- Volume 72, Issue 4, 1991
Volume 72, Issue 4, 1991
- Animal
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A novel subgroup of exogenous avian leukosis virus in chickens
More LessAn avian leukosis virus with a wide host range belonging to a new subgroup for chickens was isolated from meat-type chicken lines. The virus, of which HPRS-103 strain is the prototype, was of low oncogenicity in chickens but appeared to behave like an exogenous leukosis virus. Neutralizing antibodies to the virus were found in three of five meat-type chicken lines, but not in seven layer lines. The virus and its Rous sarcoma virus pseudotype did not replicate in, or transform, mammalian cells.
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Tumour necrosis factor-α, interferon-γ and interferon-β exert antiviral activity in nervous tissue cells
The individual and synergistic antiviral effects of cytokines released by infiltrating immune cells or by cells of the nervous system may play an important role in inhibiting virus spread during infections of the central nervous system (CNS). We examined the antiviral activity against the neurotropic pseudorabies virus (PRV) of interferon-γ (IFN-γ) and tumour necrosis factor-α (TNF-α), and combinations of these cytokines, as compared to that of IFN-β, in rat nervous tissue cells. PRV replicated efficiently in all neural cell types tested, including neurons, astrocytes and oligodendrocytes. The inhibitory effects were determined by quantifying the inhibition of virus plaque formation, yields of infectious virus at various times after infection and synthesis of viral proteins. At a low m.o.i., IFN-γ and IFN-β inhibited viral plaque formation in all cell types; TNF-α was effective only in astrocytes but showed synergy with IFN-γ. At a higher m.o.i., IFN-β inhibited yields of infectious virus more effectively than IFN-γ, whereas TNF-γ had no effect on virus yields and was only marginally synergistic with the antiviral activity of IFN-γ. The yield-reduction assays correlated well with cytokine-induced inhibition of viral protein synthesis. Our results show that both IFN-γ and IFN-β can induce a state of antiviral resistance in neural cells whereas TNF-α is effective only in astrocytes at low m.o.i.; they suggest an antiviral role of cytokines in the immune response to virus infections of the CNS.
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Location of amino acid residues important for the structure and biological function of the haemagglutinin—neuraminidase glycoprotein of Sendai virus by analysis of escape mutants
More LessTo locate sites important for the structure and function of the haemagglutinin—neuraminidase glycoprotein (HN) of Sendai virus, the biological characteristics of antibody-selected escape mutants were correlated with mutations in the primary HN amino acid sequence. An escape mutant virus deficient only in neuraminidase function but with an HN content equal to that of the wild-type virus had an amino acid change at residue 184, implying that this position may be important for maintaining a functionally active enzymic site. In contrast, other escape mutant viruses with reductions in haemagglutination (eightfold) and neuraminidase activities (70 to 80%) had a sharply diminished HN content and substitutions either at residue 375, or double mutations at residues 279 and 461. The loss of biological activity with the concomitant loss of HN content suggests that these sites may be important for the processing and transport of HN, or in maintaining a structure resistant to proteolytic degradation; residue 451 was shown to have an undefined role in fusion activity. The monoclonal antibodies (MAbs) used to isolate the mutant viruses included those of the IgA and IgG classes and were divided into four operational groups based on their haemagglutination-inhibition pattern against the selected mutants. MAbs of the IgA class recognized epitopes overlapping with (group A) as well as epitopes distinct from (groups C and D) those recognized by the IgG class; group B included only IgG antibodies. The epitopes recognized by IgA antibodies may identify residues important for the secretory immune response to the HN molecule.
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Detection of phocid distemper virus RNA in seal tissues using slot hybridization and the polymerase chain reaction amplification assay: genetic evidence that the virus is distinct from canine distemper virus
More LessSlot hybridization and the polymerase chain reaction (PCR) after reverse transcription (RT) were used to detect RNA extracted from tissues of seals after naturally occurring disease and experimental infection with phocid distemper virus (PDV). A phosphoprotein (P) gene-specific cDNA served as a probe for both slot hybridization and the identification of PCR-generated fragments by Southern blotting. As primers for the PCR assay PDV P gene-derived oligonucleotides were used. Hybridization, PCR and partial nucleic acid sequence analysis clearly demonstrated that PDV is a distinct virus (most closely related to canine distemper virus) within the morbillivirus group. PCR, when combined with Southern blot hybridization, was clearly superior to slot hybridization and more sensitive than cell culture isolation and immunofluorescence assays for the detection of virus in tissues. Considerable amounts of viral RNA could be demonstrated in the lungs and spleens. In experimentally infected animals a large quantity of virus-specific RNA was additionally found in colon samples. Using RT-PCR in combination with Southern blotting, PDV could be demonstrated in buffy coat cells using a simple and fast cell lysis procedure.
