- Volume 78, Issue 1, 1997
Volume 78, Issue 1, 1997
- Articles
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The cleavage activities of aphthovirus and cardiovirus 2A proteins.
More LessThe primary 2A/2B polyprotein cleavage of aphtho- and cardioviruses is mediated by their 2A proteins cleaving C-terminally. Whilst the aphthovirus 2A region is only 16 aa (possibly 18 aa) long, the cardiovirus 2A protein is some 150 aa. We have previously shown that foot-and-mouth disease virus (FMDV) 2A is able to mediate cleavage in an artificial (chloramphenicol acetyltransferase/FMDV 2A/β-glucuronidase [CAT-2A-GUS]) polyprotein system devoid of any other FMDV sequences with high (~85%), although not complete, cleavage. In this paper we show that insertion of upstream FMDV capsid protein 1D sequences increases the activity. In addition, we have demonstrated that the cardiovirus Theiler’s murine encephalomyelitis virus (TME) 2A protein, when linked to GUS in a single ORF, is able to cleave at its own C terminus with high efficiency - if not completely. The C-terminal 19 aa of TME 2A, together with the N-terminal proline residue of protein 2B, were inserted into the CAT/GUS artificial polyprotein system (in a single ORF). This recombinant [CAT-ΔTME2A-GUS] polyprotein was able to mediate cleavage with high (~85%) efficiency-directly comparable to the activity observed when FMDV 2A was inserted. A similar insertion into [CAT-GUS] of the C-terminal 19 aa of the cardiovirus encephalomyocarditis virus (EMC) 2A, together with the N-terminal proline residue of protein 2B, produced a [CAT-Δ EMC2A- GUS] polyprotein which also mediated cleavage at ~85%. Analysis of the products of expression of these artificial polyproteins in a prokaryotic translation system did not, apparently, reveal any GUS cleavage product.
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Molecular characterization of virus-specific RNA produced in the brains of flavivirus-susceptible and -resistant mice after challenge with Murray Valley encephalitis virus
More LessNatural resistance to flaviviruses in mice is controlled by a single genetic locus, Flv, on chromosome 5. Although the mechanism of this resistance is not fully understood, it is believed to operate at the level of virus replication rather than the immune response. It has been hypothesized that enhanced production of viral defective interfering (DI) particles is responsible for a substantial reduction in the titres of infectious virus in resistant mice. However, this has never been established at the molecular level since such particles have not been isolated and characterized. We have studied the products of virus replication in the brains of flavivirus-susceptible C3H/HeJ (Flvs ) and -resistant congenic C3H/RV (Flvr ) mice after an intracerebral challenge (i.c.) with Murray Valley encephalitis (MVE) virus and have found no evidence for the accumulation of truncated viral RNA in the brains of resistant mice. All three major viral RNA species, the replicative intermediate (RI), replicative form (RF) and virion RNA (vRNA) together with a subgenomic RNA species of 0·6 kb, which has not been previously described, were present in the brains of both mouse strains. However, the viral RF and RI RNA forms preferentially accumulated in the brains of resistant mice. Thus, we confirm that the resistance allele Flvr interferes with discrete steps in flavivirus replication, although the precise mechanism remains to be determined.
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Characterization of monoclonal antibody-escape mutants of tick-borne encephalitis virus with reduced neuroinvasiveness in mice
More LessEscape mutants of tick-borne encephalitis (TBE) virus were selected using neutralizing monoclonal antibodies (MAbs) that react with three different and previously unrecognized epitopes in the envelope protein E of TBE virus. Two of these variants (V-IC3 and V-IE3) exhibited a significantly reduced reactivity with their selecting MAbs, as determined by ELISA, whereas with one variant (V-IO3), reactivity was completely unchanged. Comparative sequence analyses demonstrated that each of the variants differed from the wild-type virus by a single amino acid substitution located at exposed positions within domains I, II and III of protein E. In the mouse model, all three mutants were still neurovirulent but exhibited a significantly reduced neuroinvasiveness after subcutaneous inoculation. Virus replication, however, was sufficient to induce a specific antibody response. The observed alterations in virulence properties were not associated with reduced growth rates in vertebrate cell cultures, but one variant (V-IE3) exhibited a small plaque phenotype. The mutation of variant V-IO3 resulted in a temperature-sensitive phenotype and a significant elevation of the pH-threshold of the conformational change necessary for fusion activity.
