Artykuły w czasopismach: „Orf virus”

1

Bergqvist, Christina, Mazen Kurban i Ossama Abbas. "Orf virus infection". Reviews in Medical Virology 27, nr 4 (8.05.2017): e1932. http://dx.doi.org/10.1002/rmv.1932.

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Gemeniano, Malou C., Earl T. Sawai, Christian M. Leutenegger i Ellen E. Sparger. "Feline Immunodeficiency Virus Orf-A Is Required for Virus Particle Formation and Virus Infectivity". Journal of Virology 77, nr 16 (15.08.2003): 8819–30. http://dx.doi.org/10.1128/jvi.77.16.8819-8830.2003.

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ABSTRACT The orf-A (orf-2) gene of feline immunodeficiency virus (FIV) is a small open reading frame predicted to encode a 77-amino-acid protein that contains putative domains similar to those of the ungulate lentiviral Tat protein. Orf-A is reported to be critical for efficient viral replication in vitro and in vivo. A series of FIV-pPPR-derived proviruses with in-frame deletions and point mutations within orf-A were constructed and tested for replication in feline lymphoid cells. Orf-A mutant proviruses were also tested for viral gene and protein expression, viral particle formation, and virion infectivity. Deletions within orf-A severely restricted FIV replication in feline peripheral blood mononuclear cells (PBMC) and interleukin-2-dependent T-cell lines. In addition, substitutions of alanines for leucines in the putative leucine-rich domain, for cysteines in the putative cysteine-rich domain, and for a tryptophan at position 43 in Orf-A restricted the replication of FIV mutants. Deletions and point mutations in orf-A imposed a small effect or no effect on FIV long-terminal-repeat-driven viral gene expression and had no effect on viral protein expression. However, release of cell-free, virion-associated viral RNA in supernatants from cells transfected with orf-A mutant proviruses was severely restricted but was rescued by cotransfection with a wild-type Orf-A expression vector. In addition, virions derived from orf-A mutant proviruses expressed reduced infectivity for feline PBMC. Our findings suggest that Orf-A functions involve multiple steps of the FIV life cycle including both virion formation and infectivity. Furthermore, these observations suggest that Orf-A represents an FIV-encoded analog more similar to the accessory gene vpr, vpu, or nef than to the regulatory gene tat encoded by the primate lentiviruses.

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Nettleton, P. F., J. Brebner, I. Pow, J. A. Gilray, G. D. Bell i H. W. Reid. "Tissue culture-propagated orf virus vaccine protects lambs from orf virus challenge". Veterinary Record 138, nr 8 (24.02.1996): 184–86. http://dx.doi.org/10.1136/vr.138.8.184.

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Tobler, Caroline, Céline Ritter-Schenk i Petra Zimmermann. "Orf Virus Infection: Ecthyma Contagiosum". Journal of Pediatrics 243 (kwiecień 2022): 236–37. http://dx.doi.org/10.1016/j.jpeds.2021.11.067.

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Querol Nasarre, Ignacio, Mariano Ara Martín i Estrella Simal Gil. "Infección por el virus orf". Piel 21, nr 5 (maj 2006): 247–52. http://dx.doi.org/10.1016/s0213-9251(06)72478-9.

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Parwanto, Edy. "Virus Corona (SARS-CoV-2) penyebab COVID-19 kini telah bermutasi". Jurnal Biomedika dan Kesehatan 4, nr 2 (17.06.2021): 47–49. http://dx.doi.org/10.18051/jbiomedkes.2021.v4.47-49.

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Telah dikemukakan bahwa virus corona menjadi penyebab COVID-19.(1) Virus corona yang dimaksud yaitu SARS-CoV-2, sedangkan COVID-19 kependekan dari corona virus disease-19. COVID-19 adalah penyakit yang disebabkan oleh SARS-CoV2 yang muncul awal Desember tahun 2019 di Wuhan, China. Sifat virus corona tersebut mudah menginfeksi manusia dan mudah menyebar hampir keseluruh penjuru dunia. Oleh karena itu terjadilah wabah (pandemi) COVID-19. Seiring berjalannya waktu, virus corona mengalami mutasi gen. Mutasi gen merupakan perubahan gen secara spontan dan bersifat turun menurun dari partikel virus induk ke partikel virus anakannya. Kita mengetahui bahwa gen virus corona terusun atas rangkaian ribo nucleic acid (RNA), oleh karena itu virus corona digolongkan sebagai virus RNA. Rangkaian gen pada virus corona tersebut menyusun genom virus corona. Genom virus corona mengandung 29 903 nukleotida (nt). Komponen genom virus corona yaitu 5’ untranslated region (5‘ UTR), rangkaian gen virus corona pengkode protein dan 3’ untranslated region (3’ UTR). Bagian 5’ UTR terdapat pada up stream (pangkal) sedangkan 3’ UTR terdapat di bagian down stream (ujung), keduanya tidak mengkode protein. Secara berurutan dari arah up stream ke down stream, rangkaian gen virus corona terdiri atas gen ORF 1ab, gen S, gen ORF 3a, gen E, gen M, gen ORF 6, gen ORF 7a, gen ORF 7b, gen ORF 8, gen N, gen ORF 10.(2)

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Leat, Neil, Brenda Ball, Vandana Govan i Sean Davison. "Analysis of the complete genome sequence of black queen-cell virus, a picorna-like virus of honey bees". Journal of General Virology 81, nr 8 (1.08.2000): 2111–19. http://dx.doi.org/10.1099/0022-1317-81-8-2111.

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A virus with picorna-like biophysical properties was isolated from South African honey bees. On the basis of serology, it was identified as an isolate of black queen-cell virus (BQCV). Nucleotide sequence analysis revealed an 8550 nt polyadenylated genome containing two large ORFs. The 5′-proximal ORF (ORF 1) represented 4968 nt while the 3′-proximal ORF (ORF 2) represented 2562 nt. The ORFs were separated by a 208 nt intergenic region and were flanked by a 657 nt 5′-untranslated region and a 155 nt 3′-untranslated region. Deduced amino acid sequences for ORF 1 and ORF 2 were most similar to the non-structural and structural proteins, respectively, of Drosophila C virus (DCV), Rhopalosiphum padi virus (RhPV), Himetobi P virus (HiPV) and Plautia stali intestine virus (PSIV). It is proposed that BQCV belongs to the group of picorna-like, insect-infecting RNA viruses constituted by DCV, RhPV, HiPV and PSIV.

