- Volume 69, Issue 6, 1988
Volume 69, Issue 6, 1988
- Bacterial
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Genome Homology and Host Range of Some SPβ-related Bacteriophages of Bacillus Subtilis and Bacillus amyloliquefaciens
More LessSummaryTemperate Bacillus subtilis bacteriophages SBβ, ø3T and SPR and B. amyloliquefaciens phage H2 were compared with respect to DNA-DNA homology by Southern blot analysis to each other and to members of the genus Bacillus. The results show that H2 is a distantly related member of the group III B. subtilis phages. Detectable homology to group III phages could be found in the DNA of several other Bacillus species, including B. natto and B. amyloliquefaciens, demonstrating the widespread occurrence of this group of phages. The host ranges for the phages SPβ, SPR and H2 were determined by adsorption efficiency and by the ability of erythromycin resistance- and chloramphenicol resistance-transducing phages to convert susceptible host strains. Of the three phages examined, only H2 was capable of infecting B. amyloliquefaciens. Based on these results we propose that group III phages should be divided into three subgroups: SPβ, ø3T, Rho11, IG1, IG3 and Z (subgroup 1), SPR (subgroup 2) and H2 (subgroup 3).
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- Animal
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Early Events of Importance in Determining Host Cell Permissiveness to Mouse Hepatitis Virus Infection
More LessSummaryThree categories of cell lines are described which differ with respect to their permissiveness to mouse hepatitis virus (MHV), strain A59. Fully permissive L-2 cells gave rise to 100- to 1000-fold higher numbers of infectious centres than did semipermissive LM, LM-K or C-1300 cells, whereas non-permissive Vero or C-6 cells were refractory to MHV infection. On an infected cell basis, semi-permissive cells (LM, LM-K or C-1300) were as efficient in replicating viral RNA, protein and progeny virions as fully permissive L-2 cells. This result suggested that LM, LM-K and C-1300 cells were deficient in their ability to permit full expression (as compared to L-2 cells) of an early event in MHV infection. Assays of radiolabelled MHV binding to cells of all three categories (L-2, LM, LM-K and C-6) and of infectious MHV binding to L-2 and LM-K cells showed no correlation between virion binding and degree of permissiveness to MHV infection. Internalization of MHV virions into L-2 and LM-K cells, as assayed by proteinase K-resistant infectious centres, showed that, in both cases, maximum virion uptake was complete by approximately 40 min post-inoculation. Direct assays of infectious virion uptake showed similar numbers of internalized viruses (only a threefold difference between L-2 and LM-K cells, as compared to a 500-fold difference in infectious centres). Attempts to enhance MHV uptake into LM-K cells relative to L-2 cells, with DEAE-dextran or the cytoskeleton-disrupting drugs colchicine and cytochalasin B, were unsuccessful, further suggesting that the ability of LM-K cells to internalize the virus was not lacking. The results suggest that MHV infection of at least some semi-permissive cells, such as the LM-K line, is limited by a process which chronologically correlates with virion uncoating. Since LM-K cells have been shown previously to be resistant to membrane fusion in MHV infection, it is postulated that they may also restrict uncoating of MHV by limiting the degree of normal endosomal membrane fusion with the viral envelope.
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Interaction of Polylysine with the Cellular Receptor for Herpes Simplex Virus Type 1
More LessSummaryWe earlier reported that neomycin blocked reversibly the binding of herpes simplex virus type 1 (HSV-1) to the receptor of BHK cells, while the binding of HSV-2 to the receptor was unaffected. We could not determine whether the effect was on the virus particle, the receptor, or both. We have now tested several other cationic substances, and report that polylysine (and polyarginine) block the binding of HSV-1 to the receptor by interfering with the cellular receptor function; higher molecular weight polylysines were more potent than those of lower molecular weight. Polylysine and neomycin showed additive effects. In vitro, polylysine showed the same strong binding to the plasma membrane phosphoinositides as did neomycin. Together these data suggest that the drugs may have a common target in the cell membrane. The HSV-1 and HSV-2 virus particles were unaffected by the drugs, as was the cellular HSV-2 receptor.