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Purification and characterization of the NS3 serine protease domain of hepatitis C virus expressed in Saccharomyces cerevisiae
cDNA encoding the putative core of the hepatitis C virus NS3 serine protease domain (residues 1–181 of NS3; NS3181) was expressed as an N-terminally (His)6-tagged fusion protein in Saccharomyces cerevisiae. NS3181 protease activity was found in soluble cell lysates, and the N-terminal metal-chelating domain facilitated the efficient purification of active enzyme, using immobilized metal affinity chromatography. The purified NS3181 protease activity was characterized by assaying the trans-cleavage of in vitro transcription-translation generated substrates, and subsequently a previously unobserved cleavage site within the NS5A region was identified. The inhibitory effect of known protease inhibitors was also examined. It is hoped that availability of this method for the expression and purification of the NS3181 protease will facilitate the development of anti-hepatitis C therapies.
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Classification of hepatitis C virus variants in six major types based on analysis of the envelope 1 and nonstructural 5B genome regions and complete polyprotein sequences
More LessThe phylogenetic status of recently described isolates of hepatitis C virus (HCV) from Vietnam, Thailand and Indonesia (previously classified as types 7, 8, 9, 10 and 11) was re-analysed by the neighbour-joining method instead of the unweighted pair-group method with arithmetic mean (UPGMA) that was first used by the discoverers of these strains. The analysis of complete amino acid sequences and of nucleotide sequences of the envelope 1 (672 nt) and nonstructural 5B (1092 nt) genomic regions permitted the re-assignment of the type 7, 8, 9 and 11 isolates to type 6, and that of type 10 strains to type 3. Finally, this study made possible the classification of the previously described HCV strains (including these South-East Asian isolates) in six major types and at least 30 subtypes. It confirms that analysis of the E1 and NS5B genomic regions using the neighbourjoining method is a reliable tool for the assignment of most new isolates.
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Genetic diversity between hepatitis G virus isolates: analysis of nucleotide variation in the NS-3 and putative ‘core’ peptide genes
More LessSignificant variation was found, between 46 isolates of hepatitis G virus (HGV), following direct sequencing of subgenomic PCR fragments from either or both the NS-3 and putative ‘core’ peptide. Nucleotide sequences of most HGV NS-3 fragments varied by 10–30% and of most putative ‘core’ peptide fragments by 2–20%. HGV was therefore shown to be much less variable than hepatitis C virus (HCV) and pairwise comparisons ofHGVsequencesdemon- strated a single distinct distribution of evolutionary distances. Construction of phylogenetic trees, bootstrap analysis and calculation of mean distances between possible subtypes also indicated one level of variation between HGV NS-3 and putative ‘core’ peptide sequences, and the suggested degree of variation between isolates was similar to that between HCV subtypes. No evidence for clustering of sequences into multiple subtypes or genotypes was found. Although very small subgenomic fragments of HCV are indicative of the viral genotype it seems that the assignment of genetic groups is not possible for HGV using such small subgenomic fragments. The relatively limited genetic variation observed in HGV may reflect a relatively low level of host selection pressure stemming from the low level of host immunity stimulated by this virus.
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Mouse hepatitis virus strain A59 is released from opposite sides of different epithelial cell types
More LessCoronaviruses infect humans and animals through epithelial cells of the gastrointestinal and respiratory tracts that serve as their primary target. When studying infections in cultured polarized epithelial cells, we found previously that coronaviruses are released from specific plasma-membrane domains; thus, mouse hepatitis virus (strain A59; MHV-A59) leaves murine epithelial kidney cells from the baso- lateral surface, whereas release of transmissible gastroenteritis virus from porcine epithelial kidney cells is confined to the apical membrane. This observation begged the question whether a particular coronavirus is consistently shed through the same membrane, irrespective of the nature of the epithelial cell. We therefore extended our studies with MHV-A59 to Madin-Darby canine kidney (MDCK) strain I and human colon carcinoma (Caco-2) cells, both of which are naturally refractory to MHV-A59 but were made susceptible to infection by transfection with recombinant MHV receptor cDNA. The release of MHV-A59 from CacoMHVR cells occurred preferentially from the basolateral side, consistent with our previous observations. In contrast, release from MDCK mhvr cells occurred almost exclusively from the apical surface. Because of this difference, we studied MHV-A59 infection of MDCKmhvr cells in more detail. The virus entered the cells preferentially from the apical side, a situation similar to that in murine epithelial cells, where the highest density of MHV receptor glycoprotein was found. The results from this and previous studies show that targeting of vesicles containing MHV-A59 to a specific side of epithelial cells may vary in different epithelial cell types.