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Randall, Glenn, Michael Lagunoff i Bernard Roizman. "Herpes Simplex Virus 1 Open Reading Frames O and P Are Not Necessary for Establishment of Latent Infection in Mice". Journal of Virology 74, nr 19 (1.10.2000): 9019–27. http://dx.doi.org/10.1128/jvi.74.19.9019-9027.2000.

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ABSTRACT Open reading frame (ORF) O and ORF P partially overlap and are located antisense to the γ134.5 gene within the domain transcribed during latency. In wild-type virus-infected cells, ORF O and ORF P are completely repressed during productive infection by ICP4, the major viral transcriptional activator/repressor. In cells infected with a mutant in which ORF P was derepressed there was a significant delay in the appearance of the viral α-regulatory proteins ICP0 and ICP22. The ORF O protein binds to and inhibits ICP4 binding to its cognate DNA site in vitro. These characteristics suggested a role for ORF O and ORF P in the establishment of latency. To test this hypothesis, two recombinant viruses were constructed. In the first, R7538(P−/O−), the ORF P initiator methionine codon, which also serves as the initiator methionine codon for ORF O, was replaced and a diagnostic restriction endonuclease was introduced upstream. In the second, R7543(P−/O−)R, the mutations were repaired to restore the wild-type virus sequences. We report the following. (i) The R7538(P−/O−) mutant failed to express ORF O and ORF P proteins but expressed a wild-type γ134.5 protein. (ii) R7538(P−/O−) yields were similar to that of the wild type following infection of cell culture or following infection of mice by intracerebral or ocular routes. (iii) R7538(P−/O−) virus reactivated from latency following explanation and cocultivation of murine trigeminal ganglia with Vero cells at a frequency similar to that of the wild type, herpes simplex virus 1(F). (iv) The amount of latent R7538(P−/O−) virus as assayed by quantitative PCR is eightfold less than that of the repair virus. The repaired virus could not be differentiated from the wild-type parent in any of the assays done in this study. We conclude that ORF O and ORF P are not essential for the establishment of latency in mice but may play a role in determining the quantity of latent virus maintained in sensory neurons.

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Duchateau, Nathalie C., Olivier Aerts i Julien Lambert. "Autoinoculation with Orf virus (ecthyma contagiosum)". International Journal of Dermatology 53, nr 1 (3.01.2013): e60-e62. http://dx.doi.org/10.1111/j.1365-4632.2012.05622.x.

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Haig, David M. "Orf virus infection and host immunity". Current Opinion in Infectious Diseases 19, nr 2 (kwiecień 2006): 127–31. http://dx.doi.org/10.1097/01.qco.0000216622.75326.ef.

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Friebel, T. R., i J. F. A. van der Werff. "The orf virus: a case report". Journal of Hand Surgery (European Volume) 40, nr 6 (16.12.2013): 648–49. http://dx.doi.org/10.1177/1753193413516403.

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GALLINA, L., F. VERONESE, P. FARINELLI, R. BOLDORINI, G. DELROSSO, E. COLOMBO, E. MALDI, A. PELI i A. SCAGLIARINI. "Erythema multiforme after orf virus infection". Epidemiology and Infection 144, nr 1 (26.06.2015): 88–89. http://dx.doi.org/10.1017/s0950268815001077.

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López-Cedeño, Angella, Gustavo Cañedo, Nicole Knöpfel, Isabel Colmenero, Esperanza Pérez-Pastrana i Antonio Torrelo. "Erythema multiforme after orf virus infection". Pediatric Dermatology 35, nr 4 (15.05.2018): e237-e238. http://dx.doi.org/10.1111/pde.13526.

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Mercer, Andrew A., Katherine M. Fraser i Joseph J. Esposito. "Gene homology between orf virus and smallpox variola virus". Virus Genes 13, nr 2 (1996): 175–78. http://dx.doi.org/10.1007/bf00568910.

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Fleming, Stephen B., Ian E. Anderson, Jackie Thomson, David L. Deane, Colin J. McInnes, Catherine A. McCaughan, Andrew A. Mercer i David M. Haig. "Infection with recombinant orf viruses demonstrates that the viral interleukin-10 is a virulence factor". Journal of General Virology 88, nr 7 (1.07.2007): 1922–27. http://dx.doi.org/10.1099/vir.0.82833-0.

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Orf virus is the prototype parapoxvirus that causes the contagious skin disease orf. It encodes an orthologue of the cytokine interleukin (IL)-10. Recombinant orf viruses were constructed in which the viral interleukin-10 (vorfIL-10) was disabled (vorfIL-10ko) and reinserted (vorfrevIL-10) at the same locus and compared to wild-type virus for their ability to induce skin lesions in sheep. After either primary infection or reinfection, smaller less severe lesions were recorded in the vorfIL-10ko-infected animals compared with either of the vorfIL-10-intact virus-infected animals. Thus, the vorfIL-10ko virus was attenuated compared with the vorfIL-10 intact viruses, demonstrating that orf virus IL-10 is a virulence factor. The virus IL-10 is one of several virulence or immuno-modulatory factors expressed by orf virus. Removal of any one of these genes would be expected to have only a partial effect on virulence, which is what was observed in this study with vorfIL-10.

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Deane, David, Colin J. McInnes, Ann Percival, Ann Wood, Jackie Thomson, Andrea Lear, Janice Gilray, Stephen Fleming, Andrew Mercer i David Haig. "Orf Virus Encodes a Novel Secreted Protein Inhibitor of Granulocyte-Macrophage Colony-Stimulating Factor and Interleukin-2". Journal of Virology 74, nr 3 (1.02.2000): 1313–20. http://dx.doi.org/10.1128/jvi.74.3.1313-1320.2000.

