Academic literature on the topic 'Capsid coding region'

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Journal articles on the topic "Capsid coding region"

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Chinsangaram, Jarasvech, Clayton Beard, Peter W. Mason, Marla K. Zellner, Gordon Ward, and Marvin J. Grubman. "Antibody Response in Mice Inoculated with DNA Expressing Foot-and-Mouth Disease Virus Capsid Proteins." Journal of Virology 72, no. 5 (May 1, 1998): 4454–57. http://dx.doi.org/10.1128/jvi.72.5.4454-4457.1998.

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ABSTRACT Candidate foot-and-mouth disease (FMD) DNA vaccines designed to produce viral capsids lacking infectious viral nucleic acid were evaluated. Plasmid DNAs containing a portion of the FMDV genome coding for the capsid precursor protein (P1-2A) and wild-type or mutant viral proteinase 3C (plasmids P12X3C or P12X3C-mut, respectively) were constructed. Cell-free translation reactions programmed with pP12X3C (wild-type 3C) and pP12X3C-mut produced a capsid precursor, but only the reactions programmed with the plasmid encoding the functional proteinase resulted in P1-2A processing and capsid formation. Baby hamster kidney (BHK) cells also produced viral capsid proteins when transfected with these plasmids. Plasmid P12X3C was administered to mice by intramuscular, intradermal, and epithelial (gene gun) inoculations. Anti-FMD virus (FMDV) antibodies were detected by radioimmunoprecipitation (RIP) and plaque reduction neutralization assays only in sera of mice inoculated by using a gene gun. When pP12X3C and pP12X3C-mut were inoculated into mice by using a gene gun, both plasmids elicited an antibody response detectable by RIP but only pP12X3C elicited a neutralizing antibody response. These results suggest that capsid formation in situ is required for effective immunization. Expression and stimulation of an immune response was enhanced by addition of an intron sequence upstream of the coding region, while addition of the FMDV internal ribosome entry site or leader proteinase (L) coding region either had no effect or reduced the immune response.
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Jia, Xi-Yu, Marc Van Eden, Marc G. Busch, Ellie Ehrenfeld, and Donald F. Summers. "trans-Encapsidation of a Poliovirus Replicon by Different Picornavirus Capsid Proteins." Journal of Virology 72, no. 10 (October 1, 1998): 7972–77. http://dx.doi.org/10.1128/jvi.72.10.7972-7977.1998.

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ABSTRACT A trans-encapsidation assay was established to study the specificity of picornavirus RNA encapsidation. A poliovirus replicon with the luciferase gene replacing the capsid protein-coding region was coexpressed in transfected HeLa cells with capsid proteins from homologous or heterologous virus. Successfultrans-encapsidation resulted in assembly and production of virions whose replication, upon subsequent infection of HeLa cells, was accompanied by expression of luciferase activity. The amount of luciferase activity was proportional to the amount oftrans-encapsidated virus produced from the cotransfection. When poliovirus capsid proteins were supplied in trans, >2 × 106 infectious particles/ml were produced. When coxsackievirus B3, human rhinovirus 14, mengovirus, or hepatitis A virus (HAV) capsid proteins were supplied in trans, all but HAV showed some encapsidation of the replicon. The overall encapsidation efficiency of the replicon RNA by heterologous capsid proteins was significantly lower than when poliovirus capsid was used.trans-encapsidated particles could be completely neutralized with specific antisera against each of the donor virus capsids. The results indicate that encapsidation is regulated by specific viral nucleic acid and protein sequences.
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Bouslama, Lamjed, Dorsaf Nasri, Lionel Chollet, Khaoula Belguith, Thomas Bourlet, Mahjoub Aouni, Bruno Pozzetto, and Sylvie Pillet. "Natural Recombination Event within the Capsid Genomic Region Leading to a Chimeric Strain of Human Enterovirus B." Journal of Virology 81, no. 17 (May 30, 2007): 8944–52. http://dx.doi.org/10.1128/jvi.00180-07.

