- Volume 70, Issue 9, 1989
Volume 70, Issue 9, 1989
- Articles
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- Animal
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Vaccinia Virus Encodes a Family of Genes with Homology to Serine Proteinase Inhibitors
More LessSummaryNucleotide sequencing of a region of the vaccinia virus genome proximal to the right inverted terminal repeat (ITR) identified two open reading frames (ORFs) encoding proteins of 39K and 40K with amino acid homology to each other, to another vaccinia virus gene near the opposite end of the virus genome and to the superfamily of serine proteinase inhibitors (serpins). Serpins have now been found in poxviruses from the genera orthopox (cowpox and vaccinia viruses), leporipox (myxoma virus) and avipox (fowlpox virus). One of the vaccinia virus serpins identified here (B13R) shares 92% amino acid identity with the serpin from cowpox virus and 46% and 19% identity with vaccinia serpins B24R and K2L, respectively. The amino acid sequence of B13R reported here differs at 11 positions from a recently reported sequence and contains an additional three internal residues. The serpin genes near the right ITR are separated by 8 kb of DNA. Both genes contain early transcriptional termination signals just downstream of the ORFs and are transcribed in a rightward direction towards the end of the genome. Analysis of mRNAs from virus-infected cells demonstrated that all three vaccinia virus serpin genes are transcribed early during infection. The amino acid sequences at the active sites of these serpins suggest that they may inhibit serine proteinases of differing biochemical specificities. The possible functions of these genes are discussed.
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Detection of Herpes Simplex Virus Type 1 Gene Expression in Latently and Productively Infected Mouse Ganglia Using the Polymerase Chain Reaction
SummaryThe polymerase chain reaction (PCR) was employed to detect herpes simplex virus (HSV) sequences in the DNA, and HSV gene expression in total cell RNA, extracted from cervical and trigeminal ganglia of mice during productive and latent infection with HSV-1, strain SC16. Such gene expression was detected in 1 μg or less of RNA, the quantity anticipated to be present in one or two cervical ganglia. Within the limits of the primers available, gene expression during latency appeared to be restricted to the latency-associated transcript (LAT). The 195 base portion of the LAT amplified by the PCR was sequenced and found to contain several base changes and deletions with respect to published sequences for different HSV strains. These mutations, within the putative open reading frame 2 of the LAT, formed stop or terminator signals, which suggests that the LAT does not act to establish or maintain latency through translation to a protein. The primers for the LAT also amplified a 300 bp fragment from any murine and some other mammalian RNAs. Apart from the oligonucleotide primers, this fragment did not show any homology with HSV.
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Mapping of Epitopes on the 65K DNA-binding Protein of Herpes Simplex Virus Type 1
SummaryPreviously we have described the isolation of seven monoclonal antibodies (MAbs) and two polyvalent rabbit sera directed against the product of herpes simplex virus type 1 (HSV-1) gene UL42, a 65K DNA-binding protein (65KDBP) which is essential for HSV DNA replication and virus growth. We now report the synthesis of all 483 overlapping hexapeptides of this 488 amino acid protein and describe their use for the identification of epitopes recognized by these MAbs and polyvalent sera. MAb 6898, derived from one fusion, recognizes the peptides EDLDGAand DLDGAA which correspond to amino acids 363 to 369 of 65KDBP. MAbs Z4D4, Z6F3, Z1A8, Z10C1, Z3H12 and Z1F11, derived from a second fusion, all recognize the peptides GDPEDL and DPEDLD which correspond to amino acids 360 to 366. As expected both polyvalent sera recognize several different epitopes.