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ABSTRACT The parapoxvirus orf virus encodes a novel soluble protein inhibitor of ovine granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-2 (IL-2). The GM-CSF- and IL-2-inhibitory factor (GIF) gene was expressed as an intermediate-late viral gene in orf virus-infected cells. GIF formed homodimers and tetramers in solution, and it bound ovine GM-CSF with a Kd of 369 pM and ovine IL-2 with a Kd of 1.04 nM. GIF did not bind human GM-CSF or IL-2 in spite of the fact that orf virus is a human pathogen. GIF was detected in afferent lymph plasma draining the skin site of orf virus reinfection and was associated with reduced levels of lymph GM-CSF. GIF expression by orf virus indicates that GM-CSF and IL-2 are important in host antiviral immunity.

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Glass, Pamela J., Laura J. White, Judith M. Ball, Isabelle Leparc-Goffart, Michele E. Hardy i Mary K. Estes. "Norwalk Virus Open Reading Frame 3 Encodes a Minor Structural Protein". Journal of Virology 74, nr 14 (15.07.2000): 6581–91. http://dx.doi.org/10.1128/jvi.74.14.6581-6591.2000.

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ABSTRACT Norwalk virus (NV) is a causative agent of acute epidemic nonbacterial gastroenteritis in humans. The inability to cultivate NV has required the use of molecular techniques to examine the genome organization and functions of the viral proteins. The function of the NV protein encoded by open reading frame 3 (ORF 3) has been unknown. In this paper, we report the characterization of the NV ORF 3 protein expressed in a cell-free translation system and in insect cells and show its association with recombinant virus-like particles (VLPs) and NV virions. Expression of the ORF 3 coding region in rabbit reticulocyte lysates resulted in the production of a single protein with an apparent molecular weight of 23,000 (23K protein), which is not modified by N-linked glycosylation. The ORF 3 protein was expressed in insect cells by using two different baculovirus recombinants; one recombinant contained the entire 3′ end of the genome beginning with the ORF 2 coding sequences (ORFs 2+3), and the second recombinant contained ORF 3 alone. Expression from the construct containing both ORF 2 and ORF 3 resulted in the expression of a single protein (23K protein) detected by Western blot analysis with ORF 3-specific peptide antisera. However, expression from a construct containing only the ORF 3 coding sequences resulted in the production of multiple forms of the ORF 3 protein ranging in size from 23,000 to 35,000. Indirect-immunofluorescence studies using an ORF 3 peptide antiserum showed that the ORF 3 protein is localized to the cytoplasm of infected insect cells. The 23K ORF 3 protein was consistently associated with recombinant VLPs purified from the media of insect cells infected with a baculovirus recombinant containing the entire 3′ end of the NV genome. Western blot analysis of NV purified from the stools of NV-infected volunteers revealed the presence of a 35K protein as well as multiple higher-molecular-weight bands specifically recognized by an ORF 3 peptide antiserum. These results indicate that the ORF 3 protein is a minor structural protein of the virion.

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KARABASANAVAR, NAGAPPA, PRASHANTH S. BAGALKOTE, D. B. RAJASHEKARA, S. S. MANJUNATHA i K. C. VEERANNA. "Phylogenetic analysis of Orf virus associated with contagious ecthyma (orf) outbreak in Tellicherry goats (Capra hircus)". Indian Journal of Animal Sciences 88, nr 2 (2.05.2018): 144–49. http://dx.doi.org/10.56093/ijans.v88i2.79288.

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Orf virus (ORFV) is a member of genus Parapoxvirus that causes contagious ecthyma in goats. A pox-like disease was investigated in Tellicherry goats (31 female) maintained at a semi-organized farm. History revealed recent introduction of Tellicherry goats for breeding purpose and housing of the new entrants in to a farm already having a mild form of pox-like disease. Newly introduced and stressed Tellicherry goats developed severe form of infection with 100% morbidity. Affected goats showed lesions around lips (100%), commissure (53%) and oral cavity (65%); exanthematic dermatitis was evident in 94% of the affected goats followed by ulceration (47%) and nodular lesions (24%). Scab samples were collected from affected goats to confirm the clinical diagnosis. Genus Parapoxvirus was confirmed by the amplification of specific 594 bp and 235 bp amplicons. Further, Orf virus specific amplicon of size 1,206 bp was also amplified for the confirmation. Sequence analysis of PCR amplicons showed close resemblance of the outbreak strain with reported Indian Orf virus isolates. Based on the homology of the outer envelope protein B2L gene sequence of Orf virus, the source of infection to the Tellicherry goats was traced to the local goat. Although Orf virus is zoonotic; however, no occupational transmission was noticed in the present outbreak.

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Robinson, A. J., i A. A. Mercer. "Orf virus and vaccinia virus do not cross-protect sheep". Archives of Virology 101, nr 3-4 (wrzesień 1988): 255–59. http://dx.doi.org/10.1007/bf01311006.

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Whitehouse, Adrian, Matthew Cooper, Kersten T. Hall i David M. Meredith. "The Open Reading Frame (ORF) 50a Gene Product Regulates ORF 57 Gene Expression in Herpesvirus Saimiri". Journal of Virology 72, nr 3 (1.03.1998): 1967–73. http://dx.doi.org/10.1128/jvi.72.3.1967-1973.1998.

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ABSTRACT We have previously demonstrated that open reading frame (ORF) 50 and ORF 57 encode transcriptional regulating genes in herpesvirus saimiri. ORF 50, a homolog of Epstein-Barr virus R protein, is a sequence-specific transactivator, whereas ORF 57 acts posttranscriptionally. In this report, we demonstrate that the ORF 57 gene is regulated by the ORF 50a gene product. We show that the ORF 57 gene is expressed at basal levels early in the virus replication cycle and that thereafter it is transactivated by the ORF 50a gene product, due to an increase in RNA levels. As it has been shown that the ORF 57 gene product downregulates ORF 50a due to the presence of its intron, these combined observations identify a feedback mechanism modulating gene expression in herpesvirus saimiri, whereby ORF 50a transcription is downregulated by the ORF 57 gene product, a gene which it specifically transactivates. Furthermore, we propose that the intron-containing ORF 57 gene downregulates itself by the same mechanism as that for ORF 50a, as both genes are downregulated at similar times during the replication cycle.

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Tzeng, Wen-Pin, i Teryl K. Frey. "Mapping the Rubella Virus Subgenomic Promoter". Journal of Virology 76, nr 7 (1.04.2002): 3189–201. http://dx.doi.org/10.1128/jvi.76.7.3189-3201.2002.