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Excretion of Non-infectious Virus Particles Lacking Glycoprotein H by a Temperature-sensitive Mutant of Herpes Simplex Virus Type 1: Evidence that gH Is Essential for Virion Infectivity
More LessSummaryA temperature-sensitive mutant of herpes simplex virus type 1, tsQ26, was shown to contain an amino acid substitution in glycoprotein H (gH). The mutant entered cells efficiently at the non-permissive temperature and replicated to give nearly normal yields of intracellular infectivity. The intracellular virions contained, predominantly, an immature form of gH and no gH was found on the surface of infected cells. Excreted virions were devoid of gH and were not infectious. Virions excreted at the permissive temperature were infectious and contained gH and no loss of gH resulted from incubation of these virions at the non-permissive temperature. The temperature-sensitive phenotype apparently results from the loss of gH from virions during their transport to the cell surface, and since loss of gH is accompanied by loss of infectivity we conclude that gH is an essential component of the infectious virion.
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Limited Efficacy of Inhibitors of Herpes Simplex Virus DNA Synthesis in Murine Models of Recrudescent Disease
More LessSummaryThe herpesvirus DNA polymerase inhibitor foscarnet, applied topically, and the anti-herpesvirus guanosine analogue buciclovir, given orally, decreased virus replication and disease development in primary skin infections of mice caused by herpes simplex virus type 1 (HSV-1). If the same tissues were infected via sensory nerves, following zosteriform spread of the virus the same treatments showed strongly decreased efficacy, or were inefficacious, when started before development of clinical signs in the infected tissues. These results were obtained in murine models of zosteriform spread of HSV-1 to the ear (following inoculation of the ventral side of the neck) or to the lower flank (following inoculation of the upper flank). In these models the immune system played a dominant role in virus clearance. The topically applied foscarnet could not prevent disease development in these models of recrudescent disease even when applied before the virus was detected in the skin, but a decrease in virus titre was obtained. Orally administered buciclovir lost efficacy when administered at the time of virus entry into the skin, i.e. 1 or 2 days before development of clinical signs. In the flank model, measuring lesion development, orally administered acyclovir also had a strongly decreased efficacy, when compared with its effect during infections in which lesion development did not involve translocation of virus through nerves. In the presence of developing immunity the inhibitors could not accelerate the clearance of virus from infected tissues. Furthermore, all treatments (topical foscarnet and oral buciclovir or acyclovir) were without effect on disease development when treatment was initiated on appearance of the first clinical signs of disease. As disease development following zosteriform spread of HSV resembles that in recurrent herpes in humans, and as the limited efficacy of the inhibitors observed resembles the poor results obtained with inhibitors of herpesvirus DNA synthesis in clinical studies on the treatment of symptomatic recurrent herpes, we suggest the use of animal models of zosteriform spread for pre-clinical evaluation of new antiherpes drugs.
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Inhibition of Transcription of Herpes Simplex Virus Immediate Early Genes in Interferon-treated Human Cells
More LessSummaryThe effect of interferon (IFN) treatment on the early stages of herpes simplex virus type 1 (HSV-1) replication in three types of human cells was investigated. Interferon pretreatment was shown to reduce the steady state levels of both total and polysome-bound HSV-1 immediate early α mRNAs. Using the nuclear run-off transcription assay, we showed that IFN selectively inhibited transcription of the HSV-1 genes, with no effect on transcription of total cellular RNA or that of the β-tubulin RNA. Thus, IFN appears to inhibit the initiation of HSV-1 α gene transcription rather than affect the stability of the respective mRNAs. IFN did not prevent the HSV-1-induced early shut-off of host cellular protein synthesis caused by a structural protein of the infecting virus. This observation indicated that the IFN-mediated inhibition of HSV-1 replication is at a stage beyond viral penetration into the cytoplasm. These results suggested that IFN blocked HSV-1 replication primarily at a very early stage, during the onset of α mRNA transcription.