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Expression and characterization of a recombinant murine coronavirus 3C-like proteinase
More LessThe replication of coronaviruses involves proteolytic processing of the gene 1 translation products, pp1a and pp1ab. One of the key enzymes in this process is predicted to be a virus-encoded 3C-like proteinase. In this report, we describe a bacterial system that has allowed us to express and characterize a recombinant murine coronavirus (MHV- JHM) 3C-like proteinase. The partially purified protein has been shown to exhibit proteolytic activity in trans and mutation analysis has been used to demonstrate the indispensability of Cys- 3495 for enzymatic activity. Finally, the effect of class-specific proteinase inhibitors on the trans cleavage activity of the MHV 3C-like proteinase has been used to demonstrate the functional and structural homology of this enzyme to the picorna- virus 3C proteinases.
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Organization of the M genomic segment of Toscana phlebovirus
More LessThe nucleotide sequence of the Toscana (TOS) virus M RNA segment contains a single major open reading frame in the viral-complementary sequence, which can encode a polyprotein of 1339 amino acids. To map the TOS M segment product(s), different regions of the putative M polypeptide were expressed as glutathione S-transferase fusion proteins, which were purified and inoculated into mice to produce hyperimmune sera. By Western blot analysis, a protein of approximately 30 kDa and two glycoproteins, G1 and G2, with the same molecular mass (approximately 65 kDa) were identified in TOS virus-infected cells. The 30 kDa protein, which reacted with antibodies raised to the NH2-terminal, was found to be a non-structural protein (designated NSm). By immunoprecipitation analysis of TOS virus-infected cell lysates, both treated or untreated with tunicamycin, the relative positions of glycoproteins G1 and G2 were determined. The gene order, with respect to the genomic M RNA, was found to be 3′ NSm-G1-G2 5′.
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An anti-fusion regulatory protein-1 monoclonal antibody suppresses human parainfluenza virus type 2-induced cell fusion
Fusion regulatory protein-1 (FRP-1) regulates virus-mediated cell fusion and induces polykaryocyte formation of monocytes without any fusogen. We have recently reported that FRP-1 and the 4F2/CD98 heavy chain are identical molecules. Cell fusion in Newcastle disease virus (NDV)-infected HeLa cells was enhanced when cells were incubated with anti-FRP-1 MAb. Anti-FRP-1 MAbs also induced human immunodeficiency virus gp160-mediated cell fusion. However, HBJ127, an anti-FRP- 1/4F2/CD98 MAb that enhanced cell fusion in NDV- infected cells, delayed human parainfluenza virus type 2 (HPIV-2)-induced cell fusion in HeLa cells, although these viruses belong to the same genus Rubulavirus. No anti-FRP-1 MAbs enhanced cellfusion in HPIV-2-infected HeLa cells. Anti-FRP-1 MAbs including HBJ127 showed no effect on virus growth and expression levels of virus-specific polypeptides in HPIV-2-infected HeLa cells, indicating thatthe delay in cell fusion by an anti-FRP-1 MAb is not due to suppression of virus replication. When HeLa cells were transfected with an expression vector harbouring HPIV-2 HN and F genes, cell fusion was also suppressed by HBJ127, but the effect was weak in comparison with virus-infected cells. These data indicate anti-FRP-1 antibodies not only induce/enhance, but also inhibit/delay virus- induced cell fusion and therefore FRP-1 molecules are multifunctional.
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Characterization of five conserved genotypes of the mumps virus small hydrophobic (SH) protein gene.
More LessTwenty-one different mumps virus isolates from Sweden and Japan collected over 25 years were compared by nucleotide sequence analysis of the small hydrophobic (SH) protein gene, and the deduced 57 amino acid sequences of the coding part of the gene were aligned with published sequences of viral isolates from the USA, the UK, Sweden and Japan. Five genotypes were found which, in accordance with previously used nomenclature, were named A to E. Genotypes A, C, D and E were found in Europe and genotype B was found in Japan. Amino acid signature sequence motifs specific for each genotype were identified. A triplet of three amino acids at positions 28-30 was the most characteristic. Different genotypes can circulate simultaneously in a given geographical location. In Stockholm, genotypes A and D or C and D were found over different time periods. In contrast, only genotype B was found in Japan.
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Sequence divergence of measles virus haemagglutinin during natural evolution and adaptation to cell culture.
