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Academic literature on the topic 'Orf virus'

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Published: 4 June 2021
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Journal articles on the topic "Orf virus"

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Bergqvist, Christina, Mazen Kurban, and Ossama Abbas. "Orf virus infection." Reviews in Medical Virology 27, no. 4 (May 8, 2017): e1932. http://dx.doi.org/10.1002/rmv.1932.

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Gemeniano, Malou C., Earl T. Sawai, Christian M. Leutenegger, and Ellen E. Sparger. "Feline Immunodeficiency Virus Orf-A Is Required for Virus Particle Formation and Virus Infectivity." Journal of Virology 77, no. 16 (August 15, 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, and H. W. Reid. "Tissue culture-propagated orf virus vaccine protects lambs from orf virus challenge." Veterinary Record 138, no. 8 (February 24, 1996): 184–86. http://dx.doi.org/10.1136/vr.138.8.184.

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

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Querol Nasarre, Ignacio, Mariano Ara Martín, and Estrella Simal Gil. "Infección por el virus orf." Piel 21, no. 5 (May 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, no. 2 (June 17, 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, and 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, no. 8 (August 1, 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, and 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, no. 19 (October 1, 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, and Julien Lambert. "Autoinoculation with Orf virus (ecthyma contagiosum)." International Journal of Dermatology 53, no. 1 (January 3, 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, no. 2 (April 2006): 127–31. http://dx.doi.org/10.1097/01.qco.0000216622.75326.ef.

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Dissertations / Theses on the topic "Orf virus"

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Gemeniano, Maria Lourdes Charmaine. "Characterization of Orf-A of feline immunodeficiency virus /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2002. http://uclibs.org/PID/11984.

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Westphal, Dana, and n/a. "Characterisation of a novel inhibitor of apoptosis expressed by Orf virus." University of Otago. Department of Microbiology & Immunology, 2008. http://adt.otago.ac.nz./public/adt-NZDU20080922.162136.

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Apoptosis plays important roles in host defences against virus infection. It is therefore not surprising that viruses have developed a vast array of modulators that block this process at different stages within the apoptotic pathways. Intrestingly, Orf virus (ORFV), a member of the Parapoxvirus genus, did not reveal any of the known poxviral inhibitors of apoptosis, but was found to express a unique anti-apoptotic protein, ORFV125. The aim of this PhD project was to determine the subcellular localisation of this protein and to further characterise its anti-apoptotic activity. This included exploring its ability to inhibit early, intermediate and late events of apoptosis and identifying the mechanism by which this viral protein functions to prevent cell death. Experiments revealed that ORFV125 was localised to the mitochondria through a C-terminal mitochondrial-targeting motif, and this specific location was necessary for the protein�s anti-apoptotic function. Furthermore, the viral protein inhibited UV-induced apoptotic events at and downstream of the mitochondria such as cytochrome c release, caspase activation and DNA fragmentation. However, it was not able to prevent UV-induced activation of the c-Jun-NH₂ kinase (JNK), an event occurring upstream of the mitochondria, consistent with its localisation to this organelle. The ability to prevent apoptosis was comparable with that of the cellular anti-apoptotic protein Bcl-2, which belongs to a family of mitochondrial regulators of apoptosis. Although standard BLAST analysis failed to detect homology to anti-apoptotic members of the Bcl-2 family, a manual alignment of the primary sequence of ORFV125 with these proteins revealed characteristic residues of Bcl-2 homology (BH) domains within ORFV125. These motifs are conserved within the Bcl-2 proteins and important for their structure and function. In addition, mutating amino acids within the ORFV125 BH domains led to a loss of the anti-apoptotic function of the mutated proteins, indicating the functional importance of these residues for the viral protein. These observations suggest that ORFV125 might be classified as a viral Bcl-2-like protein. To provide evidence for this hypothesis, it was investigated if ORFV125 acts in a Bcl-2-like manner to inhibit apoptosis. The viral protein was able to entirely block the activation of the pro-apoptotic Bcl-2 family members Bak and Bax, although it did not directly bind to these proteins. Instead, ORFV125 interacted with a subset of the pro-apoptotic BH3-only proteins, which can trigger the activation of Bax and Bak. Furthermore, this study demonstrated that ORFV125 could inhibit apoptosis induced by BH3-only proteins to which the viral protein could bind. On the other hand, ORFV125 was not able to prevent the activity of pro-apoptotic proteins that it failed to interact with. This shows that ORFV125�s mechanism of action is to inhibit the activity of BH3-only proteins by binding and neutralising their function. Overall, these results provided evidence that ORFV125 is potent anti-apoptotic protein that can prevent UV-induced cell death without the participation of other ORFV proteins. Furthermore, the viral protein shared primary sequence and secondary structure similarities to Bcl-2 family members and acted in a Bcl-2-like manner to inhibit apoptosis.
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McKeever, Declan James. "Studies of the immunology and epidemiology of orf." Thesis, University of Edinburgh, 1987. http://hdl.handle.net/1842/30488.

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Mo, Min, and n/a. "Characterization of an Orf virus RING-H2 protein, B5L : a mimic of cellular anaphase promoting complex subunit 11." University of Otago. Department of Microbiology & Immunology, 2009. http://adt.otago.ac.nz./public/adt-NZDU20090220.085825.

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The anaphase promoting complex (APC/C) is an ubiquitin ligase that is an essential regulator of multiple steps in the cell cycle. The complex consists of at least 12 subunits with a catalytic core formed by a scaffold protein, APC2, and a RING-H2 protein, APC11. The Parapoxvirus, Orf virus (OV), encodes a RING-H2 protein, B5L, with clear sequence similarities to APC11. The disruption of APC/C function leads to pre-mature entry into S phase and a delayed M phase exit and, potentially, apoptosis. This investigation explored the functional significance of the similarity between B5L and APC11 and specifically sought to determine if B5L manipulates cell cycle regulation by targeting APC/C function. Co-immunoprecipitation experiments from lysates of cells expressing a range of constructs revealed an interaction between B5L and APC2 in the same manner as seen with APC11. Furthermore, B5L was found to associate with endogenous APC/C. However, although APC11 promoted the formation of polyubiquitin chains in substrate-independent in vitro assays, B5L was inactive in this assay. Bioinformatics comparisons of APC11 and other known RING ubiquitin ligases with B5L and its poxviral homologues revealed some subtle differences. In particular a domain of APC11 (amino acids 61-74), that is essential for its ubiquitin ligase activity is not conserved in B5L or its homologues. When this APC11 domain was incorporated in place of the corresponding region of B5L (amino acids 59-67), the mutated B5L acquired ubiquitin ligase activity. On the other hand, APC11 protein in which the domain was replaced with that of B5L lost ubiquitin ligase activity. Stable cell lines expressing B5L showed an increased number of cells in G2/M phase (30�4%) compared with cell lines expressing APC11 (11�2%, n=3, p<0.05, ANOVA, Tukey�s), consistent with impaired APC/C function. APC/C substrates such as cyclin A, cyclin B and the thymidine kinase were stablized in B5L-expressing cells compared with control cells. Furthermore, transient hyper-expression of B5L induced apoptosis in 25�2% (n=3, p<0.05) of the cell population compared with only 6�1% apoptotic cells when APC11 was hyper-expressed. Analysis of the DNA content of OV-infected cells revealed enhanced DNA synthesis compared with cells infected with a B5L knockout OV. These observations indicate that B5L is a non-functional mimic of APC11. It associates with APC/C, but lacks ubiquitin ligase activity, and hence disrupts APC/C function. These abilities may enable OV to induce a cellular environment that enhances viral replication.
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Chand, Puran. "Molecular and immunological characterisation of a major envelope protein of capripoxvirus." Thesis, University of Surrey, 1992. http://epubs.surrey.ac.uk/2774/.