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Clinical and Serological Outcome of Genital Herpes Simplex Virus (HSV) Type 2 Inoculation following Oral HSV Type 1 Infection in Guinea-pigs
More LessSummaryThe clinical and serological outcome of genital herpes simplex virus type 2 (HSV-2) inoculation in animals previously orally infected with HSV type 1 was evaluated. A prior HSV-1 oral infection modified the genital HSV-2 infection so that only four of 18 (22%) animals were initially symptomatic although all but one animal shed HSV-2 from the cervicovaginal area for at least 5 days following inoculation. Three of four animals with symptomatic initial disease also developed recurrences, as did an additional six animals that did not manifest acute genital disease. Anti-glycoprotein gG-1 antibody was found in 17 of 18 animals with only an HSV-1 infection and anti-gG-2 antibody in all of nine animals with only an HSV-2 infection. Anti-gG-2 antibody was detected in eight of 17 animals with a prior HSV-1 infection following HSV-2 inoculation and one had an indeterminate response. Eight of these nine animals developed recurrent genital disease compared to one of eight that did not respond to gG-2 (P < 0·006). Thus a prior oral HSV-1 infection modified both the initial presentation of HSV-2 infection and the HSV type-specific serological response.
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Isolation and Preliminary Characterization of Temperature-sensitive Mutants of Mouse Cytomegalovirus of Differing Virulence for 1-week-old Mice
More LessSummaryTo study the pathogenicity of murine cytomegalovirus (MCMV) and to identify virulence determinants, we have isolated and phenotypically characterized a set of temperature-sensitive mutants. One mutant, PP269/38, was avirulent for 1-week-old BALB/c mice and restricted in its plaque formation and replication at 39 °C. Mutants PP242/68 and PP268/38 were 100-fold less virulent than salivary gland-grown virus (SGV), even after two passages in the salivary glands of 1-week-old mice. The former mutant was unable to replicate or form plaques at 39 °C whereas the latter replicated poorly at 39 °C but not at all at 40 °C although it was able to form plaques at 40 °C with a reduced plaque size. PP31/15 exhibited a 40-fold reduction in virulence compared to SGV after two passages in vivo and was unable to form plaques or to replicate at 40 °C; at 39 °C it was able to, with reduced efficiency. The remaining two mutants, PP99/3 and PP392/31, were 10-fold less virulent than SGV and were restricted at 40 °C. The six mutants have been classified into at least four complementation groups. These mutants may be useful for studying various aspects of MCMV pathogenicity.
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Human Cytomegalovirus RNAs Immunoprecipitated by Multiple Systemic Lupus Erythematosus Antisera
More LessSummaryThe association of human cytomegalovirus (HCMV) RNAs with ribonucleoprotein particles that react with antibodies from patients with systemic lupus erythematosus was tested by immunoprecipitation with multiple patients’ sera. A major late 2·8 kb RNA and several minor RNAs encoded by the HCMV long repeat region were immunoprecipitated from HCMV-infected cells by La, Ro and, much less abundantly, Sm autoimmune antisera. The exact location of these RNAs was determined by high resolution R-loop mapping and found to be between 0·8093 and 0·8189 map units. The 2·8 kb RNA is polyadenylated and associated with polysomes but does not appear to be spliced. Immunoprecipitation was not seen using normal or other autoimmune antisera. In addition, immunoprecipitation was specific to these RNAs in that other abundant HCMV RNAs were not immunoprecipitated. It was also found that the addition of increasing amounts of purified La antigen to infected cell lysates inhibited immunoprecipitation of the 2·8 kb RNA by La antiserum. The data suggest that specific HCMV RNAs may interact with cellular ribonucleoproteins known to be involved in post-transcriptional regulation of gene expression.