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ABSTRACT Rubella virus (RUB), the sole member of the Rubivirus genus in the Togaviridae family of positive-strand RNA viruses, synthesizes a single subgenomic (SG) RNA containing sequences from the 3′ end of the genomic RNA including the open reading frame (ORF) that encodes the virion proteins. The synthesis of SG RNA is initiated internally on a negative-strand, genome-length template at a site known as the SG promoter (SGP). Mapping the RUB SGP was initiated by using an infectious cDNA vector, dsRobo402/GFP, in which the region containing the SGP was duplicated (K. V. Pugachev, W.-P. Tzeng, and T. K. Frey, J. Virol. 74:10811-10815, 2000). In dsRobo402/GFP, the 5′-proximal nonstructural protein ORF (NS-ORF) is followed by the first SGP (SGP-1), the green fluorescent protein (GFP) gene, the second SGP (SGP-2), and the structural protein ORF. The duplicated SGP, SGP-2, contained nucleotides (nt) −175 to +76 relative to the SG start site, including the 3′ 127 nt of the NS-ORF and 47 nt between the NS-ORF and the SG start site. 5′ Deletions of SGP-2 to nt −40 (9 nt beyond the 3′ end of the NS-ORF) resulted in a wild-type (wt) phenotype in terms of virus replication and RNA synthesis. Deletions beyond this point impaired viability; however, the analysis was complicated by homologous recombination between SGP-1 and SGP-2 that resulted in deletion of the GFP gene and resurrection of viable virus with one SGP. Since the NS-ORF region was not necessary for SGP activity, subsequent mapping was done by using both replicon vectors, RUBrep/GFP and RUBrep/CAT, in which the SP-ORF is replaced with the reporter GFP and chloramphenical acetyltransferase genes, respectively, and the wt infectious clone, Robo402. In the replicon vectors, 5′ deletions to nt −26 resulted in the synthesis of SG RNA. In the infectious clone, deletions through nt −28 gave rise to viable virus. A series of short internal deletions confirmed that the region between nt −28 and the SG start site was essential for viability and showed that the repeated UCA triplet at the 5′ end of SG RNA was also required. Thus, the minimal SGP maps from nt −26 through the SG start site and appears to extend to at least nt +6, although a larger region is required for the generation of virus with a wt phenotype. Interestingly, while the positioning of the RUB SGP immediately adjacent the SG start site is thus similar to that of members of the genus Alphavirus, the other genus in the Togaviridae family, it does not include a region of nucleotide sequence homology with the alphavirus SGP that is located between nt −48 and nt −23 with respect to the SG start site in the RUB genome.

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van Munster, M., A. M. Dullemans, M. Verbeek, J. F. J. M. van den Heuvel, A. Clérivet i F. van der Wilk. "Sequence analysis and genomic organization of Aphid lethal paralysis virus: a new member of the family Dicistroviridae". Journal of General Virology 83, nr 12 (1.12.2002): 3131–38. http://dx.doi.org/10.1099/0022-1317-83-12-3131.

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The complete nucleotide sequence of the genomic RNA of an aphid-infecting virus, Aphid lethal paralysis virus (ALPV), has been determined. The genome is 9812 nt in length and contains two long open reading frames (ORFs), which are separated by an intergenic region of 163 nt. The first ORF (5′ ORF) is preceded by an untranslated leader sequence of 506 nt, while an untranslated region of 571 nt follows the second ORF (3′ ORF). The deduced amino acid sequences of the 5′ ORF and 3′ ORF products respectively showed similarity to the non-structural and structural proteins of members of the newly recognized genus Cripavirus (family Dicistroviridae). On the basis of the observed sequence similarities and identical genome organization, it is proposed that ALPV belongs to this genus. Phylogenetic analysis showed that ALPV is most closely related to Rhopalosiphum padi virus, and groups in a cluster with Drosophila C virus and Cricket paralysis virus, while the other members of this genus are more distantly related. Infectivity experiments showed that ALPV can not only infect aphid species but is also able to infect the whitefly Trialeurodes vaporariorum, extending its host range to another family of the order Hemiptera.

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Spyrou, V., i G. Valiakos. "Orf virus infection in sheep or goats". Veterinary Microbiology 181, nr 1-2 (grudzień 2015): 178–82. http://dx.doi.org/10.1016/j.vetmic.2015.08.010.

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Şevik, Murat. "Orf virus circulation in cattle in Turkey". Comparative Immunology, Microbiology and Infectious Diseases 65 (sierpień 2019): 1–6. http://dx.doi.org/10.1016/j.cimid.2019.03.013.

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Robinson, Anthony J., Gillian Barns, Kate Fraser, Elizabeth Carpenter i Andrew A. Mercer. "Conservation and variation in orf virus genomes". Virology 157, nr 1 (marzec 1987): 13–23. http://dx.doi.org/10.1016/0042-6822(87)90308-4.

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Cottone, R., M. Büttner, C. J. McInnes, A. R. Wood i H. J. Rziha. "Orf virus encodes a functional dUTPase gene". Journal of General Virology 83, nr 5 (1.05.2002): 1043–48. http://dx.doi.org/10.1099/0022-1317-83-5-1043.

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The present study is the first report on the functional activity of a parapoxvirus-encoded dUTPase. The dUTPase gene of the attenuated orf virus (ORFV), strain D1701, was expressed as a bacterial thioredoxin fusion protein. In vitro assays showed that ORFV dUTPase was highly specific for dUTP as substrate. The enzyme was active over a broad pH range (pH 6·0–9·0), with maximal enzymatic activity at pH 7·0 in the presence of Mg2+ cations. Kinetic studies of the recombinant ORFV dUTPase revealed an apparent K m of 4·0 μM, which is more similar to that of the mammalian or African swine fever virus enzyme than to the K m of vaccinia virus dUTPase. Enzyme activity was also found with purified ORFV particles, indicating its virion association.

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Wang, Ruixue, Yong Wang, Fang Liu i Shuhong Luo. "Orf virus: A promising new therapeutic agent". Reviews in Medical Virology 29, nr 1 (28.10.2018): e2013. http://dx.doi.org/10.1002/rmv.2013.