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Analysis of the proteins of capripoxvirus (KS-1) revealed a 32kd protein that is one of the major structural proteins of the virus and is localised in the virus envelope. Monospecific serum prepared against the 32kd envelope protein neutralised the virus indicating that this protein contains neutralising epitopes. Lymphocyte proliferation studies, using the 32kd protein and peripheral blood mononuclear cells from capripoxvirus (KS-i) vaccinated sheep, showed that this protein strongly induced cellmediated immune responses. The 32kd protein is capripoxvirus specific and induced antibodies in early stages of capripoxvirus infections. Immunoblot analysis of antibody responses against this protein has provided a basis for the differential diagnosis of capripoxvirus and orf virus infections. The 32kd protein bound to the surface of cultured lamb testis cells. The binding of the 32kd protein was completely inhibited by prior incubation of cells with purified capripoxvirus (KS-1) but not by bovine serum albumin. Trypsin treatment of capripoxvirus (KS-1) degraded the majority of the 32kd protein with a minimal effect on a few other virus proteins. Trypsin removed an external 10kd fragment from the 32kd protein, leaving a 22kd fragment associated with the virus. In addition, the trypsin treatment reduced the virus infectivity by at least ten fold, suggesting that the cell surface binding domain of the 32kd protein is located within the external 10kd fragment. The monospecific serum to the 32kd protein had no effect of the infectivity titre of the trypsin treated virus further supporting the concept that the external 10kd fragment of the 32kd protein is involved in binding of the virus particle to the cell surface. A degenerate oligonucleotide probe, based on an internal amino acid sequence obtained from V8 protease cleavage products of the 32kd protein, was used to identify the gene encoding the 32kd protein. The gene encoding the 32kd protein was identified within the 2.8kb HindI1l Q1 fragment of the capripoxvirus (KS-1) genome. The nucleotide sequence analysis of the Hindu Q1 fragment revealed five open reading frames (Q11L, Q12R, Q13L, Q14R and Q15L), one of these open reading frames, Q13L, is capable of encoding a 30.6kd protein and contains the complete internal amino acid sequence obtained from the V8 protease cleavage products of the 32kd protein, indicating that the Q13L encodes the 32kd envelope protein of capripoxvirus (KS-1). The deduced amino acid sequence of the Q13L shows a 34.1% identity and 61.3% similarity with that of H3L open reading frame of vaccinia virus.
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Dickinson, Victoria Jane. "The cloning and subcellular localisation of maize streak virus ORF V1." Thesis, University of Hull, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321050.

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Lear, Andrea. "The characterisation of the ovine skin response to orf virus infection." Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/20625.

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Orf is a highly contagious, eruptive skin disease of sheep and goats caused by a parapox virus. The virus enters through abrasions in the skin, where it replicates in the regenerating epidermal keratinocytes. Despite the generation of a specific antiviral response, orf virus reinfections can be established easily, although the lesions are milder and generally regress more rapidly than after primary exposure. The cutaneous response to orf involves the formation of a dense network of MHC class II+ dendritic cells at the lesion. The primary aim of this project was to characterise these dendritic cells and to identify the cytokines produced by orf infected keratinocytes in vitro, that might be involved in the accumulation of the dendritic cells in vivo. In vivo studies of primary and secondary orf virus lesions identified the class II+ dendritic cells to be a population of CD1- cells, which are also found within the dermis of normal ovine skin. A subpopulation of these cells also expressed the antigen, coagulation factor XIIIa. Factor XIIIa+ dendritic cells comprised over half the dendritic cells seen in the network of a primary orf lesion but were only observed in small numbers, transiently, in the secondary orf lesion. All the dendritic cells lacked the expression of ovine macrophage markers. The proliferative response of the primary and secondary orf lesions also differed. High proliferative activity was observed in the epidermis and dermis in the primary response to orf but not in the secondary response. A few of the proliferating cells were identified as dendritic cells but it would appear that the dendritic cell network in both primary and secondary orf lesions does not arise by local cell division.
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Cargnelutti, Juliana Felipetto. "Infecção experimental de coelhos e camundongos com o vírus do ectima contagioso." Universidade Federal de Santa Maria, 2010. http://repositorio.ufsm.br/handle/1/10060.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
Contagious ecthyma (orf) is a cutaneous disease that affects sheep and goats, and may be occasionally transmitted to humans. The disease is caused by orf virus (ORFV). ORFV infection produces croustous and proliferative lesions, usually on the nostrils and labial commissures of lambs, and also in the udder, teat skin and coronary bands of adults animals. The pathogenesis of ORFV infection is poorly understood and a search for an adequate animal model is required, yet the disease has been already reproduced in sheep, goats and rabbits. This dissertation relates the clinical, virological and pathological aspects of ORFV infection in rabbits and mice experimental inoculated. Ten rabbits, ten mice and two lambs were inoculated intradermally after skin scarification with an hypodermic needle. A viral suspension of ORFV IA-82 strain (108.5TCID50/mL) was inoculated in the internal face of the ear, back skin and labial commissure of rabbits; internal face of the ear of mice. Lambs were inoculated in the labial commissures and in the internal face of hind limbs. All animals were monitored clinically, virologically, and pathologically for 21 days. All rabbits developed clinical signs in the inoculation sites, begining with mild hyperemia that evolved to macules, papules, vesicle, pustules and scabs. Lesions appeared at days 3 and 4 post-inoculation (pi) and lasted to 3 to 10 days. Viral shedding was detected from days 2 to 14pi. Histological examination of lesions revealed focal proliferative dermatitis with ballooning degeneration and eosinophilic intracytoplasmic inclusions in keratinocytes, histological hallmarks of contagious ecthyma in sheep. A similar, albeit much milder clinical course was observed in 5 out of 10 inoculated mice. All lambs presented characteristic contagious ecthyma clinical and histopathologycal lesions from days 3 to 18pi, and the virus was recovered from lesions between days 2 and 19pi. At day 28pi, seroneutralization test (SN) was unable to detect neutralizing antibodies in all inoculated animals. These findings show that ORFV replicates and produce local lesions in rabbits and mice. However, rabbits are more susceptible to infection and disease, and may be used as an animal model to study some aspects of ORFV pathogenesis.
O ectima contagioso (ou orf) é uma doença infecto-contagiosa de pele que afeta principalmente ovinos e caprinos, e que ocasionalmente pode acometer o homem. O seu agente etiológico é o vírus da orf (ORFV). O ORFV produz lesões proliferativas, geralmente na comissura labial e no plano naso-labial de cordeiros, e também na pele do úbere, nos tetos e no rodete coronário dos cascos de animais adultos. A patogenia da infecção pelo ORFV é pouco conhecida, embora a doença já tenha sido reproduzida em ovinos, caprinos e coelhos. Essa dissertação relata os achados clínicos, virológicos e histopatológicos da infecção experimental de coelhos e camundongos pelo ORFV. Para isso, coelhos, camundongos e cordeiros foram inoculados pela via intradérmica (ID), após escarificação da pele com agulha hipodérmica. A inoculação dos cordeiros serviu como controle positivo. Uma suspensão viral da cepa IA-82 do ORFV (108,5DICC50/mL) foi inoculada na face interna da orelha, na pele do dorso e na comissura labial dos coelhos; na face interna da orelha dos camundongos; e na comissura labial e face interna do membro pélvico dos cordeiros. Os animais foram monitorados por 21 dias nos aspectos clínicos, virológicos e patológicos. Todos os coelhos inoculados apresentaram lesões semelhantes nos locais de inoculação, iniciando com hiperemia, evoluindo para máculas, pápulas, vesículas, pústulas e crostas. Os sinais surgiram 3 a 4 dias pós inoculação (pi) e duraram por 3 a 10 dias. Excreção viral foi detectada entre os dias 2 e 14pi. A análise histológica das lesões revelou dermatite focal proliferativa, com degeneração balonosa e corpúsculos de inclusão intracitoplasmáticos eosinofílicos nos queratinócitos, semelhante às alterações histológicas observadas nos cordeiros. Lesões similares, mas de menor intensidade foram observadas em 5 de 10 camundongos. Os cordeiros, utilizados como controles positivos, apresentaram lesões clínicas e histopatológicas características de ectima contagioso entre os dias 3 e 18pi, sendo que o vírus foi recuperado das lesões entre os dias 2 e 19dpi. No dia 28pi, pelo teste de soroneutralização (SN), não foram detectados anticorpos neutralizantes no soro dos animais inoculados. Esses resultados demonstram que a inoculação de ORFV resulta em replicação viral e produção de lesões em coelhos e camundongos, porém a doença é reproduzida de forma mais consistente em coelhos. Portanto, sugere-se que coelhos possam ser utilizados como modelos para estudos in vivo com o ORFV.
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Coelho, João Nuno Santos. "Molecular characterization and functional analysis of ORF P1192R from African swine fever virus." Doctoral thesis, Universidade de Lisboa. Faculdade de Medicina Veterinária, 2016. http://hdl.handle.net/10400.5/10907.