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Syncytium Formation and Destruction of Bystander CD4+ Cells Cocultured with T Cells Persistently Infected with Human Immunodeficiency Virus as Demonstrated by Flow Cytometry
More LessSummaryWe have developed a flow cytometric method for demonstrating cell fusion between human immunodeficiency virus type 1 (HIV-1)- or HIV-2-infected HUT-78 cells and uninfected CD4-bearing MOLT-4 cells. Syncytium formation due to an interaction between the gp120 glycoprotein expressed on HIV-infected HUT-78 cells and the CD4 receptor present on MOLT-4 cells, resulted in an immediate decrease in the number of MOLT-4 cells; after a 24 h incubation period almost all MOLT-4 cells had disappeared from the culture. To show that the target MOLT-4 cells and not the aggressor HUT-78 cells were destroyed, specific monoclonal antibodies (MAbs) that reacted with antigens expressed on either MOLT-4 or HUT-78 cells were used. The formation of giant cells andthe concomitant disappearance of MOLT-4 cells was blocked by MAbs specific for OKT4A and Leu3a, and, to a much lower level, by the MAbs specific for OKT4 and gp120. MAbs specific for OKT3,Leu2a, HLA-DR, Leu18 and LeuM3 did not prevent the disappearance of MOLT-4 cells. Sera from two AIDS patients containing antibodies to the HIV envelope glycoproteins did not protect MOLT-4cells against the destructive effect of the HIV-infected HUT-78 cells. The fusion index, thepercentage fusion inhibition and the 50% fusion inhibitory concentration of the MAbs can be accurately determined with the flow cytometric assay. The method can be readily implemented to evaluate any therapeutic treatment by examining its capacity to block cell-to-cell fusion, and hence destruction of the target bystander cells. Five anti-HIV compounds which have been previously shown to interfere with HIV binding to cells (namely pentosan polysulphate, heparin, suramin, aurintricarboxylic acid and Evans Blue) were further evaluated by this new method. With the exception of heparin, all of these compounds were found to inhibit cell-to-cell fusion andthe concomitant destruction of the target bystander cells. Azidothymidine failed to inhibit fusion or bystander T cell destruction.
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Isolation and Characterization of Canine Distemper Virus Nucleocapsid Variants
More LessSummaryNucleocapsid (NC) variants expressed by the Onderstepoort strain of canine distemper virus (CDV) were ultrastructurally and biochemically characterized. Three isolated variants were defined which corresponded to the three variants observed within the cytoplasm of infected cells. Dense NC (D-NC), isolated on discontinuous caesium chloride (CsCl) isopycnic gradients, had an average density of 1·2971 ± 0·0042 g/ml. Ultrastructurally, D-NC were 1620·0 ± 112·1 nm in length with a 20·1 ± 1·3 nm outer and a 5·8 ± 0·7 nm inner core diameter. The D-NC protein composition was 89·7% of a 61K protein (N), 8·4% of a 75K protein (P) and 1·9% of a 160K to 200K protein (L). A single species of nucleic acid, 15 kb in length, was isolated from D-NC. Light NC (L-NC), similarly isolated, had an average density of 1·2894 ± 0·0040 g/ml. L-NC differed ultrastructurally from D-NC in that poor resolution of NC subunits, a larger outer diameter (32·0 ± 2·8 nm), and a greater inner core diameter (10·4 ± 0·6 nm) were observed. The average L-NC strand length was 1574·4 ± 115·8 nm. The protein composition was the same as D-NC with the exception of an additional 70K protein, representing 4·0 to 7·7% of the total L-NC protein mass. A 15 kb nucleic acid was also identified in L-NC, although heightened sensitivity of encapsidated L-NC nucleic acid to non-specific nuclease degradation was observed. The ratio of D-NC to L-NC isolated from individual virus preparations varied and was independent of viral infectivity. A third NC variant, defective-NC (Df-NC), was also identified. This had the lowest density on CsCl gradients (1·2460 ± 0·0046 g/ml). The Df-NC structures were truncated to a uniform length of 87·0 ± 5·8 nm. Diameter measurements were between those of D-NC and L-NC, being 24·4 ± 1·4 nm (outer) and 6·9 ± 0·4 nm (inner core). Like L-NC, the 70K protein was present but in greater amounts, representing as much as 43·7% of the total Df-NC protein mass. RNase A-sensitive nucleic acid was isolated from Df-NC which ranged in size from 1·16 to 0·67 kb with a majority of the material being 0·86 kb in length. For both L-NC and Df-NC, canine CDV convalescent serum reacted with viral N and P proteins in Western blot analyses but not with the 70K protein, suggesting a host cellular origin for the latter.
