Effect of Virus Pathogenicity on Antibody Production in Marek's Disease

Smith, M. W.; Calnek, B. W.

doi:10.2307/1589040

Cited by 25 publications

(9 citation statements)

References 14 publications

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“…The MDV clone JM/102W (12) and the CS strain of REV (13) were used for coinfection experiments. Other MDV strains used were CU2 (14), Md5 (15), and Mdll (16). Viruses were propagated in DEFs or chicken embryo fibroblasts as described (17).…”

Section: Methodsmentioning

confidence: 99%

Retroviral insertions into a herpesvirus are clustered at the junctions of the short repeat and short unique sequences.

Jones

Isfort

Witter

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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We previously described the integration of a nonacute retrovirus, reticuloendotheliosis virus (REV), into the genome of a herpesvirus, Marek disease virus (MDV), following both long-term and short-term coinfection in cultured fibroblasts. The long-term coinfection occurred in the course of attenuating the oncogenicity of the JM strain of MDV and was sustained for >100 passages. The short-term coinfection, which spanned only 16 passages, was designed to recreate the insertion phenomenon under controlled conditions. We found that REV integrations into MDV were common and could occur within the first passage following coinfection. Now we have mapped the integration sites. After 5-16 passages in vitro, 17 out of 19 REV junction sites are clustered in two

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Section: Methodsmentioning

confidence: 99%

Retroviral insertions into a herpesvirus are clustered at the junctions of the short repeat and short unique sequences.

Jones

Isfort

Witter

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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“…Cloned MDV isolates CU-2 (low oncogenicity) and JM-16 (moderate oncogenicity) have been described (Smith & Calnek, 1973;Calnek et al, 1984). All inocula for these experiments were from stocks of infected chicken kidney cell cultures stored at -196 °C.…”

Section: Methodsmentioning

confidence: 99%

Effect of Immunocompetence on the Establishment and Maintenance of Latency with Marek's Disease Herpesvirus

Buscaglia

Calnek

Schat

1988

Journal of General Virology

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SUMMARYMarek's disease virus (MDV) infections normally have an early cytolytic phase in lymphoid organs at 3 to 6 days post-infection followed by a period of latent infection. Little is known about the mechanisms that govern latency with herpesvirus infections, including Marek's disease (MD). To investigate the importance of immunocompetence for either the establishment or the maintenance of latency in MD, immunosuppressive treatments were applied prior to infection with MDV or after latency was established. These included cyclosporin (Cs) or betamethasone (BM) treatments, neonatal thymectomy plus cyclophosphamide treatment (Tx/Cy), and infection at a young age before full competence. The effect of all the treatments was determined by examining tissues and spleen cells for evidence of virus replication before and after cultivation in vitro. Induced (Cs or Tx/Cy treatments) or natural (infection at a young age) incompetence resulted in prolonged and more widespread early cytolytic infection. Immunosuppression by Cs after latency had developed resulted in a reappearance of cytolytic infection in the spleen and it enhanced the cytolytic infection in the thymus and the bursa of Fabricius. After immunosuppression with Cs, cytolytic infection was found mostly in T cells, although many of the virus-positive cells did not have markers for either T cells or B cells. Immunosuppression by BM after latency had developed also resulted in the reappearance of cytolytic infection in the spleen but only at a very low level. These results suggest that immunocompetence is required for the establishment and maintenance of latency.

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“…We now present the nucleotide sequence of a mildly virulent strain known as CU-2. This strain was originally isolated and cloned by Smith and Calnek [45] and pathotyped as mildly virulent (mv) in susceptible chickens [3,14,46]. To identify mutations, which may be responsible for its less virulent phenotype, CU-2 ORFS were compared with those found within the genomes of the attenuated strain CVI988 [34,49] and the very virulent strains Md5, Md11, and RB-1B [26,50,53].…”

Section: Introductionmentioning

confidence: 99%

Sequence determination of a mildly virulent strain (CU-2) of Gallid herpesvirus type 2 using 454 pyrosequencing

Spatz

Rue

2008

Virus Genes

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The complete DNA sequence of the mildly virulent Gallid herpesvirus type 2 strain CU-2 was determined and consists of 176,922 bp with an overall gene organization typical of class E herpesviruses. Phylogenetically, this strain partitions in its own branch between the virulent strains RB-1B, Md11, and Md5, and the vaccine strain CVI988. Overall, the genome of CU-2 is more similar to that of CVI988, with identically sized unique short regions of 11,651 bp. As in CVI988, an insertion of 177 bp was identified in the overlapping genes encoding the Meq, RLORF6, and 23 kDa proteins within the repeat long region of the genome. A total of 15 single nucleotide polymorphisms (SNPs) common to both CU-2 and CVI988, and not occurring in virulent strains, were identified in the genes encoding UL29, UL45, UL50, UL52, LORF10, RLORF14a, RLORF12, Meq(RLORF7), 23kDa, ICP4, US3, and two hypothetical proteins MDV071.4 and MDV076.4. Each gene encoding UL29 and Meq contained two SNPs. Only one major open reading frame (ORF) encoding UL41, the virus host shutoff (VHS) ribonuclease, was disrupted in the CU-2 genome. An additional cytosine after the 25 codon is predicted to produce a truncated protein of 97 aa. Since GaHV-2 mutants lacking UL41 have been reported to retain their virulence, other factors are likely responsible for the low virulence of CU-2. It is largely suspected that SNPs in common with CVI988 along with the insertions in the Meq loci are responsible for its phenotype. Conversely, we identified 43 nonsynonymous mutations (within 23 genes) that may contribute to the virulence of CU-2. These SNPs are shared exclusively with all sequenced virulent strains (Md5, Md11, and RB-1B) and not present within the CVI988 genome. Although most occur in proteins of unknown function, a significant percentage is in proteins involved in virion assembly.

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Effect of Virus Pathogenicity on Antibody Production in Marek's Disease

Cited by 25 publications

References 14 publications

Retroviral insertions into a herpesvirus are clustered at the junctions of the short repeat and short unique sequences.

Retroviral insertions into a herpesvirus are clustered at the junctions of the short repeat and short unique sequences.

Effect of Immunocompetence on the Establishment and Maintenance of Latency with Marek's Disease Herpesvirus

Sequence determination of a mildly virulent strain (CU-2) of Gallid herpesvirus type 2 using 454 pyrosequencing

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