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Tese de Doutoramento em Ciências Veterinárias. Especialidade de Ciências Biológicas e Biomédicas
African swine fever virus (ASFV) is a nucleo-cytoplasmic large DNA arbovirus and the single member of the family Asfarviridae. It infects soft ticks of the genus Ornithodoros as well as all members of the family Suidae, representing a global threat for pig husbandry for which there is currently no effective vaccine or treatment. Since the ASFV viral cycle is mainly cytoplasmic, it has been found/predicted to code for many components of the replicative and transcriptional machineries. Of these, and based in sequence homologies, a putative type II DNA topoisomerase-coding ORF (P1192R) was identified in the ASFV genome. DNA topoisomerases are enzymes that modulate the topological state of DNA molecules. They are ubiquitous and essential, participating in processes such as DNA replication, recombination and repair and also in transcription. Since ASFV has a large linear genome, with 170 to 190 kbp depending on the isolate, containing terminal inverted repeats and covalently closed ends, a type II topoisomerase may be indispensable for viral replication and/or transcriptional events. The main objectives of this work were to deepen the study on ORF P1192R and determine if it indeed codes for a type II DNA topoisomerase and, if so, to characterize its activity. Bioinformatics and phylogenetic analyses showed that ORF P1192R is highly conserved among the fourteen ASFV isolates analyzed and, although its amino acid sequence clearly diverges from other type II topoisomerases, the structural organization is preserved and conserved motifs and domains essential for activity are present. Transient expression of GFP-pP1192R in COS-7 cells revealed an exclusively cytoplasmic distribution of the protein, which remained unaltered by treatment with leptomycin B. Using Vero cells or swine macrophages infected with ASFV isolate Ba71V or L60, respectively, expression of pP1192R was observed in the late phase of infection, co-localizing with the viral factories, where the bulk of viral replication and transcription occurs. Heterologous expression of pP1192R in Saccharomyces cerevisiae demonstrated that it functionally complements a top2 thermo-sensitive mutation and that it exhibits ATP-dependent decatenation activity. The purified recombinant pP1192R was found to efficiently decatenate kDNA and to processively relax supercoiled plasmid DNA, which are characteristics of a type II topoisomerase. The optimal requirements in terms of pH, temperature and salt, divalent ions and ATP concentrations for pP1192R activity in vitro were determined and its sensitivity to a panel of topoisomerase poisons and inhibitors was tested. Our results indicate that P1192R may be a target for studying, and possibly controlling, ASFV transcription and replication.
RESUMO - O vírus da peste suína africana (VPSA) é um arbovírus icosaédrico núcleo-citoplasmático de DNA de cadeia dupla, classificado no género Asfivirus da família Asfarviridae, da qual é o único membro conhecido. Este vírus infecta carraças do género Ornithodoros assim como todos os membros da família Suidae, constituindo uma ameaça global para a suinicultura para a qual não existe actualmente qualquer vacina ou tratamento. A prevenção da peste suína africana é feita através de medidas que visam reduzir o risco de introdução de animais ou produtos de origem animal infectados em regiões livres da doença, enquanto o controlo de um surto se baseia exclusivamente em medidas que incluem o abate sanitário de todos os animais susceptíveis na área do foco e a proibição de movimentos e comercialização de animais. Embora o VPSA tenha sido inicialmente descrito como um vírus com replicação exclusivamente citoplasmática, actualmente sabe-se que o núcleo da célula hospedeira é indispensável na fase inicial da infecção. Contudo, a grande maioria do ciclo infeccioso ocorre no citoplasma da célula infectada, não sendo por isso surpreendente que, das 150 a 167 grelhas de leitura aberta (ORF, do inglês “open reading frame”) identificadas no genoma do VPSA, algumas codifiquem para componentes das maquinarias de replicação e de transcrição. Dentre estas, prevê-se, com base em homologia de sequências aminoacídicas, que a ORF P1192R codifique para uma topoisomerase de DNA do tipo II. As topoisomerases de DNA estão presentes em todas as células e são responsáveis pela modulação do estado topológico do DNA, estado esse que se altera durante processos como a replicação, a recombinação e a reparação do DNA, assim como a transcrição, e dos quais resultam torções das moléculas de DNA que, não sendo resolvidas, podem comprometer a integridade genómica e consequentemente a viabilidade celular. Todas as topoisomerases exercem a sua actividade através da criação de quebras no DNA devido ao ataque nucleofílico de um resíduo de tirosina catalítico ao esqueleto fosfodiéster da molécula de DNA, gerandose assim uma ligação fosfotirosina covalente. As topoisomerases são classificadas em dois tipos, tendo por base a forma como quebram a molécula de DNA: as topoisomerases do tipo I, cuja actividade é independente de ATP e que geram quebras em cadeia única no DNA, facilitando assim o desenrolamento; e as topoisomerases do tipo II, que necessitam de ATP para gerar uma quebra nas duas cadeias do DNA, através da qual fazem passar uma dupla cadeia intacta. Considerando que o VPSA tem um genoma linear de grandes dimensões, com 170 a 190 quilopares de bases dependendo do isolado, e que contém repetições terminais invertidas fechadas covalentemente, uma topoisomerase do tipo II pode efectivamente ser essencial para eventos de replicação e/ou transcrição virais. Os objectivos centrais deste trabalho foram os seguintes: (i) realização de um estudo bioinformático e filogenético aprofundado da ORF P1192R do VPSA; (ii) estudo da proteína codificada por esta ORF (pP1192R), através da sua clonagem, expressão em sistema heterólogo, purificação da proteína recombinante e caracterização in vitro da sua actividade; (iii) determinação do efeito sobre a actividade da proteína recombinante dum painel de compostos químicos descritos como sendo inibidores de topoisomerases; (iv) identificação dos níveis de expressão e da localização intracelular da pP1192R em células infectadas pelo VPSA, a diferentes tempos de infecção; (v) avaliação do efeito de mutações dirigidas em resíduos ou motivos identificados como reguladores da actividade enzimática ou localização subcelular da pP1192R, tendo por base a informação gerada nos estudos bioinformáticos acima mencionados. A ORF P1192R do isolado L60 do VPSA foi amplificada por PCR e clonada e a sua sequência nucleotídica foi determinada e utilizada em análises bioinformáticas e filogenéticas. Verificou-se que esta ORF é altamente conservada entre os catorze isolados do VPSA cujo genoma se encontrava disponível nas bases de dados e, embora a sua sequência aminoacídica seja claramente divergente das de outras topoisomerases do tipo II incluídas neste estudo, quer sejam elas de origem procariota, eucariota ou viral, a organização estrutural da proteína está preservada e estão presentes motivos e domínios conservados que são essenciais para a actividade enzimática. O estudo da localização celular da pP1192R iniciou-se com a construção de plasmídeos quiméricos para a expressão da pP1192R em fusão com a proteína verde fluorescente (GFP) ou com uma variante vermelha (RFP). Transfectaram-se transientemente células de linha COS-7 com estas construções tendo-se observado que a proteína de fusão se distribuía exclusivamente pelo citoplasma. Esta distribuição não foi alterada após tratamento com leptomicina B que bloqueia uma das vias de exportação de proteínas do núcleo. Já a infecção das células a expressarem GFP-pP1192R com um isolado do VPSA adaptado a células Vero (Ba71V) induziu uma redistribuição da proteína de fusão, deixando de estar homogeneamente distribuída pelo citoplasma para estar principalmente concentrada nas fábricas virais a partir das 8 horas pós-infecção. Utilizando células de linha Vero infectadas com o isolado Ba71V, utilizado como modelo de infecção, ou macrófagos derivados de monócitos de sangue periférico de suíno (células alvo do vírus na infecção natural) infectados com o isolado virulento L60, e utilizando um soro anti-pP1192R produzido no decurso destes trabalhos, foi possível constatar que a pP1192R viral é produzida na fase intermédia/tardia da infecção (observável a partir das 6/8 horas pós-infecção) e que acumula nas fábricas virais ao longo da infecção. A expressão em sistema heterólogo da pP1192R iniciou-se num sistema procariota, baseado em Escherichia coli, mas embora tenha sido possível obter proteína recombinante em grandes quantidades, a sua purificação só foi conseguida recorrendo a agentes desnaturantes, impedindo a obtenção de proteína activa. Assim, avançou-se para um novo sistema de expressão baseado na levedura Pichia pastoris que apresenta diversas vantagens sobre o anterior, nomeadamente o facto de ser um sistema eucariota e por isso mais semelhante ao contexto em que a pP1192R é expressa em condições naturais. Contudo, neste sistema não foi possível obter proteína recombinante e o sistema foi abandonado. Tentou-se por fim a expressão heteróloga na levedura Saccharomyces cerevisiae. Neste organismo, a utilização das estirpes JCW26 e SD117 que contêm uma mutação termo-sensível no gene que codifica para a topoisomerase do tipo II endógena, permitiu demonstrar, quer in vivo através da complementação da mutação termo-sensível, quer in vitro recorrendo a ensaios funcionais de decatenação, que a pP1192R é efectivamente uma topoisomerase do tipo II funcional. Utilizando ainda S. cerevisiae como sistema de expressão, foi possível obter e purificar pP1192R recombinante para caracterização da sua actividade em ensaios funcionais in vitro. Observou-se que a pP1192R é capaz de relaxar DNA superenrolado, de decatenar DNA catenado e, quando em elevadas concentrações, de catenar DNA plasmídico, não tendo sido detectada actividade de superenrolamento de DNA relaxado. Determinaram-se também as condições óptimas de funcionamento em termos de temperatura, pH e concentrações de sal (NaCl ou KCl), ATP ou iões divalentes (Mg2+, Mn2+, Zn2+, Cu2+ e Ca2+), que foram posteriormente utilizadas para avaliar a sensibilidade da pP1192R recombinante a um painel de inibidores de topoisomerases, entre os quais se incluem drogas frequentemente utilizadas como agentes antimicrobianos ou antitumorais. Dos compostos testados, aqueles para os quais foram obtidos resultados mais promissores, i.e., os que revelaram níveis de inibição mais elevados, foram a coumermicina A1, a doxorubicina, a amsacrina e a genisteína. Pelo contrário, as quinolonas, normalmente utilizadas como antibióticos visando infecções provocadas por organismos procariotas, foram dos compostos com menor eficácia. Em suma, os resultados deste trabalho indicam que a ORF P1192R é um alvo promissor para o estudo e, eventualmente, o controlo dos processos replicativos e transcricionais do vírus da peste suína africana.
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Housawi, Fadhel Mohammed Taher. "Studies on parapoxvirus antigens through the development of monoclonal antibodies to orf virus." Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/30287.