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Induction of Gene Expression under Human Cytomegalovirus Immediate Early Enhancer-Promoter Control by Inhibition of Protein Synthesis Is Cell Cycle-dependent
More LessSummaryIn this paper we describe stably transfected rat cell lines which harbour either the human cytomegalovirus (HCMV) immediate early (IE) gene encoding the 72K IE nuclear antigen (IEA) or the bacterial chloramphenicol acetyltransferase (CAT) gene both under transcriptional control of the HCMV IE enhancer-promoter (-484 to -19 relative to the IE cap site, +1). In these cell lines IE gene or CAT gene expression is repressed but can be induced by heat-shock, by sodium arsenite and by inhibitors of protein synthesis such as cycloheximide (CH). In addition, we present evidence suggesting that CH-mediated activation is cell cycle-dependent. Thus CH-mediated induction of the 72K IEA as well as CAT gene expression was impaired and accumulation of mRNAs did not occur when cellular DNA synthesis was inhibited. Activation of IE genes by CH occurred almost exclusively in those cells which were in S-phase. In contrast, activation of gene expression by sodium arsenite occurred independently of cellular DNA synthesis and was not restricted to cells in S-phase. The data are consistent with, but not proof of, the hypothesis that the activation of IE transcription, brought about by inhibition of protein synthesis, resulted from a disturbed chromatin conformation due to DNA synthesis continuing in the absence of a supply of chromatin-organizing proteins. The possible relevance of these observations with regard to HCMV latency and reactivation is discussed.
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Prokaryotic Expression of Immunogenic Polypeptides of the Large Phosphoprotein (pp150) of Human Cytomegalovirus
SummaryThe large phosphorylated matrix protein pp150 of human cytomegalovirus (HCMV) is the polypeptide most frequently reactive in immunoblotting analyses with human antisera when compared with other viral proteins. Several defined regions of pp150 were expressed as β-galactosidase fusion proteins and these were tested for their immunoreactivity with human sera and their immunogenicity. One antigenic region could be expressed in large amounts and was found to carry immunodominant epitopes, as shown by immunoblotting and ELISA. A rabbit antiserum raised against recombinant pp150 antigens produced in bacteria proved to be useful for immunofluorescence and immunohistochemistry studies of HCMV-infected cells and tissues. The results suggest that this anti-pp150 serum will help to elucidate the process of virus assembly and antigen detection in infected cells.
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Characterization of a Human Cytomegalovirus Glycoprotein Complex (gcI)
More LessSummaryThree distinct families of glycoprotein complexes present in the envelopes of human cytomegalovirus and designated gcI, gcII and gcIII have been described recently. The synthesis of the gcI family was analysed using either inhibitors of glycoprotein processing and transport or endoglycosidase treatments of purified glycoproteins. The initial step in gcI synthesis involved the glycosylation of a 95K protein (p95) to form a high-mannose, simple N-linked glycoprotein of M r 158K (gp158), which was detected only in the presence of the glycoprotein processing inhibitor castanospermine. This intermediate was rapidly trimmed in the virus-infected cell to form a more stable simple N-linked precursor glycoprotein of M r 138K (gp138). Treatment of either gp158 or gp138 with endoglycosidase H produced p95. Both molecules, gp158 and gp138, were found in disulphide-linked complexes which are presumably infected cell precursors to gcI since they were not found in virions. The processing of these complexes involved complete cleavage of gp138 and conversion of some but not all of its oligosaccharide to complex N-linked chains. Both processing events were inhibited by the ionophore monensin. Mature gcI contained the gp138 cleavage product, gp55, in a disulphide-linked complex with a heterogeneous glycoprotein designated gp93-130. The latter glycoprotein could be separated into two electrophoretic forms, gp93 and gp130. The deglycosylated form of gp55 had a discrete banding pattern with an apparent M r of 46K (p46). In contrast, the deglycosylated forms of gp93 and gp130 had diffuse banding patterns with apparent M r values of 46K to 56K (p46–56) and 60K to 70K (p60–70) respectively. Peptide profiles comparing gp93 with gp130 indicated that they have highly similar polypeptide backbones. Since the deglycosylated forms of gp55 and gp130, 46K and 60K to 70K, respectively, together exceed the 95K precursor/deglycosylated intermediate in M r, we propose that the above glycoproteins are derived by an alternative proteolytic cleavage of the precursor. The heterogeneous electrophoretic properties of the deglycosylated forms of gp93 and gp130 may be due to additional post-translational modifications other than glycosylation.
