HPRS-103 (exogenous avian leukosis virus, subgroup J) has an env gene related to those of endogenous elements EAV-0 and E51 and an E element found previously only in sarcoma viruses

Bai, Jirong; Payne, L. N.; Skinner, Michael A.

doi:10.1128/jvi.69.2.779-784.1995

Cited by 146 publications

(61 citation statements)

References 35 publications

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“…However, it seems unlikely that the RSV stimulator is the only member of this group. Within the avian-leukosis sarcoma genus, the frameshift sequences present at the gag/pol overlap region of two sequenced avian leukosis virus (ALV) strains (one subgroup A, Bieth & Darlix, 1992; one subgroup J [ALV103 J], Bai et al, 1995) are closely conserved and PK2 and PK4 are identical. The same is also true for the gag/pol overlap region of two proviral clones (pSRA2, De Lorbe et al, 1980;pRCAS, Hughes et al, 1987) of the related Schmidt-Ruppin subgroup A strain which we have sequenced (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Secondary structure and mutational analysis of the ribosomal frameshift signal of rous sarcoma virus 1 1Edited by D. E. Draper

Marczinke

Fisher

Vidakovic

et al. 1998

Journal of Molecular Biology

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Expression of the Gag-Pol polyprotein of Rous sarcoma virus (RSV) requires a -1 ribosomal frameshifting event at the overlap region of the gag and pol open reading frames. The signal for frameshifting is composed of two essential mRNA elements; a slippery sequence (AAAUUUA) where the ribosome changes reading frame, and a stimulatory RNA structure located immediately downstream. This RNA is predicted to be a complex stem-loop but may also form an RNA pseudoknot. We have investigated the structure of the RSV frameshift signal by a combination of enzymatic and chemical structure probing and site-directed mutagenesis. The stimulatory RNA is indeed a complex stem-loop with a long stable stem and two additional stem-loops contained as substructures within the main loop region. The substructures are not however required for frameshifting. Evidence for an additional interaction between a stretch of nucleotides in the main loop and a region downstream to generate an RNA pseudoknot was obtained from an analysis of the frameshifting properties of RSV mutants translated in the rabbit reticulocyte lysate in vitro translation system. Mutations that disrupted the predicted pseudoknot-forming sequences reduced frameshifting but when the mutations were combined and should re-form the pseudoknot, frameshifting was restored to a level approaching that of the wild-type construct. It was also observed that the predicted pseudoknot-forming regions had reduced sensitivity to cleavage by the single-stranded probe imidazole. Overall, however, the structure probing data indicate that the pseudoknot interaction is weak and may form transiently. In comparison to other characterised RNA structures present at viral frameshift signals, the RSV stimulator falls into a novel group. It cannot be considered to be a simple hairpin-loop yet it is distinct from other well characterised frameshift-inducing RNA pseudoknots in that the overall contribution of the RSV pseudoknot to frameshifting is less dramatic.

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Section: Discussionmentioning

confidence: 99%

Secondary structure and mutational analysis of the ribosomal frameshift signal of rous sarcoma virus 1 1Edited by D. E. Draper

Marczinke

Fisher

Vidakovic

et al. 1998

Journal of Molecular Biology

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“…The most outstanding example for in vivo recombination, led to the creation of the new avian leukosis virus, subgroup J (ALV-J). ALV-J emerged following a spontaneous recombination between exogenous and endogenous retroviral sequences (Bai et al, 1995;Venugopal, 1999). Very soon the new virus disseminated worldwide with the extensive international trade of the specific genetic breed, in which ALV-J was created, leading to a very severe outcome with a devastating economic impact on the poultry industry (Malkinson et al, 2004).…”

Section: Molecular Interactions Between Two Rna Virusesmentioning

confidence: 99%

“…Very soon the new virus disseminated worldwide with the extensive international trade of the specific genetic breed, in which ALV-J was created, leading to a very severe outcome with a devastating economic impact on the poultry industry (Malkinson et al, 2004). ALV-J genetic sequence revealed several recombinations between the exogenous ALV gag and pol genes and the env gene of the endogenous avian erythoblastosis virus (Bai et al, 1995;Benson et al, 1998;Fadly and Smith, 1999). In the respect of viral evolution through genetic recombination, ALV-J represents a viable recombinant that occurred spontaneously in vivo between exogenous and endogenous avian retroviruses, ALV and AEV, respectively.…”

Section: Molecular Interactions Between Two Rna Virusesmentioning

confidence: 99%

Biotic concerns in generating molecular diagnosis matrixes for 4 avian viruses with emphasis on Marek’s disease virus