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Twenty-five monoclonal antibodies (mabs) against orf virus, a parapoxvirus (ppv), were produced following the immunisation of mice with a lysate of cells infected with orf-11 virus. These mabs, together with 2 others recloned from an earlier fusion, were identified by ELISA and IFT and characterised. No neutralising activity was shown by any of the mabs. The size of orf proteins detected by the mabs was measured using western blotting and radioimmunoprecipitation (RIP). Western blotting was conducted with two types of orf-11 antigen preparations - gradient purified virus or a lysate of orf-11 infected cells. Five mabs detected a protein of approximately 40 kDa with both purified virus and infected lysate antigens. These mabs detected a protein approximately 65 kDa in size, but only with infected cell lysate antigen. In RIP studies, 21 mabs produced bands 13 of which were against the 65 kDa protein, 7 against that 40 kDa protein while one was against a 50 kDa protein. Twenty-one of the 27 mabs reacted with at least two of 18 vaccinia virus orf virus (VVOV) recombinants expressing a library of orf genome fragments of the NZ-2 virus strain. Four of the mabs which had identified the native 40kDa protein reacted with 2 overlapping recombinants (245 and 247). Seventeen of the mabs, 16 of which had identified the native 65 kDa protein recognised three recombinants 79, 285 and 286 all of which contain different inserts from the same region of the orf virus genome. Subsequent sequencing of the overlapping site between recombinants 245 and 247 by New Zealand collaborators has identified a new orf gene, designated FIL which has been shown to be analogous to the H3L vaccinia virus gene which codes for an immunodominant 35 kDa envelope protein. Cells infected with a new VVOV recombinant expressing only the FIL orf gene showed positive fluorescence with 3 or the 4 mabs which reacted with the 245 and 246 recombinants, confirming the target of these mabs is the product of the FIL gene.
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Books on the topic "Orf virus"

