Insertion of reticuloendotheliosis virus long terminal repeat into a bacterial artificial chromosome clone of a very virulent Marek's disease virus alters its pathogenicity

Isolation and full-genome sequence of two reticuloendotheliosis virus strains from mixed infections with Marek’s disease virus in China

“…The recombinant virus produced a unique 4-kb transcript, which was also detected in RM-1, but not in rMd5 BAC. Subsequently, Mays et al [20] found that the virus rMd5-RM1-LTR was attenuated at cell culture passage 40, but could still cause severe thymic and bursal atrophy, early immunosuppression, and early cytolytic infection. More importantly, a field MDV strain (GX0101) that contained the REV LTR was isolated, which means that it was possible for the REV LTR to integrate into the MDV genome in the field.…”

Influence of avian leukosis virus long terminal repeat on biological activities of Marek's disease virus

“…Genomic sequencing has confirmed that a single REV LTR insert resides in the genome of GX0101 and is located upstream of the sorf2 gene (Su et al, 2012. Unlike the artificial constructed virus strain rMd5-RM1-LTR, in which the REV LTR insert was particularly unstable, existing for only one week after infection of chickens (Mays et al, 2012), the inserted REV LTR fragment in GX0101 remained stable following 20 passages in chickens. The differences in stability of the REV LTR insert for GX0101 and rMd5-RM1-LTR may be related to different integration or different genome structure.…”

“…RM1 was a recombinant MDV containing REV LTR produced during cocultivation of REV and MDV. The REV LTR insert was not stable during passage in chickens when it was inserted into Md5 at the same site (Kim et al, 2011;Mays et al, 2012). In contrast, GX0101 maintained its REV LTR insert even after 20 passages in chickens.…”

A recombinant field strain of Marek's disease (MD) virus with reticuloendotheliosis virus long terminal repeat insert lacking the meq gene as a vaccine against MD

“…Moreover, the insertion of the REV LTR into the genome of CVI988/Rispens results in enhanced growth ability and protective efficacy [40]. REV LTR only remained stable in the Md5 genome for 1 week post-inoculation with the virus, but in vivo experiments still demonstrated a reduction in the pathogenicity of Md5 following the insertion of REV LTR [37,38].…”

“…Although the reasons for this difference are still unknown, we suggest that it is due to differences in the viral genome. Previous whole sequence analyses have demonstrated significant differences between the genomes of GX0101 and Md5, and the REV LTR was not stable when it was artificially inserted into Md5 genome [37,38]. In addition, this difference may be due to the insertion of the REV LTR, which is a strong promoter or enhancer that trans-activates different genes depending upon the insertion site [39].…”