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Characterization of the Serological Response in Man to the Latent Membrane Protein and the Six Nuclear Antigens Encoded by Epstein-Barr Virus
More LessSummaryA total of 116 sera from healthy individuals and from patients with Burkitt’s lymphoma (BL), nasopharyngeal carcinoma (NPC) or rheumatoid arthritis (RA) were studied with respect to antibody responses to each of the seven known transformation-associated Epstein-Barr virus (EBV)-encoded antigens [latent membrane protein (LMP) and six nuclear proteins (EBNAs 1 to 6)]. The antibodies were detected using modified standard immunoblotting techniques. Antibodies to LMP were detected for the first time in sera from 6/27 (22%) healthy, EBV-immune individuals (seropositive for the viral capsid antigens). An increased incidence of anti-LMP antibodies was found in EBV-immune sera from patients with BL (17/24 positive; 71%), NPC (21/33; 64%), and RA (16/21; 76%). Antibodies to EBNA 1 were detected in all EBV-immune sera at a standard 1:20 dilution. Antibodies to the other EBNAs were detected in only a proportion of these sera (20 to 95%) at the same dilution. Only minor disease-associated differences in the incidence of these antibodies were observed, the most consistent being that RA sera had a higher incidence of antibodies to EBNAs 2 to 6 compared with healthy controls. Testing of the sera at a 1:100 dilution suggested that there were some disease-related differences in the titres of anti-EBNA antibodies. At this serum dilution, a reduced incidence of antibodies to EBNA 2 was seen in NPC (6/31) compared with RA (18/19) and healthy EBV-seropositives (16/26); antibodies to EBNA 3 were detected at an increased incidence in BL (8/15) and NPC (16/31) compared with control sera (7/26); antibodies to EBNA 4 were detected at increased incidence in BL (5/15) and RA (6/19) compared with control sera (1/26); and antibodies to EBNA 6 were detected at increased incidence in NPC (19/31) and RA (7/19) compared with control sera (3/26).
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The Response of Infants with Bronchiolitis to the Proteins of Respiratory Syncytial Virus
More LessSummaryAcute phase sera were collected from 28 infants hospitalized with bronchiolitis due to respiratory syncytial (RS) virus and convalescent sera were collected from 24 of them. The sera were assayed for neutralizing antibodies by plaque inhibition, for antibodies to the viral proteins by Western blot against partially purified RS virus, and for their ability to inhibit attachment and fusion. Among the 28 acute phase sera, 27 had antibody to the attachment glycoprotein (G), 16 had antibody to the fusion glycoprotein (F), but none had antibody to the matrix protein (VPM). Both the geometric mean anti-G titre, and the geometric mean anti-F titre correlated with the 50% neutralizing dose (ND50) titre in the acute phase serum. Among the 24 convalescent sera, only four exhibited an increase in neutralizing antibody titre. The response to G appeared to be related to the acute phase ND50 titre. Of 17 infants with acute phase titres of less than 100 ND50/ml, 10 responded to G while there was no response to this protein in seven infants with acute phase titres greater than 100 ND50/ml. While only one infant responded to F, 18 responded to the phosphorylated nucleocapsid protein, VP32, and none responded to VPM. The ability of the acute phase sera to inhibit virus attachment to HeLa cells and to inhibit fusion correlated with the anti-G titre and the anti-F titre, respectively. However, there was no correlation between the inhibition of fusion and the anti-F titre in the convalescent sera, almost all of which inhibited fusion. These results suggest that the infected infants were responding to RS virus, but that their response to the viral proteins was either masked or slowed by residual maternal antibody. The inability to detect VPM in the acute and convalescent phase sera, as well as in 20 paired maternal and cord sera at a 1:50 dilution suggested that VPM, although it is one of the most prevalent viral proteins in both the virion and the infected cell, may be poorly antigenic in humans.
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Reduction of Yellow Fever Virus Mouse Neurovirulence by Immunization with a Bacterially Synthesized Non-structural Protein (NS1) Fragment
More LessSummaryPart of a yellow fever virus-specified non-structural protein (NS1) was expressed in Escherichia coli as a fusion protein with β-galactosidase. Immunization of mice with this partially purified NS1-β-galactosidase fusion protein induced yellow fever virus-specific antibodies and provided some protection against intracerebral challenge with the virus.