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Differential Phosphorylation of the Nucleoprotein of Influenza A Viruses
More LessSummaryAn analysis of the nucleoprotein (NP) of 29 different influenza A viruses by phosphopeptide fingerprinting revealed three prototype patterns. The first, which was a complex pattern consisting of six to seven phosphopeptides, another which was relatively simple consisted of two or three phosphopeptides, and a third one which was complex but was missing the main phosphopeptide shared by the two other patterns. Phosphoserine was the only labelled phosphamino acid detected. A tentative deduction of two of the phosphate attachment sites (serine residues at positions 3 and 473) could be made by comparison of the known amino acid sequences of the NPs of 25 strains. No correlation was found between species specificity or subtype or year of isolation of the strains. During the infectious cycle the fingerprint underwent significant changes, indicating subtle phosphorylation and dephosphorylation of the NP at various stages during viral multiplication. Most of the phosphopeptides were metabolically stable; however one major phosphopeptide, which was not found in the NP of mature virions, exhibited a high turnover (presumably serine at position 3). The phosphopeptide fingerprint could be significantly influenced in vivo by the specific stimulation of cellular protein kinase C by the phorbol ester 12-O-tetradecanolyphorbol 13-acetate or by its inhibition with the isoquinoline sulphonamide H7. H7 specifically inhibited the replication of influenza A viruses by deregulation of viral protein synthesis without interfering with the multiplication of a parainfluenza virus (Newcastle disease virus), an alphavirus (Semliki Forest virus) or a flavivirus (West Nile). Therefore the correct phosphorylation of the NP of influenza viruses appears to be essential for influenza virus replication.
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Gangliosides Influence Experimental Influenza Virus Infection in Mice
SummaryInfluenza virus infection in mice may be either stimulated or partially prevented by certain gangliosides, depending on the experimental conditions employed. When injected prior to virus infection gangliosides increased the mortality rate, whereas preincubation with the virus before infection had a protecting effect. Hybrid mice resistant to influenza virus became highly susceptible to infection after injection of a specific ganglioside whereas the corresponding antiganglioside antiserum protected virus-susceptible mice against infection by the virus. These results are discussed in the light of earlier findings that various gangliosides enhance non-specific binding of influenza virus, whereas gangliosides of the GT1b and GD1b type are able to act as specific virus receptors and to promote virus penetration.
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The Immunoglobulin G Subclass Responses of Mice to Influenza A Virus: the Effect of Mouse Strain, and the Neutralizing Abilities of Individual Protein A-purified Subclass Antibodies
More LessSummaryThe IgG subclass responses to cold-adapted (ca) influenza A/Queensland/6/72 virus and purified haemagglutinin H3 was assessed in C57BL/6 and BALB/c mice. In BALB/c mice IgG2a was present as the major subclass in serum, lung and salivary secretions after two doses of ca virus. In contrast, the serum response in C57BL/6 mice was predominantly IgG1 after primary and secondary inoculations of ca virus. However, in lung and salivary secretions no specific subclass was dominant. When purified H3 was used as the inoculum, serum responses were dominated by IgG1 inBALB/c mice after two inoculations whereas all four subclasses were present at equal levels in C57BL/6 mice. Overall the lung and salivary responses detected in C57BL/6 mice were lower than those observed in BALB/c mice with all four subclasses contributing equally to the response in BALB/c mice. The neutralizing and haemagglutination inhibition abilities of the four Protein A–Sepharose-purified IgG subclasses differed between the BALB/c, C57BL/6 and CBA/CaH mice strains. IgG1 and IgG2a were most effective in BALB/c mice and in C57BL/6 and CBA/CaH mice, IgG2a and IgG2b. These results are discussed in terms of the differing abilities of replicating and non-replicating virus to stimulate differential responses in mice and the TH1 and TH2 helper cell concept.