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ABSTRACT Recombination between two strains is a known phenomenon for enteroviruses replicating within a single cell. We describe a recombinant strain recovered from human stools, typed as coxsackievirus B4 (CV-B4) and CV-B3 after partial sequencing of the VP1 and VP2 coding regions, respectively. The strain was neutralized by a polyclonal CV-B3-specific antiserum but not by a CV-B4-specific antiserum. The nucleotide sequence analysis of the whole structural genomic region showed the occurrence of a recombination event at position 1950 within the VP3 capsid gene, in a region coding for the 2b antigenic site previously described for CV-B3. This observation evidences for the first time the occurrence of an interserotypic recombination within the VP2-VP3-VP1 capsid region between two nonpoliovirus enterovirus strains. The neutralization pattern suggests that the major antigenic site is located within the VP2 protein.
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Déjardin, Jérôme, Guillaume Bompard-Maréchal, Muriel Audit, Thomas J. Hope, Marc Sitbon, and Marylène Mougel. "A Novel Subgenomic Murine Leukemia Virus RNA Transcript Results from Alternative Splicing." Journal of Virology 74, no. 8 (April 15, 2000): 3709–14. http://dx.doi.org/10.1128/jvi.74.8.3709-3714.2000.

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ABSTRACT Here we show the existence of a novel subgenomic 4.4-kb RNA in cells infected with the prototypic replication-competent Friend or Moloney murine leukemia viruses (MuLV). This RNA derives by splicing from an alternative donor site (SD′) within the capsid-coding region to the canonical envelope splice acceptor site. The position and the sequence of SD′ was highly conserved among mammalian type C and D oncoviruses. Point mutations used to inactivate SD′ without changing the capsid-coding ability affected viral RNA splicing and reduced viral replication in infected cells.
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Sasaki, Jun, and Nobuhiko Nakashima. "Translation Initiation at the CUU Codon Is Mediated by the Internal Ribosome Entry Site of an Insect Picorna-Like Virus In Vitro." Journal of Virology 73, no. 2 (February 1, 1999): 1219–26. http://dx.doi.org/10.1128/jvi.73.2.1219-1226.1999.

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ABSTRACT AUG-unrelated translation initiation was found in an insect picorna-like virus, Plautia stali intestine virus (PSIV). The positive-strand RNA genome of the virus contains two nonoverlapping open reading frames (ORFs). The capsid protein gene is located in the 3′-proximal ORF and lacks an AUG initiation codon. We examined the translation mechanism and the initiation codon of the capsid protein gene by using various dicistronic and monocistronic RNAs in vitro. The capsid protein gene was translated cap independently in the presence of the upstream cistron, indicating that the gene is translated by internal ribosome entry. Deletion analysis showed that the internal ribosome entry site (IRES) consisted of approximately 250 bases and that its 3′ boundary extended slightly into the capsid-coding region. The initiation codon for the IRES-mediated translation was identified as the CUU codon, which is located just upstream of the 5′ terminus of the capsid-coding region by site-directed mutagenesis. In vitro translation assays of monocistronic RNAs lacking the 5′ part of the IRES showed that this CUU codon was not recognized by scanning ribosomes. This suggests that the PSIV IRES can effectively direct translation initiation without stable codon-anticodon pairing between the initiation codon and the initiator methionyl-tRNA.
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Dahourou, George, Sophie Guillot, Olivier Le Gall, and Radu Crainic. "Genetic recombination in wild-type poliovirus." Journal of General Virology 83, no. 12 (December 1, 2002): 3103–10. http://dx.doi.org/10.1099/0022-1317-83-12-3103.

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Poliovirus isolates were screened for recombinants by combined analysis of two distant polymorphic segments of the poliovirus genome (one in the capsid and the other in the polymerase-coding region). Using a restriction fragment length polymorphism (RFLP) assay, a high number of recombinant genomes was found among vaccine-derived strains excreted by poliovirus vaccine vaccinees or vaccine-associated paralytic poliomyelitis cases. Some of these subjects carried a wild-type poliovirus (non-vaccine-specific) nucleotide sequence in the 3′ part of the genome. Using a similar approach, a collection of wild-type poliovirus strains isolated in South India between 1985 and 1993 was screened for recombinants. Genotypes were defined by the parallel application of RFLP assays and genomic sequencing of the capsid protein VP1 and the 3D polymerase polypeptide. Analyses revealed several instances where the position of an isolate on the phylogenic tree for the capsid protein-coding segment did not agree with its position on the tree for the polymerase-coding region. In this way, several wild-type/wild-type and wild-type/vaccine recombinants could be identified, indicating that recombination is encountered commonly in the natural evolution of poliovirus strains.
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Savolainen, Carita, Pia Laine, Mick N. Mulders, and Tapani Hovi. "Sequence analysis of human rhinoviruses in the RNA-dependent RNA polymerase coding region reveals large within-species variation." Journal of General Virology 85, no. 8 (August 1, 2004): 2271–77. http://dx.doi.org/10.1099/vir.0.79897-0.