Davidson¹

2019

Journal of Virological Methods

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A B S T R A C TThe great advance in the field of diagnosis of avian viruses is reflecting the highly sophisticated molecular assays of the human and general virology in providing highly sensitive and fast methods of diagnosis. The present review will discuss the biotic factors and the complexities that became evident with the evolution of the novel molecular diagnostic assays with emphasis on 4 avian viruses, chicken anemia, infectious laryngotracheitis, turkey meningoencephalitis, but mainly on Marek's disease virus.To create a biologically meaningful diagnosis, attention should be dedicated to various biotic factors and not only of the diagnostic assay. Included among the important factors are, (a) the sample examined and the sampling strategy, (b) the outcomes of the pathogen amplification ex vivo, (c) the sampling time and its reflection on the disease diagnosis, (d) the impact of simultaneous multiple virus-infections regarding the ability to demonstrate all pathogens and inter-and intra-interactions between the pathogens. A concerted consideration of the relevant factors and the use of advanced molecular diagnostic assay would yield biologically significant diagnosis in real-time that would beneficiate the poultry industry. Recently Shojaei et al. (2015) and Astill et al. (2018) described novel methodologies developed to detect rapidly avian viruses, such as

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“…As two oncogenic retroviruses, avian leukosis virus subgroup J (ALV-J) and reticuloendotheliosis virus (REV) are the optimal model to study the synergistic tumorigenesis mechanisms. Both ALV-J and REV consist of a set of retroviral genes, gag, pol, env and LTR, and mainly induce myelocytomas and reticuloendotheliosis, respectively (1, 2). Due to similar transmission routes, co-infection of ALV-J and REV can readily occur (3, 4), and spread very rapidly (5-7).…”

Section: Introductionmentioning

confidence: 99%

ALV-J and REV synergistically activate a new oncogene of KIAA1199 via NF-κB and EGFR signaling regulated by miR-147

Zhou

Xue

Zhuang

et al. 2018

Preprint

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22The tumorigenesis is the result of the accumulation of multiple oncogenes and tumor 23 suppressor genes changes. Co-infection of avian leucosis virus subgroup J (ALV-J) 24 and reticuloendotheliosis virus ( REV) , as two oncogenic retroviruses, showed 25 synergistic pathogenic effects characterized by enhanced tumor initiation and 26 progression. The molecular mechanism underlying synergistic effects of ALV-J and 27 REV on the neoplasia remains unclear. Here, we found co-infection of ALV-J and 28 REV enhanced the ability of virus infection, increased viral life cycle, maintained cell 29 survival and enhanced tumor formation. We combined the high-throughput proteomic 30 readout with a large-scale miRNA screening to identify which molecules are involved 31 in the synergism. Our results revealed co-infection of ALV-J and REV activated a 32 latent oncogene of KIAA1199 and inhibited the expression of tumor suppressor miR-33 147. Further, enhanced KIAA1199, down-regulated miR-147, activated NF-κB and 34 EGFR were demonstrated in co-infected tissues and tumor. Mechanistically, we 35 showed ALV-J and REV synergistically enhanced KIAA1199 by activation of NF-κB 36 and EGFR signalling pathway, and the suppression of tumor suppressor miR-147 37 was contributed to maintain the NF-κB/KIAA1199/EGFR pathway crosstalk by 38 targeting the 3'UTR region sequences of NF-κB p50 and KIAA1199. Our results 39 contributed to the understanding of the molecular mechanisms of viral synergistic 40 tumorgenesis, which provided the evidence that suggested the synergistic actions of 41 two retroviruses could result in activation of latent pro-oncogenes. 42 Author summary 3 43The tumorigenesis is the result of the accumulation of multiple oncogenes and tumor 44 suppressor genes changes. Co-infection with ALV-J and REV showed synergistic 45 pathogenic effects characterized by enhanced tumor progression, however, the 46 molecular mechanism on the neoplasia remains unclear. Our results revealed co-47 infection of ALV-J and REV promotes tumorigenesis by both induction of a latent 48 oncogene of KIAA1199 and suppression of the expression of tumor suppressor miR-49 147. Mechanistic studies revealed that ALV-J and REV synergistically enhance 50 KIAA1199 by activation of NF-κB and EGFR signalling pathway, and the suppression 51 of tumor suppressor miR-147 was contributed to maintain the NF-52 κB/KIAA1199/EGFR pathway crosstalk by targeting the 3'UTR region sequences of 53 NF-κB p50 and KIAA1199. These results provided the evidence that suggested the 54 synergistic actions of two retroviruses could result in activation of latent pro-55 oncogenes, indicating the potential preventive target and predictive factor for ALV-J 56 and REV induced tumorigenesis. 57 Introduction 58 Viral synergism occurs commonly in the nature when co-infection of two or more 59 unrelated viruses invades the same host. As two oncogenic retroviruses, avian 60 leukosis virus subgroup J (ALV-J) and reticuloendotheliosis virus (REV) are the 61 optimal model to study the synergisti...

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HPRS-103 (exogenous avian leukosis virus, subgroup J) has an env gene related to those of endogenous elements EAV-0 and E51 and an E element found previously only in sarcoma viruses

Cited by 146 publications

References 35 publications

Secondary structure and mutational analysis of the ribosomal frameshift signal of rous sarcoma virus 1 1Edited by D. E. Draper

Secondary structure and mutational analysis of the ribosomal frameshift signal of rous sarcoma virus 1 1Edited by D. E. Draper

Biotic concerns in generating molecular diagnosis matrixes for 4 avian viruses with emphasis on Marek’s disease virus

ALV-J and REV synergistically activate a new oncogene of KIAA1199 via NF-κB and EGFR signaling regulated by miR-147

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