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Vellucci, Ashley, Melina Manolas, Sarah Jin, John Dwyer, Garrett Vick, Alun Wang, Edwin Swiatlo i Crystal Zheng. "Orf virus infection after Eid al-Adha". IDCases 21 (2020): e00854. http://dx.doi.org/10.1016/j.idcr.2020.e00854.

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Nettleton, P. F., J. A. Gilray, D. L. Yirrell, G. R. Scott i H. W. Reid. "Natural transmission of orf virus from clinically normal ewes to orf-naive sheep". Veterinary Record 139, nr 15 (12.10.1996): 364–66. http://dx.doi.org/10.1136/vr.139.15.364.

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Tan, Joanne L., Norihito Ueda, Andrew A. Mercer i Stephen B. Fleming. "Investigation of orf virus structure and morphogenesis using recombinants expressing FLAG-tagged envelope structural proteins: evidence for wrapped virus particles and egress from infected cells". Journal of General Virology 90, nr 3 (1.03.2009): 614–25. http://dx.doi.org/10.1099/vir.0.005488-0.

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Orf virus (ORFV) is the type species of the genus Parapoxvirus, but little is known about the structure or morphogenesis of the virus. In contrast, the structure and morphogenesis of vaccinia virus (VACV) has been extensively studied. VACV has two main infectious forms, mature virion (MV) and extracellular virion (EV). The MV is wrapped by two additional membranes derived from the trans-Golgi to produce a wrapped virion (WV), the outermost of which is lost by cellular membrane fusion during viral egress to form the EV. Genome sequencing of ORFV has revealed that it has homologues of almost all of the VACV structural genes. Notable exceptions are A36R, K2L, A56R and B5R, which are associated with WV and EV envelopes. This study investigated the morphogenesis and structure of ORFV by fusing FLAG peptide to the structural proteins 10 kDa, F1L and ORF-110 to form recombinant viruses. 10 kDa and F1L are homologues of VACV A27L and H3L MV membrane proteins, whilst ORF-110 is homologous to VACV A34R, an EV membrane protein. Immunogold labelling of FLAG proteins on virus particles isolated from lysed cells showed that FLAG–F1L and FLAG–10 kDa were displayed on the surface of infectious particles, whereas ORF-110–FLAG could not be detected. Western blot analysis of solubilized recombinant ORF-110–FLAG particles revealed that ORF-110–FLAG was abundant and undergoes post-translational modification indicative of endoplasmic reticulum trafficking. Fluorescent microscopy confirmed the prediction that ORF-110–FLAG localized to the Golgi in virus-infected cells. Finally, immunogold labelling of EVs showed that ORF-110–FLAG became exposed on the surface of EV-like particles as a result of egress from the cell.

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Ahasan, Mohammad M., i Clive Sweet. "Murine cytomegalovirus open reading frame m29.1 augments virus replication both in vitro and in vivo". Journal of General Virology 88, nr 11 (1.11.2007): 2941–51. http://dx.doi.org/10.1099/vir.0.83133-0.

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Murine cytomegalovirus mutant Rc29, with a premature stop codon mutation in the m29 open reading frame (ORF), produced no apparent phenotype in cell culture or following infection of BALB/c mice. In contrast, a similar mutant virus, Rc29.1, with a premature stop codon mutation in its m29.1 ORF, showed reduced virus yields (2–3 log10 p.f.u. ml−1) in tissue culture. Mutant virus yields in BALB/c mice were delayed, reduced (∼1 log10 p.f.u. per tissue) and persisted less well in salivary glands compared with wild-type (wt) and revertant (Rv29.1) virus. In severe combined immunodeficiency mice, Rc29.1 virus showed delayed and reduced replication initially in all tissues (liver, spleen, kidneys, heart, lung and salivary glands). This delayed death until 31 days post-infection (p.i.) compared with wt (23 days p.i.) but at death virus yields were similar to wt. m29 gene transcription was initiated at early times post-infection, while production of a transcript from ORF m29.1 in the presence of cycloheximide indicated that it was an immediate-early gene. ORFs m29.1 and M28 are expressed from a bicistronic message, which is spliced infrequently. However, it is likely that each ORF expresses its own protein, as antiserum derived in rabbits to the m29.1 protein expressed in bacteria from the m29.1 ORF detected only one protein in Western blot analysis of the size predicted for the m29.1 protein. Our results suggest that neither ORF is essential for virus replication but m29.1 is important for optimal viral growth in vitro and in vivo.

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Dal Pozzo, F., G. Andrei, A. Holý, J. Van Den Oord, A. Scagliarini, E. De Clercq i R. Snoeck. "Activities of Acyclic Nucleoside Phosphonates against Orf Virus in Human and Ovine Cell Monolayers and Organotypic Ovine Raft Cultures". Antimicrobial Agents and Chemotherapy 49, nr 12 (grudzień 2005): 4843–52. http://dx.doi.org/10.1128/aac.49.12.4843-4852.2005.

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ABSTRACT Orf virus, a member of the Parapoxvirus genus, causes a contagious pustular dermatitis in sheep, goats, and humans. Previous studies have demonstrated the activity of (S)-1-[3-hydroxy-2-(phosphonomethoxy)propyl]cytosine (HPMPC; cidofovir; Vistide) against orf virus in cell culture and humans. We have evaluated a broad range of acyclic nucleoside phosphonates (ANPs) against several orf virus strains in primary lamb keratinocytes (PLKs) and human embryonic lung (HEL) monolayers. HPMPC, (S)-9-[3-hydroxy-2-(phosphonomethoxy)propyl]-2,6- diaminopurine (HPMPDAP), and (R)-9-[3-hydroxy-2-(phosphonomethoxy)propoxy]-2,4-diaminopyrimidine (HPMPO-DAPy) were three of the most active compounds that were subsequently tested in a virus yield assay with PLK and HEL cells by virus titration and DNA quantification. HPMPC, HPMPDAP, and HPMPO-DAPy were evaluated for their activities against orf virus replication in organotypic epithelial raft cultures from differentiated PLK cells. At the highest concentrations (50 and 20 μg/ml), full protection was provided by the three drugs, while at 5 μg/ml, only HPMPDAP and HPMPC offered partial protection. The activities of the three compounds in the raft culture system were confirmed by quantification of infectious virus and viral DNA. These findings provide a rationale for the use of HPMPC and other ANPs in the treatment of orf (contagious ecthyma) in humans and animals.