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Sequence, Transcription and Translation of a Late Gene of the Autographa californica Nuclear Polyhedrosis Virus Encoding a 34·8K Polypeptide
More LessSummaryA 1·4 kb region downstream of the DNA polymerase gene of Autographa californica nuclear polyhedrosis virus was sequenced. Two open reading frames (ORFs) were identified of 927 and 474 bases in length. The 927 base ORF encodes a 34·8K protein as determined by in vitro translation of both hybrid-selected RNA and RNA synthesized in vitro from a 927 base ORF template. The predicted amino acid sequence of the 34·8K polypeptide (p34·8) reveals a hydrophobic N terminus, two potential N-glycosylation sites, and potential sites for phosphorylation by casein kinase I and protein kinase C. The p34·8 gene has a strong codon usage bias which is strikingly different from that of the polyhedrin gene. The two 5′ ends of the 927 base ORF transcripts initiate from an ATAAG sequence and a GTAAG sequence 11 and 87 bases upstream of the ATG codon respectively. A short upstream reading frame is present in the leader sequence of the longer RNA. The transcripts have multiple 3′ ends; the most proximal endpoint correlates with a polyadenylation signal overlapping the translational termination codon of the 927 base ORF. Transcripts of the latter were not observed early in the infection cycle but appeared 6 h after infection and were maximally expressed at 12 to 24 h post-infection. The late nature of these transcripts was confirmed by their sensitivity to aphidicolin and cycloheximide, inhibitors of DNA replication and protein synthesis respectively. Attempts to construct viral mutants carrying a deletion of the p34·8 gene and fusion with the β-galactosidase gene suggest that the former gene is essential for viral replication.
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Viral Interference in the Tick, Rhipicephalus appendiculatus. I. Interference to Oral Superinfection by Thogoto Virus
More LessSummaryInterference between arboviruses in a naturally infected tick vector is reported for the first time. Rhipicephalus appendiculatus nymphs were dually infected with Thogoto (THO) virus, a tick-borne virus, similar to members of the family Orthomyxoviridae. In the first series of experiments examining ‘inter-stadial’ interference, larvae were orally infected with a temperature-sensitive (ts) mutant, and after moulting the nymphs were superinfected with the wild-type (wt) virus. In the second series of experiments examining ‘inter-stadial’ interference, nymphs were dually infected by interrupted feeding; the time interval between infective feeds was either shorter than 24 h or lasted for 10 days. Interference was demonstrated by the inability of wt virus to replicate in ticks previously infected with ts virus. Both inter- and intra-stadial interference were observed and complete interference was detected in 78% of dually infected nymphs. A pool of dually infected ticks, in which intra-stadial interference had been detected, failed to transmit the superinfecting virus after moulting.
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Viral Interference in the Tick, Rhipicephalus appendiculatus. II. Absence of Interference with Thogoto Virus when the Tick Gut Is By-passed by Parenteral Inoculation
More LessSummaryGenetic reassortment of Thogoto (THO) virus has been demonstrated in dually infected Rhipicephalus appendiculatus ticks. However previous results showed that oral superinfection is inhibited by interference. To ascertain the site of THO viral interference, ticks were infected parenterally or orally with a temperature-sensitive (ts) mutant of THO virus. Infected ticks were then challenged with wild-type (wt) THO virus via parenteral inoculation. Intra-stadial superinfection was carried out by parenteral inoculation of newly infected engorged ticks whereas inter-stadial superinfection involved inoculation of engorged ticks infected at the previous stage. In both instances viral interference was not observed, i.e. the challenge virus replicated and was delivered by bite to susceptible hosts. Therefore when the gut is bypassed, R. appendiculatus ticks are apparently permissive to dual infection even when there is a delay in the presentation of the superinfecting virus. These results demonstrate that interference following superinfection per os does not occur in the salivary glands, but may occur in the gut and possibly in a secondary site of viral replication such as the synganglion.
