecular Pathogenesis of Marek's Disease Virus and 1st Symposium on Avian Herpesviruses, October 17-20, 2010, Athens, Georgia, p. 23. Interpretive Summary:
Technical Abstract: Recently, we have reported on the development and pathogenicity of a bacterial artificial chromosome (BAC) clone of Marek’s disease (MD) virus (MDV) with an insert of long terminal repeat (LTR) of reticuloendotheliosis virus (REV). In the current study, we examined whether the REV LTR was retained by the rMd5 BAC virus following infection of duck embryo fibroblasts (DEFs) and one-day old ADOL line 15I5 X 71 chickens. DNA from DEFs infected with virus at various passage levels and from buffy coat (BC) cells obtained from chickens at 3 and 8 weeks post-infection with virus at hatch was tested for the presence of REV LTR by PCR. Results from in vitro evaluation revealed the presence of REV LTR in all viruses tested even in those used at levels higher than the 40th passage. In contrast, REV LTR was not detected in BC cells obtained from infected chickens, regardless of age at testing although the incidence of MD in these chickens that were inoculated with rMd5 BAC containing REV-LTR was less than that in chickens inoculated with rMd5 BAC without LTR or with wild type Md5 strain of MDV. Results from this study indicate that REV LTR was stable in cell culture, but not in chickens; and that the loss of REV LTR following replication of virus in chickens appears to occur within the first three weeks following infection with virus at hatch. The data also suggest that the influence of REV LTR on pathogenicity of MDV may not be dependent on retention of LTR for 3 weeks or longer after infection with virus at hatch.