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Ireland. Food Safety Advisory Committee. Leptospiral infections, Lyme disease, Babesiosis, Orf virus disease. Dublin: Stationery Office, 1992.

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Lapierre, Hervé. Virus and virus diseases of Poaceae (Gramineae). Edited by Signoret Pierre A and Institut national de la recherche agronomique (France). Paris: Institut National de la Recherche Agronomique (France), 2004.

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Michael, Thresh J., ed. Plant virus epidemiology. Amsterdam: Academic Press/Elsevier, 2006.

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A, Hadidi, Khetarpal R. K, and Koganezawa H, eds. Plant virus disease control. St. Paul, Minn: APS Press, 1998.

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G, Loebenstein, Lawson Roger H, and Brunt A. A, eds. Virus and virus-like diseases of bulb and flower crops. Chichester: John Wiley & Sons, 1995.

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Frank and Bobbie Fenner Conference on Medical Research. (1st 1988 John Curtin School of Medical Research). Immunology of virus diseases. [Canberra]: John Curtin School of Medical Research, 1989.

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Jornadas Internacionales De iusticia et iure en el Siglo de Oro (5th 2010 Buenos Aires, Argentina). Ius et virtus en el Siglo de Oro. Edited by Corso de Estrada, Laura E. and Zorroza Idoya. Pamplona: Eunsa, 2011.

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Matthews, R. E. F. 1921-, ed. Diagnosis of plant virus diseases. Boca Raton: CRC Press, 1993.

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Sreenivasulu, P. Physiology of virus infected plants. New Delhi: South Asian Publishers, 1989.

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Society for General Microbiology. Symposium. Molecular basis of virus disease. Cambridge [Cambridgeshire]: Published for the Society of General Microbiology [by] Cambridge University Press, 1987.

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Book chapters on the topic "Orf virus"

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Venkatesan, Gnanavel, Amit Kumar, V. Bhanuprakash, V. Balamurugan, and Raj Kumar Singh. "Capripoxvirus and Orf Virus." In Livestock Diseases and Management, 203–21. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-2651-0_9.

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Rziha, Hanns-Joachim, Jörg Rohde, and Ralf Amann. "Generation and Selection of Orf Virus (ORFV) Recombinants." In Methods in Molecular Biology, 177–200. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3008-1_12.

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Weber, Olaf, Percy Knolle, and Hans-Dieter Volk. "Immunomodulation by inactivated Orf virus (ORFV) - therapeutic potential." In Poxviruses, 297–310. Basel: Birkhäuser Basel, 2007. http://dx.doi.org/10.1007/978-3-7643-7557-7_14.

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Fleming, Stephen B., David M. Haig, Peter Nettleton, Hugh W. Reid, Catherine A. McCaughan, Lyn M. Wise, and Andrew A. Mercer. "Sequence and Functional Analysis of a Homolog of Interleukin-10 Encoded by the Parapoxvirus Orf Virus." In Molecular Evolution of Viruses — Past and Present, 85–95. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-1707-8_8.

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Czerny, Claus-Peter, Michaela Alex, Jana Pricelius, and Christiane Zeller-Lue. "Development of Quantitative PCR Tests for the Detection of the Orthopox Virus Adsorption Protein Gene (ORF D8L) on the LightCycler." In Rapid Cycle Real-Time PCR, 371–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-59524-0_40.

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Stedman, Kenneth Mark. "Virus." In Encyclopedia of Astrobiology, 1745–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-11274-4_1660.

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Stedman, Kenneth Mark. "Virus." In Encyclopedia of Astrobiology, 2605–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-44185-5_1660.

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Stedman, Kenneth Mark. "Virus." In Encyclopedia of Astrobiology, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27833-4_1660-3.

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Nahler, Gerhard. "virus." In Dictionary of Pharmaceutical Medicine, 189. Vienna: Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-89836-9_1448.

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Gooch, Jan W. "Virus." In Encyclopedic Dictionary of Polymers, 932. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_15102.

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Conference papers on the topic "Orf virus"

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Mueller, Melanie, Ralf Amann, Thomas Feger, and Hans-Georg Rammensee. "Abstract A170: The mode of action of Orf virus – a novel viral vector for therapeutic cancer vaccines." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-a170.

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Ma, Rong-Rong, Yin-Geng Wang, Mei-Jie Liao, Xian-Le Yang, Zheng Zhang, Xiao-Jun Rong, and Bin Li. "Diagnosis and ORF gene sequencing analysis of the nervous necrosis virus (NNV) isolated from cultured pearl gentian grouper, Epinephelus lanceolatus × Epinephelus fuscoguttatus, in China." In 2014 7th International Conference on Biomedical Engineering and Informatics (BMEI). IEEE, 2014. http://dx.doi.org/10.1109/bmei.2014.7002884.

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Stoicescu, Ramona, Razvan-Alexandru Stoicescu, Codrin Gheorghe, Adina Honcea, and Iulian Bratu. "CONSIDERATIONS ON SARS-COV-2 DIAGNOSIS IN THE LABORATORY OF UNIVERSITY EMERGENCY CLINICAL HOSPITAL OF CONSTANTA." In GEOLINKS Conference Proceedings. Saima Consult Ltd, 2021. http://dx.doi.org/10.32008/geolinks2021/b1/v3/07.