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Association between the pH-dependent Conformational Change of West Nile Flavivirus E Protein and Virus-mediated Membrane Fusion
More LessSummaryThe major envelope protein (E) of West Nile virus mediates fusion between the membranes of the viral envelope and the target cell at optimum pH values of just below neutrality. The fusion is critical for the entry mechanism, allowing virus to escape from the acidic endosomal compartment. To define the role of the viral E protein in the fusion reaction, the conformational change in E and concomitant change of viral infectivity were studied quantitatively, using protease digestion of the E protein and assay of viral infectivity. The results showed that the conformational change occurred in a pH-dependent manner with an upper threshold of pH 7.0 and maximum conversion occurring at pH 6.4 and below. The conversion was rapid and reached a half-maximal value within 15 s after acidification. The exposure of free or cell-bound virions to acid pH resulted in the loss of infectivity in an almost identical pH-dependent manner. Based on these findings, it is suggested that there are two distinct viral modes of entry into macrophages, i.e. infectious endocytosis and non-infectious viral fusion with plasma membranes, with the pH of the extracellular medium determining which of these predominates. The implications of these observations for the role of the E protein in membrane fusion and the probable localization of fusion epitopes are discussed.
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Protein Coding Assignment for the Genome of Epizootic Haemorrhagic Disease Virus
More LessSummaryViral genomic RNA was purified from BHK-21 cells infected with epizootic haemorrhagic disease virus and the 10 dsRNA genome segments were isolated by polyacrylamide gel electrophoresis. These genome segments were translated in vitro using the rabbit reticulocyte lysate system and the synthesized proteins were detected by immune precipitation and gel electrophoresis. This allowed the assignment of protein coding to the genome segments and the identification of two additional virus-specified proteins not readily detectable in lysates of virus-infected cells.
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Analysis of the L1 Gene Product of Human Papillomavirus Type 16 by Expression in a Vaccinia Virus Recombinant
More LessSummaryThe L1 open reading frame of human papillomavirus type 16 (HPV16) has been expressed in vaccinia virus under the control of both the 7.5K early and late promoter, and the 4b major late promoter. Antibodies to a β-galactosidase fusion protein containing a C-terminal portion of the HPV16 L1 gene product were used to compare the levels of L1 expression in the two recombinants, and showed that greater levels of expression were obtained when the gene was placed under the control of the 4b late promoter. Immunofluorescence studies revealed a nuclear location of the L1 gene product when expressed in vaccinia virus. Antibodies to the β-galactosidase fusion protein detected a major polypeptide species of 57K and a minor species of 64K in Western blots of recombinant-infected cell lysates. The 64K species was not detected when cells were infected in the presence of tunicamycin, indicating that the primary translation product of the HPV16 L1 open reading frame is modified by N-linked glycosylation when expressed in vaccinia virus. Whereas antibodies to HPV16 L1 fusion proteins and to a peptide containing amino acids from the C terminus of HPV16 L1 reacted well in Western blots with the HPV16 L1 target expressed in vaccinia virus, no reactivity was observed with antibodies to bovine papillomavirus type 1 particles or to a HPV6b fusion protein.
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Comparison of a Conserved Region in Fowlpox Virus and Vaccinia Virus Genomes and the Translocation of the Fowlpox Virus Thymidine Kinase Gene
More LessSummaryThe DNA sequence of a clustered set of genes which are conserved in orthopoxviruses has been determined for the avipoxvirus, fowlpox virus. The arrangement of the genes in fowlpox virus is nearly identical to that in vaccinia virus, and genes which are overlapping in vaccinia virus overlap in fowlpox virus. One major difference exists however, as the thymidine kinase (TK) gene is absent in fowlpox virus from the position it occupies within this cluster of genes in vaccinia virus. Instead, in fowlpox virus there is a 32 bp non-coding region present between the genes that flank the TK gene in vaccinia virus. The fowlpox virus TK gene has been cloned and sequenced. The sequences immediately flanking the TK gene show no homology to any previously reported poxvirus gene. These results are discussed in terms of genome stability in poxviruses and the use of the TK gene as a non-essential region for the introduction of foreign genes into poxviruses.