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Lawal, Nafi'u, Mubarak Ibrahim, Dauda Ayomide Onawala, Muhammad Bashir Bello, Rabiu Muhammad Aliyu, Yusha'u Shu'aibu Baraya, Abdullahi Aliyu, Aliyu Musawa Ibrahim i Aliyu Sa'adu. "Molecular characterization and phylogenetic analysis of orf virus isolated from goats in Sokoto metropolis, Nigeria". Future Science OA 7, nr 6 (lipiec 2021): FSO700. http://dx.doi.org/10.2144/fsoa-2020-0162.

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Aim: The aim of this study was to molecularly characterize orf virus isolated from clinical infections in goats in Sokoto metropolis. Materials & methods: Embryonated chicken eggs were used to isolate orf virus according to the established protocol. Viral DNA was extracted and full coding region of B2L gene was amplified by polymerase chain reaction, sequenced and blasted for identification and phylogenetically analyzed. Results and discussion: The B2L gene sequences of the isolate showed slight variability (96–98.7%) with the reference sequences as it clustered within the same clade with Korean, Zambian and Ethiopian strains, signifying a close genetic relationship. Unique amino acid substitutions were noted. This is the first genetic characterization of B2L gene of orf virus circulating in Nigeria. Conclusion: This study has provided in sight into the genetic diversity of orf virus in the study area.

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Cohrs, Randall J., Donald H. Gilden, Yasuyuki Gomi, Koichi Yamanishi i Jeffrey I. Cohen. "Comparison of Virus Transcription during Lytic Infection of the Oka Parental and Vaccine Strains of Varicella-Zoster Virus". Journal of Virology 80, nr 5 (1.03.2006): 2076–82. http://dx.doi.org/10.1128/jvi.80.5.2076-2082.2006.

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ABSTRACT The attenuated Oka vaccine (V-Oka) strain of varicella-zoster virus (VZV) effectively reduces disease produced by primary infection and virus reactivation. V-Oka was developed by propagation of the Oka parental (P-Oka) strain of VZV in guinea pig and human embryo fibroblasts. Complete DNA sequencing of both viruses has revealed 63 sites that differ between P-Oka and V-Oka, 37 of which are located within 21 unique open reading frames (ORFs). Of the ORFs that differ, ORF 62 contains the greatest number (10) of mutated sites. ORF 62 encodes IE 62, the major immediate-early transactivator of virus genes, and is essential for lytic virus replication. To determine whether a disproportionate number of mutations in ORF 62 might account for virus attenuation, we compared the global pattern of V-Oka gene expression to that of P-Oka. Transcription of ORFs 62, 65, 66, and 67 was suppressed, whereas ORF 41 was elevated in V-Oka-infected cells compared to P-Oka-infected cells (P < 0.01; z test). Suppression of ORF 62, 65, and 66 transcription was confirmed by quantitative dot blot and Western blot analyses. Transient-transfection assays to determine whether mutations within V-Oka-derived IE 62 affected its ability to transactivate VZV gene promoters revealed similar IE 62 transactivation of VZV gene 20, 21, 28, 29, 65, and 66 promoters in both P-Oka and V-Oka. Together, our results indicate that mutations in V-Oka IE 62 alone are unlikely to account for vaccine virus attenuation.

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Weber, O., A. A. Mercer, A. Friebe, P. Knolle i H. D. Volk. "Therapeutic immunomodulation using a virus—the potential of inactivated orf virus". European Journal of Clinical Microbiology & Infectious Diseases 32, nr 4 (22.11.2012): 451–60. http://dx.doi.org/10.1007/s10096-012-1780-x.

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Delhon, G., E. R. Tulman, C. L. Afonso, Z. Lu, A. de la Concha-Bermejillo, H. D. Lehmkuhl, M. E. Piccone, G. F. Kutish i D. L. Rock. "Genomes of the Parapoxviruses Orf Virus and Bovine Papular Stomatitis Virus". Journal of Virology 78, nr 1 (1.01.2004): 168–77. http://dx.doi.org/10.1128/jvi.78.1.168-177.2004.

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ABSTRACT Bovine papular stomatitis virus (BPSV) and orf virus (ORFV), members of the genus Parapoxvirus of the Poxviridae, are etiologic agents of worldwide diseases affecting cattle and small ruminants, respectively. Here we report the genomic sequences and comparative analysis of BPSV strain BV-AR02 and ORFV strains OV-SA00, isolated from a goat, and OV-IA82, isolated from a sheep. Parapoxvirus (PPV) BV-AR02, OV-SA00, and OV-IA82 genomes range in size from 134 to 139 kbp, with an average nucleotide composition of 64% G+C. BPSV and ORFV genomes contain 131 and 130 putative genes, respectively, and share colinearity over 127 genes, 88 of which are conserved in all characterized chordopoxviruses. BPSV and ORFV contain 15 and 16 open reading frames (ORFs), respectively, which lack similarity to other poxvirus or cellular proteins. All genes with putative roles in pathogenesis, including a vascular endothelial growth factor (VEGF)-like gene, are present in both viruses; however, BPSV contains two extra ankyrin repeat genes absent in ORFV. Interspecies sequence variability is observed in all functional classes of genes but is highest in putative virulence/host range genes, including genes unique to PPV. At the amino acid level, OV-SA00 is 94% identical to OV-IA82 and 71% identical to BV-AR02. Notably, ORFV 006/132, 103, 109, 110, and 116 genes (VEGF, homologues of vaccinia virus A26L, A33R, and A34R, and a novel PPV ORF) show an unusual degree of intraspecies variability. These genomic differences are consistent with the classification of BPSV and ORFV as two PPV species. Compared to other mammalian chordopoxviruses, PPV shares unique genomic features with molluscum contagiosum virus, including a G+C-rich nucleotide composition, three orthologous genes, and a paucity of nucleotide metabolism genes. Together, these data provide a comparative view of PPV genomics.