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Coronaviruses are members of the Coronaviridae family. They are enveloped, non-segmented, positive-sense, single-stranded RNA viruses. Their genome size is about 30 kilobases (kb) which consist, at the 5’ end, of non-structural open reading frames (ORFs: ORF1a, ORF 1b) which code for 16 non structural proteins, and at the 3’ end the genes which code for four structural proteins including membrane (M), envelope (E), spike (S), and nucleocapsid (N) proteins. Due to the rapid spread of COVID-19, a reliable detection method is needed for patient diagnosis especially in the early stages of the disease. WHO has recommended nucleic acid amplification tests such as real-time reverse transcription-polymerase chain reaction (RT-PCR). The assay detects three SARS-CoV-2 RNA targets: the envelope (E) gene, the nucleocapsid (N) gene and a region of the open reading frame (ORF1) of the RNA-dependent RNA polymerase (RdRp) gene from SARS-CoV-2 virus isolate Wuhan-Hu-1. Our study was made in the first 3 months of the year 2021 using the real-time RT PCR results obtained in the Cellular Biology ward of the University Emergency Clinical Hospital. In our lab we are testing the inpatients from the hospital wards (Neurology, Pediatrics, Surgery, Internal medicine, ICU, Cardiology, etc.); we are also testing the outpatients from Dialysis and Oncology, 2 days prior to their therapy; we also test the health care personnel. The number of tests we performed was: in January 1456, with 399 positive results (27.4%), 33 deaths; in February 1273 tests, 221 positive (17.36%), 16 deaths; in March 1471 tests, 373 positive (25.36%), 37 deceased.
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Nogueira, Raniery Augusto dos Santos Beserra, Ana Beatriz Silva Barbosa, Francisco Das Chagas Diassis Jácome Valentim, Sâmya Pires Batista De Azevêdo, and Jamile Rodrigues Cosme De Holanda. "MECANISMOS DE MANUTENÇÃO DA LATÊNCIA DO VÍRUS VARICELA ZÓSTER: UMA ADAPTAÇÃO NECESSÁRIA." In I Congresso Nacional de Microbiologia Clínica On-Line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1182.

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Introdução: O Vírus Varicela Zóster pertence à subfamília α-herpesviridae e é um DNA-vírus de fita dupla, possuindo 68 Fases de Leitura Aberta (ORF) únicas. Sendo responsável por varicela, em um primeiro contato, o vírus mantém-se latente por um longo período em gânglios das raízes dorsais e de nervos cranianos, disseminando-se por essas estruturas após décadas, quando reativado, configurando Herpes Zóster, cujas complicações prejudicam a qualidade de vida dos pacientes. Posteriormente à infecção primária, o vírus classifica-se como neurotrópico e seus meios de sobrevida em neurônios, ainda não são claros. Objetivo: Este estudo busca elucidar os mecanismos de latência desse patógeno, visando ao desenvolvimento do conhecimento científico no assunto. Material e Métodos: Utilizando-se da plataforma online PubMed, foram pesquisados os descritores “varicella zoster virus”, em adição a “apoptosis”, e “herpes zoster infection”, com o operador booleano “AND” tendo como filtro a delimitação temporal entre 01/01/2018 e 01/05/2021. Resultados: Ao longo do período de latência, o DNA viral é encontrado em células neuronais, estando em forma não-integrada (cita-se epissoma infinito ou comprimento concateméro) e sua transcrição é fortemente restrita. Em meio ao genoma viral, o ORF63 mostrou-se de grande relevância na proteção de neuronal em humanos. Durante monitorização, foi-se percebido a migração da proteína OFR63 quando se induz apoptose na célula, tornando-se mais citoplasmática. A partir disso, percebeu-se interação inibitória entre a proteína ORF63 e a estaurosporina, molécula indutora da apoptose. O que até então se mostrava como hipótese, foi melhor embasado pela redução dos níveis de caspase-3, marcador apoptótico celular, em neurônios infectados pelo VVZ quando comparados a outras células (infectadas ou não). Conclusão: Diante de todas as questões, ainda cientificamente obscuras, acerca da capacidade desse vírus de sobreviver durante décadas nos gânglios nervosos, ressalta-se a necessidade de mais pesquisas na área, para que se tenha melhor manejo de pacientes infectados com o Vírus Varicela Zóster. Ademais, não se pode negar que a inibição da apoptose é uma evolução adaptativa muito favorável ao microrganismo, já que as células neuronais são hospedeiras senescentes e seu aumento de vida significa aumento de vida do patógeno.
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Pack, Daniel W. "Hybrid Virus/Polymer and Virus/Lipid Gene Delivery Vectors." In 14th Asia Pacific Confederation of Chemical Engineering Congress. Singapore: Research Publishing Services, 2012. http://dx.doi.org/10.3850/978-981-07-1445-1_775.

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Statsi, M., and Y. Melnikova. "THE DEPENDENCE ON GENDER OF THE INCIDENCE OF FELINE VIRAL IMMUNODEFICIENCY AND FELINE VIRAL LEUKEMIA." In SAKHAROV READINGS 2022: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2022. http://dx.doi.org/10.46646/sakh-2022-2-91-93.

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The prevalence of feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV) in the populations of domestic and homeless cats has been analyzed. The effectiveness of diagnostic methods used for the detection of feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV) has been studied. It was found that the level of prevalence of viral diseases of cats, such as the immunodeficiency virus and the leukemia virus, depends on the lifestyle, gender, and health status of cats; the diagnosis of the immunodeficiency virus and the leukemia virus depends on the economic situation of the country and the commercial availability of test systems; Widespread vaccination has proven its effectiveness and the possibility of limiting the risks of infection. PCR is the gold standard in the diagnosis of viral diseases, but it is an expensive method.
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JOHNSON, JOHN E. "VIRUS ASSEMBLY AND MATURATION." In Folding and Self-Assembly of Biological Macromolecules Conference. WORLD SCIENTIFIC, 2004. http://dx.doi.org/10.1142/9789812703057_0013.

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Yusifova, K. Yu. "INDICATION OF RABIES VIRUS BY CYTOPATHOGENIC BIRD POISX VIRUS IN CELLULAR SYSTEMS." In DIGEST OF ARTICLES ALL-RUSSIAN (NATIONAL) SCIENTIFIC AND PRACTICAL CONFERENCE "CURRENT ISSUES OF VETERINARY MEDICINE: EDUCATION, SCIENCE, PRACTICE", DEDICATED TO THE 190TH ANNIVERSARY FROM THE BIRTH OF A.P. Stepanova. Publishing house of RGAU - MSHA, 2021. http://dx.doi.org/10.26897/978-5-9675-1853-9-2021-61.