Phylogenetic analysis of the sequence of the H gene of 75 measles virus (MV) strains (32 published and 43 new sequences) was carried out. The lineage groups described from comparison of the nucleotide sequences encoding the C-terminal regions of the N protein of MV were the same as those derived from the H gene sequences in almost all cases. The databases document a number of distinct genotype switches that have occurred in Madrid (Spain). Well-documented is the complete replacement of lineage group C2, the common European genotype at that time, with that of group D3 around the autumn of 1993. No further isolations of group C2 took place in Madrid after this time. The rate of mutation of the H gene sequences of MV genotype D3 circulating in Madrid from 1993 to 1996 was very low (5 × 10−4 per annum for a given nucleotide position). This is an order of magnitude lower than the rates of mutation observed in the HN genes of human influenza A viruses. The ratio of expressed over silent mutations indicated that the divergence was not driven by immune selection in this gene. Variations in amino acid 117 of the H protein (F or L) may be related to the ability of some strains to haemagglutinate only in the presence of salt. Adaptation of MV to different primate cell types was associated with very small numbers of mutations in the H gene. The changes could not be predicted when virus previously grown in human B cell lines was adapted to monkey Vero cells. In contrast, rodent brain-adapted viruses displayed a lot of amino acid sequence variation from normal MV strains. There was no convincing evidence for recombination between MV genotypes.
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Inhibition of measles virus infection and fusion with peptides corresponding to the leucine zipper region of the fusion protein.
More LessMeasles virus (MV) infections are characterized by the induction of syncytia, i.e. the fusion of infected cells. Two MV proteins, the haemagglutinin (HA) and fusion (F) proteins, are involved in this process. Synthetic peptides representing two α-helical regions of the MV F protein were studied for their ability to inhibit MV fusion. A peptide corresponding to the leucine zipper region (amino acids 455–490) inhibited MV fusion, whereas a peptide to amino acids 148–177, corresponding to the amphipathic α-helix region, did not. Fusion inhibition was also obtained with vaccinia virus-expressed HA and F, a recent wild-type MV isolate and the closely related canine distemper virus, but not with mumps virus. The F455–490 peptide did not affect the synthesis of MV F or its transport to the cell membrane. Virus-cell attachment was unaffected, but haemolysis and virus entry into the cell were inhibited. In one-step growth curves the virus yield was unaffected.
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Distribution and variation of NV genes in fish rhabdoviruses
More LessThe fish rhabdovirus infectious haematopoietic necrosis virus (IHNV) contains a non-virion (NV) gene between the glycoprotein (G) and polymerase (L) genes on its RNA genome. The present study investigated three other fish rhabdovirus genomes and found that the NV gene of hirame rhabdovirus is closely related to the NV of IHNV, whereas the viral haemorrhagic septicemia NV gene showed evidence of significant divergence. Most importantly, spring viraemia of carp virus, the only vesiculovirus-like fish rhabdovirus examined, did not have an NV gene at its genomic RNA G-L junction. These results suggest that the presence of an NV gene is characteristic of the unassigned fish rhabdovirus subgroup previously classified as lyssaviruses, and that the NV gene is not essential for replication in fish cells per se, since it is absent in a vesiculovirus-like fish rhabdovirus.
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Mapping of monoclonal antibody epitopes of the rabies virus P protein
More LessThirty-six monoclonal antibodies (MAbs) specific for the rabies virus P phosphoprotein were obtained from mice immunized with recombinant P (PV strain) produced in E. coli. All MAbs reacted against the corresponding rabies virus protein by ELISA and by Western blot analysis and revealed the presence of cytoplasmic inclusions in rabies virus infected cells. The epitopes of seven MAbs were mapped by testing their reactivity with protein fragments expressed from deletion mutants in transfected cells. Western blotting, immunoprecipitation and immunofluorescence assays were performed. These MAbs recognized epitopes in different domains of the P protein: 60% were directed against a region lying between residues 83-172 suggesting a major antigenic determinant of the rabies virus P protein in this region. Most of the antigenic sites appeared to be composed of linear epitopes. These MAbs will be useful as tools to dissect structural and functional properties of the rabies virus P protein.