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Lee, Lily Yeh, i Priscilla A. Schaffer. "A Virus with a Mutation in the ICP4-Binding Site in the L/ST Promoter of Herpes Simplex Virus Type 1, but Not a Virus with a Mutation in Open Reading Frame P, Exhibits Cell-Type-Specific Expression of γ134.5 Transcripts and Latency-Associated Transcripts". Journal of Virology 72, nr 5 (1.05.1998): 4250–64. http://dx.doi.org/10.1128/jvi.72.5.4250-4264.1998.

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ABSTRACT The herpes simplex virus type 1 L/S junction-spanning transcripts (L/STs) are a family of multisized transcripts expressed at high levels in cells infected with mutant viruses that (i) do not express ICP4, (ii) specify forms of ICP4 unable to bind to the consensus ICP4 binding site, or (iii) contain mutations in the ICP4 binding site located at the transcriptional start site of the L/STs. By extension, the failure to detect the L/STs in wild-type virus-infected cells is due to the repressive effect of ICP4 bound to its cognate binding site upstream of the L/ST transcription initiation site. ORF-P, the first and largest open reading frame (ORF) encoded by the L/STs, overlaps >90% of the ORF encoding ORF-34.5, a putative neurovirulence factor, which is transcribed from the opposite DNA strand. Viruses with mutations in the overlapping region of ORF-P and ICP34.5 exhibit premature shutoff of infected-cell protein synthesis and are highly attenuated following intracranial inoculation of juvenile mice. To determine whether the premature protein shutoff and neuroattenuated phenotypes of ORF-P ORF-34.5 double mutants are a consequence of alterations in ORF-P, ORF-34.5, or both, viruses containing mutations only in ORF-P or only in the ICP4 binding site in the L/ST promoter were isolated and characterized. Mutant virus L/ST-n38 contains a single-base-pair transition mutation in ORF-P codon 38, resulting in translational termination of the ORF-P protein (OPP). This mutation does not alter the amino acid sequence of ICP34.5. Expression of a truncated form of OPP by mutant virus L/ST-n38 did not result in premature shutoff of infected-cell protein synthesis and produced no other observable phenotype relative to wild-type virus in in vitro tests. Moreover, the 50% lethal dose (LD50) of L/ST-n38 was comparable to that of wild-type virus following intracranial inoculation of 3-week-old mice, as were the latency and reactivation phenotypes of the virus. These properties of L/ST-n38 indicate that the attenuated phenotype of ORF-P ORF-34.5 double mutants is a consequence of mutations that affect the function of ICP34.5 and not the function of OPP. Mutant virus L/ST-4BS contains four single-base-pair substitutions in the ICP4 binding site in the L/ST promoter that abrogate the binding of ICP4 to this site, leading to high-level expression of the L/STs and OPP. L/ST-4BS induced premature shutoff of viral and cellular protein synthesis and was slightly growth restricted in cells of neural lineage (SK-N-SH human neuroblastoma cells) but was wild type for these two parameters in cells of nonneural lineage (immortalized primate Vero cells). Of particular interest was the observation that L/ST-4BS exhibited cell-type-specific expression of both the γ134.5 transcripts and the latency-associated transcripts (LATs). Thus, expression of these transcripts was barely detectable in cells of neural lineage (NB41A3 mouse neuroblastoma cells) but was wild type in Vero cells. In vivo, L/ST-4BS was reactivated from mouse trigeminal ganglia with reduced efficiency and delayed kinetics relative to wild-type virus. L/ST-4BS was completely attenuated for neurovirulence (LD50 > 106 PFU) relative to wild-type virus (LD50 < 900 PFU), although the four single-base-pair substitutions lie outside the coding region for the neurovirulence factor, ICP34.5. Collectively, the complex in vitro and in vivo phenotypes of L/ST-4BS can be attributed to (i) disruptions of the ICP4 binding site in the L/ST promoter and subsequent overexpression of the L/STs and OPP; (ii) alterations in ORF-O, which is also mutated in L/ST-4BS; or (iii) alterations in other cryptic genes or cis-acting elements.

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Poulos, Bonnie T., Kathy F. J. Tang, Carlos R. Pantoja, Jean Robert Bonami i Donald V. Lightner. "Purification and characterization of infectious myonecrosis virus of penaeid shrimp". Journal of General Virology 87, nr 4 (1.04.2006): 987–96. http://dx.doi.org/10.1099/vir.0.81127-0.

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The causative agent of myonecrosis affecting cultured Penaeus vannamei in Brazil was demonstrated to be a virus after purification of the agent from infected shrimp tissues. Purified viral particles were injected into specific pathogen-free P. vannamei, resulting in a disease that displayed the same characteristics as those found in the original shrimp used for purification. The virus was named infectious myonecrosis virus (IMNV). The viral particles were icosahedral in shape and 40 nm in diameter, with a buoyant density of 1·366 g ml−1 in caesium chloride. The genome consisted of a single, double-stranded (dsRNA) molecule of 7560 bp. Sequencing of the viral genome revealed two non-overlapping open reading frames (ORFs). The 5′ ORF (ORF 1, nt 136–4953) encoded a putative RNA-binding protein and a capsid protein. The coding region of the RNA-binding protein was located in the first half of ORF 1 and contained a dsRNA-binding motif in the first 60 aa. The second half of ORF 1 encoded a capsid protein, as determined by amino acid sequencing, with a molecular mass of 106 kDa. The 3′ ORF (ORF 2, nt 5241–7451) encoded a putative RNA-dependent RNA polymerase (RdRp) with motifs characteristic of totiviruses. Phylogenetic analysis based on the RdRp clustered IMNV with Giardia lamblia virus, a member of the family Totiviridae. Based on these findings, IMNV may be a unique member of the Totiviridae or may represent a new dsRNA virus family that infects invertebrate hosts.

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Takemoto, Yutaka, i Tadaaki Hibi. "Genes Ia, II, III, IV and V of Soybean chlorotic mottle virus are essential but the gene Ib product is non-essential for systemic infection". Journal of General Virology 82, nr 6 (1.06.2001): 1481–89. http://dx.doi.org/10.1099/0022-1317-82-6-1481.