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The study was carried out on the cell systems of Japanese quail embryos and chicken fibroblasts infected with smallpox and rabies viruses. Interfering activity between these viruses was observed in the work. The possibility of using avian pox virus as an indicator in chronic infections has been revealed.
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Gür, A., M. Karakoç, MF Geyik, K. Nas, R. Çevik, AJ Saraç, S. Em, and F. Erdogan. "SAT0135 Association between hepatitis c virus antibody, hepatitis b virus antigen and fibromiyalgia." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.594.

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Huff, Monica L., Erin Hamilton-Spence, Karen Shattuck, Nadezda Yun, Amy Vickers, and Slobodan Paessler. "Elimination of Ebola Virus and Marburg Virus in human Milk Through Holder Pasteurization." In Selection of Abstracts From NCE 2016. American Academy of Pediatrics, 2018. http://dx.doi.org/10.1542/peds.141.1_meetingabstract.288.

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Reports on the topic "Orf virus"

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Gafny, Ron, A. L. N. Rao, and Edna Tanne. Etiology of the Rugose Wood Disease of Grapevine and Molecular Study of the Associated Trichoviruses. United States Department of Agriculture, September 2000. http://dx.doi.org/10.32747/2000.7575269.bard.

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Rugose wood is a complex disease of grapevines, characterized by modification of the woody cylinder of affected vines. The control of rugose wood is based on the production of healthy propagation material. Detection of rugose wood in grapevines is difficult and expensive: budwood from tested plants is grafted onto sensitive Vitis indicators and the appearance of symptoms is monitored for 3 years. The etiology of rugose wood is complex and has not yet been elucidated. Several elongated clostero-like viruses are consistently found in affected vines; one of them, grapevine virus A (GVA), is closely associated with Kober stem grooving, a component of the rugose wood complex. GVA has a single-stranded RNA genome of 7349 nucleotides, excluding a polyA tail at the 3' terminus. The GVA genome includes five open reading frames (ORFs 1-5). ORF 4, which encodes for the coat protein of GVA, is the only ORF for which the function was determined experimentally. The original objectives of this research were: 1- To produce antisera to the structural and non-structural proteins of GVA and GVB and to use these antibodies to establish an effective detection method. 2- Develop full length infectious cDNA clones of GVA and GVB. 3- Study the roll of GVA and GVB in the etiology of the grapevine rugose wood disease. 4- Determine the function of Trichovirus (now called Vitivirus) encoded genes in the virus life cycle. Each of the ORFs 2, 3, 4 and 5 genes of GVA were cloned and expressed in E. coli and used to produce antisera. Both the CP (ORF 4) and the putative MP (ORF 3) were detected with their corresponding antisera in-GVA infected N. benthamiana and grapevine. The MP was first detected at an early stage of the infection, 6-12 h after inoculation, and the CP 2-3 days after inoculation. The MP could be detected in GVA-infected grapevines that tested negative for CP, both with CP antiserum and with a commercially available ELISA kit. Antisera to ORF 2 and 5 encoded proteins could react with the recombinant proteins but failed to detect both proteins in GVA infected plants. A full-length cDNA clone of grapevine virus A (GVA) was constructed downstream from the bacteriophage T7 RNA polymerase promoter. Capped in vitro transcribed RNA was infectious in N. benthamiana and N. clevelandii plants. Symptoms induced by the RNA transcripts or by the parental virus were indistinguishable. The infectivity of the in vitro-transcribed RNA was confirmed by serological detection of the virus coat and movement proteins and by observation of virions by electron microscopy. The full-length clone was modified to include a gus reporter gene and gus activity was detected in inoculated and systemic leaves of infected plants. Studies of GVA mutants suggests that the coat protein (ORF 4) is essential for cell to cell movement, the putative movement protein (ORF 3) indeed functions as a movement protein and that ORF 2 is not required for virus replication, cell to cell or systemic movement. Attempts to infect grapevines by in-vitro transcripts, by inoculation of cDNA construct in which the virus is derived by the CaMV 35S promoter or by approach grafting with infected N. benthamiana, have so far failed. Studies of the subcellular distribution of GFP fusion with each of ORF 2, 3 and 4 encoded protein showed that the CP fusion protein accumulated as a soluble cytoplasmatic protein. The ORF 2 fusion protein accumulated in cytoplasmatic aggregates. The MP-GFP fusion protein accumulated in a large number of small aggregates in the cytoplasm and could not move from cell to cell. However, in conditions that allowed movement of the fusion protein from cell to cell (expression by a PVX vector or in young immature leaves) the protein did not form cytoplasmatic aggregates but accumulated in the plasmodesmata.
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Mawassi, Munir, Adib Rowhani, Deborah A. Golino, Avichai Perl, and Edna Tanne. Rugose Wood Disease of Grapevine, Etiology and Virus Resistance in Transgenic Vines. United States Department of Agriculture, November 2003. http://dx.doi.org/10.32747/2003.7586477.bard.

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Rugose wood is a complex disease of grapevines, which occurs in all growing areas. The disease is spread in the field by vector transmission (mealybugs). At least five elongated-phloem- limited viruses are implicated in the various rugose wood disorders. The most fully characterized of these are Grapevine virus A (GV A) and GVB, members of a newly established genus, the vitivirus. GVC, a putative vitivirus, is much less well characterized than GV A or GVB. The information regarding the role of GVC in the etiology and epidemiology of rugose wood is fragmentary and no sequence data for GVC are available. The proposed research is aimed to study the etiology and epidemiology of rugose wood disease, and to construct genetically engineered virus-resistant grapevines. The objectives of our proposed research were to construct transgenic plants with coat protein gene sequences designed to induce post-transcriptional gene silencing (pTGS); to study the epidemiology and etiology of rugose wood disease by cloning and sequencing of GVC; and surveying of rugose wood- associated viruses in Californian and Israeli vineyards. In an attempt to experimentally define the role of the various genes of GV A, we utilized the infectious clone, inserted mutations in every ORF, and studied the effect on viral replication, gene expression, symptoms and viral movement. We explored the production of viral RNAs in a GV A-infected Nicotiana benthamiana herbaceous host, and characterized one nested set of three 5'-terminal sgRNAs of 5.1, 5.5 and 6.0 kb, and another, of three 3'-terminal sgRNAs of 2.2, 1.8 and 1.0 kb that could serve for expression of ORFs 2-3, respectively. Several GV A constructs have been assembled into pCAMBIA 230 I, a binary vector which is used for Angrobacterium mediated transformation: GV A CP gene; two copies of the GV A CP gene arranged in the same antisense orientation; two copies of the GV A CP gene in which the downstream copy is in an antigens orientation; GV A replicase gene; GV A replicase gene plus the 3' UTR sequence; and the full genome of GV A. Experiments for transformation of N. benthamiana and grapevine cell suspension with these constructs have been initiated. Transgenic N. benthamiana plants that contained the CP gene, the replicase gene and the entire genome of GV A were obtained. For grapevine transformation, we have developed efficient protocols for transformation and successfully grapevine plantlets that contained the CP gene and the replicase genes of GV A were obtained. These plants are still under examination for expression of the trans genes. The construction of transgenic plants with GV A sequences will provide, in the long run, a means to control one of the most prevalent viruses associated with grapevines. Our many attempts to produce a cDNA library from the genome of GVC failed. For surveying of rugose wood associated viruses in California vineyards, samples were collected from different grape growing areas and tested by RT-PCR for GV A, GVB and GVD. The results indicated that some of the samples were infected with multiple viruses, but overall, we found higher incidence of GVB and GV A infection in California vineyards and new introduction varieties, respectively. In this research we also conducted studies to increase our understanding of virus - induced rootstock decline and its importance in vineyard productivity. Our results provided supporting evidence that the rootstock response to virus infection depends on the rootstock genotype and the virus type. In general, rootstocks are differ widely in virus susceptibility. Our data indicated that a virus type or its combination with other viruses was responsible in virus-induced rootstock decline. As the results showed, the growth of the rootstocks were severely affected when the combination of more than one virus was present.
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Dawson, William O., and Moshe Bar-Joseph. Creating an Ally from an Adversary: Genetic Manipulation of Citrus Tristeza. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7586540.bard.