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Inhibition of vesicular stomatitis virus in cells constitutively expressing an antisense RNA targeted against the virus RNA polymerase gene
More LessTo study the effect of virus-specific antisense RNA expression on vesicular stomatitis virus (VSV) in-fectivity in cultured cells, a HeLaS3 cell line constitutively expressing antisense RNA complimentary to a portion of the VSV large RNA-dependent RNA polymerase gene (L) was established (HeAntiL). At an m.o.i. of 0·01 or 0·1, the HeAntiL cell line was able to reduce virus titre and delay virus-induced cell death by 9 or 5 h, respectively, when compared to a HeLa cell line stably transfected with the expression vector devoid of antisense sequence. Ribonuclease protection experiments showed a 10–20-fold reduction of hybridizable virus L mRNA in infected HeAntiL cells compared to infected control cells at various times before cell death. These results indicate that the antisense RNA approach can significantly reduce VSV mRNAtran-scription and virus production for a reasonable period of time. The robust growth rate of VSV eventually overwhelms the available antisense RNA and leads to delayed cell death.
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Proteolytic activity in vivo and encapsidation of recombinant human immunodeficiency virus type 1 proteinase expressed in baculovirus-infected cells.
More LessThe activity in vivo of HIV-1 proteinase (PR) was analysed in the baculovirus expression system, using eight different constructs of the prt gene under the control of polyhedrin (PH) promoters of various strengths. None of the active PRs was expressed in substantial quantities, and only PH-fused and/or non-functional PR mutants accumulated in high amounts in insect cells. However, enough PR activity was generated from a lengthened PR construct in insect cells to process Gag polyprotein substrate co-expressed in the same cells in trans. Fusion of the first 58 residues from the PH sequence to the PR N terminus did not significantly change its activity and specificity of cleavage of the Gag substrate. When analysed under mild denaturing conditions, PH-fused or unfused full-length PR point mutants, as well as PH-fused or unfused C-terminal deletion mutants, showed a propensity to multimerize, with a predominant occurrence of dimers. The incorporation of PR into Gag particles was studied using eight Gag-PR fusion constructs, all containing a non-functional PR mutant. The PR domain was fused to the C-terminal p6 domain of Gag (p6 gag ), or translated in frame with NCp7 (as in frameshifted Gag-Pol polyprotein) and followed by downstream sequences of increasing lengths from the Pol domain or the bacterial β-galactosidase. The results suggested that the presence of the p6 gag domain was detrimental to the encapsidation of polyprotein-embedded PR.
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Infection of choroid plexus cells by human T cell leukaemia virus type I
More LessVery little is known about the factors that determine the outcome of infection by human T cell leukaemia virus type I (HTLV-I) and the neurotropism of this virus is still a controversial point. In transgenic mice, the HTLV-I LTR is active mainly in the central nervous system (CNS), in parenchyma as well as in ependymal and choroid plexus cells. The latter are of particular interest and could represent the way of entry of the virus into the CNS. In this study we show that primary cultures of sheep choroid plexus can be infected with HTLV-I, leading to characteristic multinucleated syncytial cells containing virus RNA and proteins. HTLV-I p24 Gag protein was detected in the culture medium and the presence of virus particles was observed by electron microscopy 40 days after infection. At this time post-infection HTLV-I could be transmitted to human cord blood cells.
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Long-term persistence of protective immunity in cynomolgus monkeys immunized with a recombinant vaccinia virus expressing the human T cell leukaemia virus type I envelope gene.
To develop effective vaccines against infection with human T cell leukaemia virus type I (HTLV-I), we constructed a recombinant vaccinia virus (WR- SFB5env) synthesizing the HTLV-I envelope (Env) gp46 protein under the control of a strong promoter, termed the ATI hybrid promoter. WR- SFB5env expressed a large quantity of gp46. In cynomolgus monkeys (Macaca fascicularis) immunized with WR-SFB5env, anti-HTLV-I Env antibody, including neutralizing antibody, was induced and remained at a high level until 136 weeks (2 6 years) post-infection (p.i.). These immunized monkeys had HTLV-I Env-specific cytotoxic T lymphocyte activity. At 136 weeks p.i., the immunized monkeys were challenged with an HTLV-I-produc- ing cynomolgus T lymphocyte cell line. Neither HTLV-I antigen nor HTLV-I proviruses were detected in peripheral blood mononuclear cells, lymph nodes or spleens of the WR-SFB5env- immunized monkeys, in contrast to non-immunized control monkeys. These results indicate that a single immunization with WR-SFB5env induced prolonged humoral and cellular immune responses to HTLV-I and protected the monkeys against virus challenge.
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Volumes and issues
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Volume 105 (2024)
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Volume 103 (2022)
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