Marek's disease virus-mediated enhancement of avian leukosis virus gene expression and virus production

Pulaski, James T.; Tieber, Virginia L.; Coussens, Paul M.

doi:10.1016/0042-6822(92)90065-w

Cited by 28 publications

(18 citation statements)

References 28 publications

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“…Although we noticed a small stimulation of the ASV LTR (two-to threefold) when cotransfected with plasmids coding for HCMV IE proteins (J. Knight, unpublished data), IE1 and IE2 cannot account for the extent of the increase in ASV RNA mediated by HCMV infection. It is also of interest that production of ALV in CEF has been shown to increase when accompanied by infection with the avian herpesvirus Marek's disease virus (MDV) (Pulaski et al, 1992). This increase was correlated with a concomitant increase in the level of RNA initiated from the ALV LTR promoter, suggesting that MDV may also encode or induce factors that act to increase transcription from the ALV LTR (Tieber et al, 1990).…”

Section: Discussionmentioning

confidence: 97%

Avian sarcoma virus RNA synthesis, RNA splicing and virus production in human foreskin fibroblasts: effect of co-infection with human cytomegalovirus

1993

Journal of General Virology

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The level of RNA transcripts in human foreskin fibroblast (HFF) cells initiated from the avian sarcoma virus (ASV) long terminal repeat (LTR) promoter was stimulated more than 10-fold when the cells were also infected with human cytomegalovirus (HCMV). HCMV was able to stimulate transcription from the ASV LTR promoter even when all the LTR sequence upstream of the TATA box was deleted, suggesting that only the basal LTR promoter is required for the effect. There were no significant changes in the ASV RNA splicing pattern in stimulated and unstimulated HFF cells. The mRNAs showing an increase during HCMV stimulation included aberrantly spliced ASV RNA species as well as unspliced gag-pol, single-spliced env and single-spliced src mRNAs. This pattern was quite different from ASV splicing in chicken embryo fibroblasts (CEF) but typical of that seen in other mammalian cells. A dramatic increase in infectious ASV production from the normally non-permissive HFF was correlated with the increase in amount of ASV RNA in response to HCMV. Thus, there is not an absolute block to ASV production in human cells. However, infectious ASV production was inefficent in HCMV-stimulated HFF compared to that in CEF cells.

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Section: Discussionmentioning

confidence: 97%

Avian sarcoma virus RNA synthesis, RNA splicing and virus production in human foreskin fibroblasts: effect of co-infection with human cytomegalovirus

1993

Journal of General Virology

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“…28,33 On the other hand, herpesvirus infection may be required to trigger or enhance the expression of other endogenous, latent, or coinfecting viruses (enveloped and unenveloped), which themselves may carry the genes necessary for tumorigenesis or progression to malignancy. 7,12,48,51 Additional experimental work will be needed to resolve these questions. Only experimental induction of cutaneous fibropapillomas and visceral fibromas with purified infectious herpesvirus would fulfill Koch's postulates for this agent.…”

Section: Discussionmentioning

confidence: 99%

Comparative Pathology and Pathogenesis of Spontaneous and Experimentally Induced Fibropapillomas of Green Turtles (Chelonia mydas)

Herbst

Jacobson²,

Klein

et al. 1999

Vet Pathol

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Abstract. Tumor biopsy samples from 25 Floridian and 15 Hawaiian green turtles (Chelonia mydas) with spontaneous green turtle fibropapillomatosis (GTFP) and from 27 captive-reared green turtles with experimentally induced GTFP were examined microscopically to differentiate the histologic features that result from GTFP pathogenesis and those that result from incidental factors that may vary according to geographic region. Common histologic features for spontaneous and experimentally induced tumors included fibroblast proliferation in the superficial dermis, epidermal acanthosis and hyperkeratosis, epidermal basal cell degeneration with dermalepidermal cleft formation, spinous layer degeneration with intraepidermal vesicle and pustule formation, and ulceration. Visceral tumors, found in eight of 10 (80%) free-ranging turtles with cutaneous disease that were examined after death, had extensive interstitial fibrous proliferation. The presence of spirorchid trematode eggs and associated foreign body granulomas, common secondary findings within spontaneous tumors, varied by geographic location, and these findings were not observed in experimentally induced tumors. Eosinophilic intranuclear inclusions and intranuclear herpesvirus-associated antigen immunoreactivity were found in 18 of 38 (47%) experimentally induced cutaneous tumors and nine of 119 (7.5%) spontaneous tumors from Floridian but not Hawaiian turtles. The possible involvement of GTFP-associated herpesvirus in the pathogenesis of epidermal degenerative changes and GTFP pathogenesis is discussed.Key words: Chelonia mydas; dermatitis; fibropapilloma; green turtles; herpesvirus; immunohistochemistry; tumor.Green turtle fibropapillomatosis (GTFP) is a disease of green turtles (Chelonia mydas) that is characterized by multiple cutaneous papillomas, fibromas, and fibropapillomas, as well as occasional visceral fibromas. Concern over recent increases in the prevalence of GTFP around the world has focused attention on identifying the cause and understanding the pathogenesis of this disease so that management strategies can be developed to minimize its impact on populations of endangered green turtles. 18 A thorough description of the disease process should identify the relevant histologic features seen in spontaneous lesions and distinguish these from features that are incidental or result from secondary processes. In addition, any proposed etiologic hypothesis should account for the major histologic features of the disease, and the pathogenesis of these lesions should be consistent with what is known about the pathobiology of closely related pathogens. Therefore, careful systematic evaluation of lesions from different populations can sometimes yield the etiologic agent but more effectively can eliminate candidates not present in all groups.The first histologic descriptions of GTFP were published about 60 years ago. 41,58,59 Subsequently, Jacobson et al. 31 provided a more detailed description of light and electron microscopic features of GTFP. These basic histolog...