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Citrus is one of the major agricultural crops common to Israel and the United States, important in terms of nutrition, foreign exchange, and employment. The economy of both citrus industries have been chronically plagued by diseases caused by Citrus tristeza virus (CTV). The short term solution until virus-resistant plants can be used is the use of mild strain cross-protection. We are custom designing "ideal" protecting viruses to immunize trees against severe isolates of CTV by purposely inoculating existing endangered trees and new plantings to be propagated as infected (protected) citrus budwood. We crossed the substantial technological hurdles necessary to accomplish this task which included developing an infectious cDNA clone which allows in vitro manipulation of the virus and methods to then infect citrus plants. We created a series of hybrids between decline-inducing and mild CTV strains, tested them in protoplasts, and are amplifying them to inoculate citrus trees for evaluation and mapping of disease determinants. We also extended this developed technology to begin engineering transient expression vectors based on CTV as tools for genetic improvement of tree crops, in this case citrus. Because of the long periods between genetic transformation and the ultimate assay of mature tree characteristics, there is a great need for an effective system that allows the expression or suppression of target genes in fruiting plants. Virus-based vectors will greatly expedite progress in citrus genetic improvement. We characterized several components of the virus that provides necessary information for designing virus-based vectors. We characterized the requirements of the 3 ’-nontranslated replication promoter and two 3 ’-ORF subgenomic (sg) mRNA controller elements. We discovered a novel type of 5’-terminal sgRNAs and characterized the cis-acting control element that also functions as a strong promoter of a 3 ’-sgRNA. We showed that the p23 gene controls negative-stranded RNA synthesis and expression of 3 ’ genes. We identified which genes are required for infection of plants, which are host range determinants, and which are not needed for plant infection. We continued the characterization of native dRNA populations and showed the presence of five different classes including class III dRNAs that consists of infectious and self-replicating molecules and class V dRNAs that contain all of the 3 ’ ORFs, along with class IV dRNAs that retain non-contiguous internal sequences. We have constructed and tested in protoplasts a series of expression vectors that will be described in this proposal.
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Palukaitis, Peter, Amit Gal-On, Milton Zaitlin, and Victor Gaba. Virus Synergy in Transgenic Plants. United States Department of Agriculture, March 2000. http://dx.doi.org/10.32747/2000.7573074.bard.

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Transgenic plants expressing viral genes offer novel means of engendering resistance to those viruses. However, some viruses interact synergistically with other viruses and it is now known that transgenic plants expressing particular genes of one virus may also mediate synergy with a second virus. Thus, our specific objectives were to (1) determine if transgenic plants resistant to one virus showed synergy with another virus; (2) determine what viral sequences were essential for synergy; and (3) determine whether one of more mechanisms were involved i synergy. This project would also enable an evaluation of the risks of synergism associated with the use of such transgenic plants. The conclusion deriving from this project are as follows: - There is more than one mechanism of synergy. - The CMV 2b gene is required for synergistic interactions. - Synergy between a potyvirus and CMV can break natural resistance limiting CMV movement. - Synergy operates at two levels - increase in virus accumulation and increase in pathology - independently of each other. - Various sequences of CMV can interact with the host to alter pathogenicity and affect virus accumulation. - The effect of synergy on CMV satellite RNA accumulatio varies in different systems. - The HC-Pro gene may only function in host plant species to induce synergy. - The HC-Pro is a host range determinant of potyviruses. - Transgenic plants expressing some viral sequences showed synergy with one or more viruses. Transgenic plants expressing CMV RNA 1, PVY NIb and the TMV 30K gene all showed synergy with at least one unrelated virus. - Transgenic plants expressing some viral sequences showed interference with the infection of unrelated viruses. Transgenic plants expressing the TMV 30K, 54K and 126K genes, the PVY NIb gene, or the CMV 3a gene all showed some level of interference with the accumulation (and in some cases the pathology) of unrelated viruses. From our observations, there are agricultural implications to the above conclusions. It is apparent that before they are released commercially, transgenic plants expressing viral sequences for resistance to one virus need to be evaluated fro two properties: - Synergism to unrelated viruses that infect the same plant. Most of these evaluations can be made in the greenhouse, and many can be predicted from the known literature of viruses known to interact with each other. In other cases, where transgenic plants are being generated from new plant species, the main corresponding viruses from the same known interacting genera (e.g., potexviruses and cucumoviruses, potyviruses and cucumoviruses, tobamoviruses and potexviruses, etc.) should be evaluated. - Inhibition or enhancement of other resistance genes. Although it is unlikely that plants to be released would be transformed with HC-Pro or 2b genes, there may be other viral genes that can affect the expression of plant genes encoding resistance to other pathogens. Therefore, transgenic plants expressing viral genes to engender pathogen-derived resistance should be evaluated against a spectrum of other pathogens, to determine whether those resistance activities are still present, have been lost, or have been enhanced!
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Wick, Charles H., and Patrick E. McCubbin. Recovery of Virus Samples from Various Surfaces with the Integrated Virus Detection System. Fort Belvoir, VA: Defense Technical Information Center, June 2010. http://dx.doi.org/10.21236/ada523314.

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Longnecker, Richard M. Epstein-Barr Virus: A Role for a Tumorigenic Virus in the Etiology of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada400450.

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Lan, Xi, John C. F. Hsieh, Haibo Liu, Susan J. Lamont, and Qing Zhu. Integration of Host and Virus Gene Expression for Chickens Response to Avian Leukosis Virus Challenge. Ames (Iowa): Iowa State University, January 2018. http://dx.doi.org/10.31274/ans_air-180814-388.

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Martuza, Robert L. Herpes Virus Therapy of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada402401.

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Martuza, Robert L. Herpes Virus Therapy of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada410713.

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Martuza, Robert L. Herpes Virus Therapy of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada418644.

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