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Human rhinoviruses (HRVs; family Picornaviridae), the most frequent causative agents of respiratory infections, comprise more than 100 distinct serotypes. According to previous phylogenetic analysis of the VP4/VP2-coding sequences, all but one of the HRV prototype strains distribute between the two established species, Human rhinovirus A (HRV-A) and Human rhinovirus B (HRV-B). Here, partial sequences of the RNA-dependent RNA polymerase (3D polymerase)-coding gene of 48 HRV prototype strains and 12 field isolates were analysed. The designated division of the HRV strains into the species HRV-A and HRV-B was also seen in the 3D-coding region. Phylogenetically, HRV-B clustered closer to human enterovirus (HEV) species HEV-B, HEV-C and poliovirus than to HRV-A. Intraspecies variation within both HRV-A and HRV-B was greater in the 3D-coding region than in the VP4/VP2-coding region, with the difference maxima reaching 48 % at the nucleotide level and 36 % at the amino acid level in HRV-A and 53 and 35 %, respectively, in HRV-B. Within both species, a few strains formed a separate cluster differing from the majority of strains as much as HEV-B from HEV-C. Furthermore, the tree topology within HRV-A differed from that for VP4/VP2, suggesting possible recombination events in the evolutionary history of the strains. However, all 12 field isolates clustered similarly, as in the capsid region. These results showed that the within-species variation in the 3D region is greater in HRV than in HEV. Furthermore, HRV variation in the 3D region exceeds that in the capsid-coding region.
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Harvala, Heli, Hannu Kalimo, Leif Dahllund, Juhana Santti, Pamela Hughes, Timo Hyypiä, and Glyn Stanway. "Mapping of tissue tropism determinants in coxsackievirus genomes." Journal of General Virology 83, no. 7 (July 1, 2002): 1697–706. http://dx.doi.org/10.1099/0022-1317-83-7-1697.

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Genomic regions responsible for the different tissue tropisms of coxsackievirus A9 (CAV9) and coxsackievirus B3 (CBV3) in newborn mice were investigated using recombinant viruses. Infectious cDNA clones of CAV9, a virus known to infect striated muscle, and CBV3, affecting the central nervous system, pancreas, liver, brown fat and striated muscle, were used to generate chimeric viruses. In situ hybridization analysis of different tissues from mice infected with the recombinant viruses, constructed by exchanging the 5′ non-coding region (5′NCR), structural and non-structural genes, demonstrated that the pancreo- and liver tropism map predominantly to CBV3 sequences within the capsid genes, evidently due to receptor recognition. Although the major neurotropism determinant in the CBV3 genome was in the capsid region, viruses containing the CAV9 capsid were also able to initiate infection in the central nervous system provided they contained the CBV3 5′NCR. The presence of the 5′NCR of CAV9 clearly enhanced muscle tissue tropism.
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Shibuya, Norihiro, Takashi Nishiyama, Yasushi Kanamori, Hitoshi Saito, and Nobuhiko Nakashima. "Conditional Rather than Absolute Requirements of the Capsid Coding Sequence for Initiation of Methionine-Independent Translation in Plautia stali Intestine Virus." Journal of Virology 77, no. 22 (November 15, 2003): 12002–10. http://dx.doi.org/10.1128/jvi.77.22.12002-12010.2003.

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ABSTRACT The positive-stranded RNA genome of Plautia stali intestine virus (PSIV) has an internal ribosome entry site (IRES) in an intergenic region (IGR). The IGR-IRES of PSIV initiates translation of the capsid protein by using CAA, the codon for glutamine. It was previously reported (J. Sasaki and N. Nakashima, J. Virol. 73:1219-1226, 1999) that IGR-IRES extended by several nucleotides into the capsid open reading frame (ORF). Despite the fact that the secondary structure model of the IGR-IRES is highly conserved, we were unable to find structural similarities in the 5′ region of the capsid ORFs in related viruses. Therefore, we reevaluated the role of the capsid ORF in IGR-IRES-mediated translation in PSIV. Mutation of the CAA codon with various triplets did not inhibit IGR-IRES-mediated translation. N-terminal amino acid analyses of mutated products showed that the IGR-IRES could initiate translation by using various elongator tRNAs. By replacement of the capsid ORF with exogenous coding sequences having AUG deleted, translation products were produced in most cases, but capsid-exogenous fusion proteins were produced more efficiently than were the translation products. These data indicate that the 5′ part of the capsid ORF is not an absolute requirement for the IGR-IRES-mediated translation. RNA structure probing analyses showed that the 5′ part of the capsid ORF was a single strand, while that of exogenous reading frames was structured. Exogenous sequences also caused structural distortion in the 3′ part of the IGR-IRES. We hypothesize that the single-stranded capsid ORF helps to form the tertiary structure of the IGR-IRES and facilitates precise positioning of ribosomes.
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Audit, Muriel, Jérôme Déjardin, Barbara Hohl, Christine Sidobre, Thomas J. Hope, Marylène Mougel, and Marc Sitbon. "Introduction of a cis-Acting Mutation in the Capsid-Coding Gene of Moloney Murine Leukemia Virus Extends Its Leukemogenic Properties." Journal of Virology 73, no. 12 (December 1, 1999): 10472–79. http://dx.doi.org/10.1128/jvi.73.12.10472-10479.1999.