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“…3]) containing a putative pentanucleotide response element (PRE) element (5Ј-GGTGG-3Ј) was located 36 bp upstream of the TATA box. Two PRE motifs which function as transcriptional enhancers during coinfection with Marek's disease virus are present in ALSV LTRs (7,31), although the neighboring sequences were unrelated to those of the EAV-HP PRE motifs. A purine-rich sequence (5Ј-GAGG AA-3Ј) overlapping the putative CCAAT box (nucleotides 131 to 136) was identical to the core sequence of the avian PU.1 box, which is involved in the macrophage-and B-cell-specific expression of the chicken lysozyme gene (2).…”

Section: Vol 74 2000 Nucleotide Sequence Of Full-length Eav-hp Provmentioning

confidence: 99%

Avian Endogenous Retrovirus EAV-HP Shares Regions of Identity with Avian Leukosis Virus Subgroup J and the Avian Retrotransposon ART-CH

Sacco

Flannery

Howes

et al. 2000

J Virol

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To resolve the genome structure of these retroviral elements, we have determined the complete sequence of two proviral clones of EAV-HP from a line N chicken genomic DNA yeast artificial chromosome library and from a meat-type chicken line 21 lambda library. The EAV-HP sequences from the two lines were 98% identical and had a typical provirus structure. The two EAV-HP clones showed identical large deletions spanning part of the gag, the entire pol, and part of the env genes. The env region of the EAV-HP clones was 97% identical to the env sequence of HPRS-103, the prototype subgroup J ALV. The 5 region of EAV-HP comprising the R and U5 regions of the long terminal repeat (LTR), the untranslated leader, and the 5 end of the putative gag region were 97% identical to the avian retrotransposon sequence, ART-CH. The remaining gag sequence shared less than 60% identity with other ALV sequences. The U3 region of the LTR was distinct from those of other retroviruses but contained some of the conserved motifs required for functioning as a promoter. To examine the ability of this endogenous retroviral LTR to function as a transcriptional promoter, the EAV-HP and HPRS-103 LTR U3 regions were compared in a luciferase reporter gene assay. The low luciferase activity detected with the EAV-HP LTR U3 constructs, at levels close to those observed for a control vector lacking the promoter or enhancer elements, suggested that these elements function as a weak promoter, possibly accounting for their low expression levels in chicken embryos.Endogenous retrovirus (ERV) sequences inherited as Mendelian genes have been recognized in most of the vertebrate genomes. In the chicken genome, four different families of ERVs have been identified. The CR1 (chicken repeat 1) element, a short interspersed repetitive DNA element belonging to the non-long terminal repeat (LTR) class of retrotransposons, forms one of these families (15). The majority of these elements, existing as approximately 7,000 to 20,000 repeats per haploid genome, have a common 3Ј end but show variable 5Ј truncations, with a few elements containing open reading frames encoding reverse transcriptase (13). CR1 elements have been identified in several avian and reptilian species, demonstrating that they are ancient sequences that arose before the divergence of birds and reptiles (40).The second family of chicken retrovirus-like elements, with the best-characterized ev loci, are the avian leukosis virus (ALV) subgroup E (ALV-E) ERVs. There are over 22 ev loci documented in layer-type birds and probably more in meattype breeds (17), with an average of 5 loci in each bird (33). Although the majority of the ev loci are defective, some of them encode infectious ERVs closely related to the ALVs (reviewed in reference 18). The ev2 locus, for example, encodes Rous-associated virus-0, the prototype of ALV-E (27). The ev loci are considered to represent recent germ line integrations because of their (i) low copy numbers, (ii) segregation in the population, and (iii) distribution restrict...

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Marek's disease virus-mediated enhancement of avian leukosis virus gene expression and virus production

Cited by 28 publications

References 28 publications

Avian sarcoma virus RNA synthesis, RNA splicing and virus production in human foreskin fibroblasts: effect of co-infection with human cytomegalovirus

Avian sarcoma virus RNA synthesis, RNA splicing and virus production in human foreskin fibroblasts: effect of co-infection with human cytomegalovirus

Comparative Pathology and Pathogenesis of Spontaneous and Experimentally Induced Fibropapillomas of Green Turtles (Chelonia mydas)

Avian Endogenous Retrovirus EAV-HP Shares Regions of Identity with Avian Leukosis Virus Subgroup J and the Avian Retrotransposon ART-CH

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