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Soybean chlorotic mottle virus (SbCMV) is the type species of the genus ‘Soybean chlorotic mottle-like viruses’, within the family Caulimoviridae. The double-stranded DNA genome of SbCMV (8178 bp) contains eight major open reading frames (ORFs). Viral genes essential and non-essential for the replication and movement of SbCMV were investigated by mutational analysis of an infectious 1·3-mer DNA clone. The results indicated that ORFs Ia, II, III, IV and V were essential for systemic infection. The product of ORF Ib was non-essential, although the putative tRNAMet primer-binding site in ORF Ib was proved to be essential. Immunoselection PCR revealed that an ORF Ia deletion mutant was encapsidated in primarily infected cells, indicating that ORF Ia is required for virus movement but not for replication. ORF IV was confirmed to encode a capsid protein by peptide sequencing of the capsid. Analysis of the viral transcripts showed that the SbCMV DNA genome gives rise to a pregenomic RNA and an ORF VI mRNA, as shown in the case of Cauliflower mosaic virus.

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Stavolone, Livia, Antonio Ragozzino i Thomas Hohn. "Characterization of Cestrum yellow leaf curling virus: a new member of the family Caulimoviridae". Journal of General Virology 84, nr 12 (1.12.2003): 3459–64. http://dx.doi.org/10.1099/vir.0.19405-0.

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Cestrum yellow leaf curling virus (CmYLCV) has been characterized as the aetiological agent of the Cestrum parqui mosaic disease. The virus genome was cloned and the clone was proven to be infectious to C. parqui. The presence of typical viroplasms in virus-infected plant tissue and the information obtained from the complete genomic sequence confirmed CmYLCV as a member of the Caulimoviridae family. All characteristic domains conserved in plant pararetroviruses were found in CmYLCV. Its genome is 8253 bp long and contains seven open reading frames (ORFs). Phylogenetic analysis of the relationships with other members of the Caulimoviridae revealed that CmYLCV is closely related to the Soybean chlorotic mottle virus (SbCMV)-like genus and particularly to SbCMV. However, in contrast to the other members of this genus, the primer-binding site is located in the intercistronic region following ORF Ib rather than within this ORF, and an ORF corresponding to ORF VII is missing.

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Mahalingam, Ravi, Robert Lasher, Mary Wellish, Randall J. Cohrs i Donald H. Gilden. "Localization of Varicella-Zoster Virus Gene 21 Protein in Virus-Infected Cells in Culture". Journal of Virology 72, nr 8 (1.08.1998): 6832–37. http://dx.doi.org/10.1128/jvi.72.8.6832-6837.1998.

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ABSTRACT Although four varicella-zoster virus (VZV) genes have been shown to be transcribed in latently infected human ganglia, their role in the development and maintenance of latency is unknown. To study these VZV transcripts, we decided first to localize their expression products in productively infected cells. We began with VZV gene 21, whose open reading frame (ORF) is 3,113 bp. We cloned the 5′ and 3′ ends and the predicted antigenic segments of the ORF as 1292-, 1280-, and 880-bp DNA fragments, respectively, into the prokaryotic expression vector pGEX-2T. The three VZV 21 ORFs were expressed as approximately 75-, 73-, and 59-kDa glutathione S-transferase fusion proteins in Escherichia coli. To prepare polyclonal antibodies that would recognize all potential epitopes on the VZV gene 21 protein, rabbits were inoculated with a mixture of the three fusion proteins, and antisera were obtained and affinity purified. Immunohistochemical and immunoelectron microscopic analyses using these antibodies revealed VZV ORF 21 protein in both the nucleus and cytoplasm of VZV-infected cells. When these antibodies were applied to purified VZV nucleocapsids, intense staining was seen in their central cores.

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McKeever, D., i H. Reid. "Survival of orf virus under British winter conditions". Veterinary Record 118, nr 22 (31.05.1986): 613–14. http://dx.doi.org/10.1136/vr.118.22.613.

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Koptopoulos, G., H. W. Reid i Irene Pow. "Cytotoxic Antibodies in Orf Virus Infection of Sheep". Zentralblatt für Veterinärmedizin Reihe B 29, nr 4 (13.05.2010): 284–91. http://dx.doi.org/10.1111/j.1439-0450.1982.tb01226.x.

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44

YIRRELL, D. L., J. P. VESTEY i M. NORVAL. "Immune responses of patients to orf virus infection". British Journal of Dermatology 130, nr 4 (kwiecień 1994): 438–43. http://dx.doi.org/10.1111/j.1365-2133.1994.tb03375.x.

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Mazur, C., I. I. Ferreira, F. B. Rangel Filho i R. Galler. "Molecular characterization of Brazilian isolates of orf virus". Veterinary Microbiology 73, nr 4 (maj 2000): 253–59. http://dx.doi.org/10.1016/s0378-1135(99)00151-0.

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Scagliarini, A., L. Gallina, F. Dal Pozzo, M. Battilani, S. Ciulli i S. Prosperi. "Heparin binding activity of orf virus F1L protein". Virus Research 105, nr 2 (październik 2004): 107–12. http://dx.doi.org/10.1016/j.virusres.2004.04.018.

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Haig, David, Colin McInnes, David Deane, Andrea Lear, Nyree Myatt, Hugh Reid, Jim Rothel i in. "Cytokines and their inhibitors in orf virus infection". Veterinary Immunology and Immunopathology 54, nr 1-4 (listopad 1996): 261–67. http://dx.doi.org/10.1016/s0165-2427(96)05687-5.

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Mercer, Andrew A., Kate Fraser, Gillian Barns i Anthony J. Robinson. "The structure and cloning of orf virus DNA". Virology 157, nr 1 (marzec 1987): 1–12. http://dx.doi.org/10.1016/0042-6822(87)90307-2.

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HAIG, D., C. MCINNES, D. DEANE, H. REID i A. MERCER. "The immune and inflammatory response to orf virus". Comparative Immunology, Microbiology and Infectious Diseases 20, nr 3 (czerwiec 1997): 197–204. http://dx.doi.org/10.1016/s0147-9571(96)00045-8.

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Mahmud, A. K. M. Firoj, K. M. Zillur Rahman, Shuvra Kanti Dey, Tahsina Islam i Ali Azam Talukder. "Genome Annotation and Comparative Genomics of ORF Virus". Advances in Microbiology 04, nr 15 (2014): 1117–31. http://dx.doi.org/10.4236/aim.2014.415122.

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