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Physical Maps and Comparative DNA Hybridization of Mamestra Brassicae and Panolis Flammea Nuclear Polyhedrosis Virus Genomes
More LessSummaryThe genome DNAs from the Panolis flammea (Pf) multiple nucleocapsid nuclear polyhedrosis virus (MNPV) and the Mamestra brassicae (Mb) MNPV were analysed with the restriction endonucleases BamHI, BglII, KpnI, HindIII, SmaI and XhoI. The profiles produced by each enzyme for the two virus genomes were quite dissimilar with very few comigrating fragments. The size of PfMNPV DNA was calculated to be 145 kilobase pairs (kbp) and that of MbMNPV 150 kbp. Physical maps of the two genomes were constructed utilizing the above enzymes. The two maps were oriented in relation to their putative polyhedrin genes. Alignment of the two restriction maps for PfMNPV and MbMNPV was achieved by performing cross blot hybridization between XhoI digests of the two virus genomes. This showed that despite differences in the physical maps the two genomes shared overall similarity in gene organization. The two viruses were also compared using dot blot hybridization analysis to quantify homology with Autographa californica (Ac) MNPV. These data showed that both PfMNPV and MbMNPV were distantly related to AcMNPV but exhibited a high degree of homology to each other (nearly 100% in 20% formamide, 70% in 50% formamide).
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Isolation, Complementation and Partial Characterization of Temperature-sensitive Mutants of the Baculovirus Hyphantria Cunea Nuclear Polyhedrosis Virus
More LessSummaryTwelve temperature-sensitive mutants were isolated from Hyphantria cunea nuclear polyhedrosis virus grown in Spodoptera frugiperda cells and were sorted into four groups by their properties in plaque assays at the non-permissive temperature (32 °C). The phenotypes of the four groups were as follows: (i) failure to make polyhedra, (ii) few polyhedra formed, (iii) reduced plaquing efficiency, (iv) small plaque size. Ten mutants had reduced plaque size and polyhedra formation at 32 °C. One mutant formed plaques without polyhedra, had a reduced infectious virus titre at 32 °C and also showed a defect in late gene function. Two mutants formed small plaques with few polyhedra and were temperature-sensitive with respect to production of extracellular non-occluded virions at 32 °C. Other phenotypes were also distinguished. The formation of polyhedra by all the mutants was 2 to 4 h faster at 32 °C than at 25 °C. After temperature shift-up from 25 °C to 32 °C at 12 h post-infection polyhedron formation was still 2 to 4 h faster. Complementation analyses based on polyhedron formation in double infections at 32 °C distinguished four complementation groups.
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The Genome of the Multicapsid Baculovirus of Orgyia Pseudotsugata: Restriction Map and Analysis of Two Sets of GC-rich Repeated Sequences
More LessSummaryFive cosmids containing inserts that comprise the complete genome of the multicapsid nuclear polyhedrosis virus of Orgyia pseudotsugata were mapped with four restriction enzymes (BglII, ClaI, SstI, XhoI). From these cosmid maps, composite maps of the complete genome were constructed for each restriction enzyme. A region containing repeats of the sequence GGC downstream of the polyhedrin gene was used to probe the genome. It cross-hybridized with a region which, upon sequence analysis, was found to be a highly repetitive GC-rich region of nearly 500 nucleotides. The two GC-rich regions appeared to be evolutionarily unrelated.
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The Complete Nucleotide Sequence of the Genome of a Hepatitis B Virus Isolated from a Naturally Infected Chimpanzee
More LessSummaryThe complete nucleotide sequence of a strain of hepatitis B virus, originally isolated from a naturally infected chimpanzee, has been determined. Interesting features of the sequence include the presence of an in-phase stop codon in the ‘pre-core’ region of the core antigen open reading frame. The sequence shows approximately 10% nucleotide divergence from all of the other hepatitis B virus sequences previously published and the possibility that this divergence is the result of passage through chimpanzees is discussed.
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