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A Cassette Vector for the Construction of Antigen Chimaeras of Poliovirus
SummaryA cassette vector has been constructed which allows the rapid and extensive modification of one of the neutralizing antigenic sites of the Sabin 1 poliovirus vaccine strain, P1/LSc 2ab. Unique restriction endonuclease sites flanking antigenic site 1 have been engineered into a full-length infectious Sabin 1 cDNA clone with minimal alteration to the coding sequence. This facilitates replacement of this region by oligonucleotides encoding foreign amino acid sequences. Our results indicate that this region is highly flexible in terms of the number and sequence of amino acids which can be accommodated.
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Acid Stability of Hepatitis A Virus
More LessSummaryThe acid stability of unpurified and highly purified hepatitis A virus (HAV) was tested andcompared with that of poliovirus type 1, coxsackievirus types A9 and B1 and echovirus type 9. Only HAV had a high residual infectivity after 2 h of exposure to pH 1 at room temperature, remaining infectious for up to 5 h. At 38°C, pH 1, HAV remained infectious for 90 min. Highly purified HAV was found to be infectious for 8 h at pH 1 and room temperature. This indicates that the increased stability is not due to protection by cellular material attached to the virus,but is a virus-specific marker. Under the same conditions, at pH 1 and room temperature, unpurified and highly purified HAV antigens were traceable for 5 and 4 h respectively.
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Propagation of Hepatitis A Virus in Hybrid Cell Lines Derived from Marmoset Liver and Vero Cells
More LessSummaryTo establish monkey liver cell lines with a high susceptibility to hepatitis A virus (HAV), marmoset (Saguinus labiatus) liver cells were fused with Vero cells deficient in hypoxanthine-guanine phosphoribosyltransferase and the resulting hybrid cells were selected in HAT medium. Of four hybrid cell lines obtained (S. 1a/Ve-1 to -4), three (S. 1a/Ve-1, -3 and -4) were equally susceptible to HAV infection. When inoculated with a virus isolated from marmoset liver tissue (10% liver tissue extract) or a faecal virus (10% stool extract) from a human hepatitis A patient, all susceptible cell lines showed a significant elevation of viral antigen activity as seen in radioimmunoassay and/or immunofluorescent antibody assays, at 4 to 6 weeks post-infection (p.i.) with the liver-derived inoculum and at 6 to 8 weeks p.i. with the stool-derived inoculum. In S. 1a/Ve-1 cells, a representative of the susceptible hybrid cell lines, full adaptation of HAV (liver tissue virus concentrate) to cell culture was attained after four serial passages. Thereafter, the virus grew to a plateau titre of 108.5 TCID50/ml at 7 days p.i. in a growth experiment. The infected cells showed no cytopathic effects but eventually a persistent infection was established when a saturated level of virus growth was reached.
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The Polypeptide of M r 14000 of Porcine Transmissible Gastroenteritis Virus: Gene Assignment and Intracellular Location
More LessSummarySynthetic oligopeptides, corresponding to an amino acid sequence encoded by a potential M r 9000 product’s open reading frame (ORF-4) at the 3′ terminus of the transmissible gastroenteritis virus genome, were used to generate rabbit antiserum. These antibodies produced immune complexes with an M r 14000 (14K) polypeptide in infected cells. The 14K product was shown by immune fluorescence to become associated with the cell nucleus, correlating with the onset of nuclear vacuolation, and suggesting a role in pathogenesis for the ORF-4 gene.
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A Herpes Simplex Virus Type 1 Mutant Containing a Deletion within Immediate Early Gene 1 Is Latency-competent in Mice
More LessSummaryWe have investigated the behaviour in mice of the herpes simplex virus type 1 (HSV-1) mutant dl 1403, which contains a deletion within the gene encoding the immediate early polypeptide Vmw110. The deletion was responsible for a reduction in virulence assayed by both the intracranial and footpad routes of inoculation. Following injection into the footpad, d11403 was able to reach the spinal cord and establish a latent infection in sensory ganglia from which virus spontaneously reactivated upon explantation. The Vmw 110 polypeptide is therefore dispensable for the establishment and maintenance of latency and for reactivation from the latent state.
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