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ABSTRACT Inoculation of newborn mice with the retrovirus Moloney murine leukemia virus (MuLV) results in the exclusive development of T lymphomas with gross thymic enlargement. The T-cell leukemogenic property of Moloney MuLV has been mapped to the U3 enhancer region of the viral promoter. However, we now describe a mutant Moloney MuLV which can induce the rapid development of a uniquely broad panel of leukemic cell types. This mutant Moloney MuLV with synonymous differences (MSD1) was obtained by introduction of nucleotide substitutions at positions 1598, 1599, and 1601 in the capsid gene which maintained the wild-type (WT) coding potential. Leukemias were observed in all MSD1-inoculated animals after a latency period that was shorter than or similar to that of WT Moloney MuLV. Importantly, though, only 56% of MSD1-induced leukemias demonstrated the characteristic thymoma phenotype observed in all WT Moloney MuLV leukemias. The remainder of MSD1-inoculated animals presented either with bona fide clonal erythroid or myelomonocytic leukemias or, alternatively, with other severe erythroid and unidentified disorders. Amplification and sequencing of U3 and capsid-coding regions showed that the inoculated parental MSD1 sequences were conserved in the leukemic spleens. This is the first report of a replication-competent MuLV lacking oncogenes which can rapidly lead to the development of such a broad range of leukemic cell types. Moreover, the ability of MSD1 to transform erythroid and myelomonocytic lineages is not due to changes in the U3 viral enhancer region but rather is the result of acis-acting effect of the capsid-coding gagsequence.
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Dissertations / Theses on the topic "Capsid coding region"

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Srinivasa, Ramya. "Flavivirus RNA replication: Probe development, structural dynamics, and role of zinc ions." Thesis, 2023. https://etd.iisc.ac.in/handle/2005/6085.

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Flaviviruses share a typical genome architecture where the highly conserved UTRs flank a central coding region. They also share a common genome replication strategy called genome cyclization where the UTRs interact to form a long-range, dynamic, 3D RNA interactome. Recent studies focused on the involvement of the capsid coding region in modulating these UTR interactions. Along similar lines, we have investigated the effect of CCR on the UTRs interactions in Dengue using ensemble FRET with cyanine dye-labeled Dengue UTRs. As a part of this study, we have developed a novel, generic chemoenzymatic, bead-based method for base-specific modification of RNA called “T7 RNA polymerase extension-based RNA modification (TERM)”. Here, we describe TERM development, demonstrate the synthesis of single, site-specific cyanine dye-labeled Dengue UTRs and discuss the UTR interaction studies performed using the TERM-synthesized cyanine dye-labeled UTRs. Our results bridge the knowledge gap in understanding the role of the capsid coding region in Flavivirus UTRs.
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Reports on the topic "Capsid coding region"

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Grubman, Marvin J., Yehuda Stram, Peter W. Mason, and Hagai Yadin. Development of an Empty Viral Capsid Vaccine against Foot and Mouth Disease. United States Department of Agriculture, August 1995. http://dx.doi.org/10.32747/1995.7570568.bard.

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Foot-and-mouth disease (FMD), a highly infectious viral disease of cloven-hoofed animals, is economically the most important disease of domestic animals. Although inactivated FMD vaccines have been succesfully used as part of comprehensive eradication programs in Western Europe, there are a number of concerns about their safety. In this proposal, we have attempted to develop a new generation of FMD vaccines that addresses these concerns. Specifically we have cloned the region of the viral genome coding for the structural proteins and the proteinase responsible for processing of the structural protein precursor into both a DNA vector and a replication-deficient human adenovirus. We have demonstrated the induction of an FMDV-specific immune response and a neutralizing antibody response with the DNA vectors in mice, but preliminary potency and efficacy studies in swine are variable. However, the adenovirus vector induces a significant and long-lived neutralizing antibody response in mice and most importantly a neutralizing and protective response in swine. These results suggest that the empty capsid approach is a potential alternative to the current vaccination strategy.
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