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Baculovirus-directed high level expression of the hepatitis delta antigen in Spodoptera frugiperda cells
More LessThe hepatitis delta antigen (HDAg) is a multifunctional protein. It forms the core-like structure of the hepatitis delta virus (HDV) but also enhances replication of HDV in the nucleus of the hepatocyte. A cDNA fragment encoding HDAg was inserted adjacent to the polyhedrin promoter of Autographa californica nuclear polyhedrosis virus present in the baculovirus transfer vector pVL941. After transfection of Spodoptera frugiperda (Sf9) cells a recombinant baculovirus Acδ1 was isolated and purified using filter hybridization techniques. Sf9 cells infected with Acδ1 express the HDAg as a non-fused, non-glycosylated protein with an abundance of up to 25% of the total cellular protein mass. Immunoblot analysis using a human polyclonal anti-HD conjugate identified a 22K and a 24K protein in the nucleus of Acδ1-infected Sf9 cells. Electron microscopic studies using immunogold labelling showed that the recombinant HDAg (recHDAg) was associated with the hetero-chromatin of the Sf9 cells. The recHDAg produced by Sf9 cells elicited anti-HD antibodies in chimpanzees when injected intramuscularly.
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Characterization of carbohydrates linked to rubella virus glycoprotein E2
More LessRubella virus contains two envelope glycoproteins, E1 and E2. The amino acid sequence for both glycoproteins is known, as is the number of N-glycosylation sites. This study has demonstrated the presence of O-linked carbohydrates bound to E2 and determined structural characteristics of the N-linked oligosaccharide chains. O-linked sugars were found to be resistant to digestion with N-glycanase but sensitive to beta-elimination with alkaline borohydride. After treatment with neuraminidase, O-linked sugars bound to peanut agglutinin, suggesting the presence of the disaccharide galactose-N-acetylgalactosamine, masked by sialic acid. The N-linked oligosaccharides were large, probably four-branched, and showed a lectin binding pattern suggesting the complex type, with terminal Gal, GlcNAc and sialic acid. No Endo H-sensitive carbohydrates were detected.
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In vitro synthesis of West Nile virus proteins indicates that the amino-terminal segment of the NS3 protein contains the active centre of the protease which cleaves the viral polyprotein after multiple basic amino acids
More LessA virus-encoded protease that cleaves after multiple basic amino acid residues has been implicated in the processing of the flavivirus polyprotein. Recently, a computer search of amino acid residues which might form the active site of a protease led to the suggestion that the amino-terminal segment of the NS3 protein represents a serine protease. To examine this possibility we constructed an mRNA which encodes a polyprotein with an amino-terminal signal sequence derived from the influenza virus haemagglutinin, followed by a segment of the West Nile flavivirus polyprotein which includes the non-structural (NS) proteins NS2A, NS2B and the amino-terminal part of the NS3 protein. This polyprotein contains two sequences, located at the termini of the NS2B protein, which are cleaved by the viral protease that cleaves after multiple basic residues in the authentic polyprotein. The proteins that are generated by this mRNA during in vitro translation in the presence of rough endoplasmic reticulum membranes indicate that these two proteolytic cleavages occur in vitro. In vitro translation of polyproteins shortened at the carboxy terminus shows that a polyprotein which does not contain the complete set of proposed catalytic residues present in the NS3 protein segment accumulates as a membrane-associated molecule without proteolytic processing. Similarly, substitution of residue histidine 51 of the NS3 polyprotein segment, which is predicted to be part of the protease catalytic centre, with an alanine residue, blocks the processing of the polyprotein in vitro.
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Breakdown of the blood-brain barrier during dengue virus infection of mice
More LessA breakdown of the blood-brain barrier occurred in mice inoculated intracerebrally (i.c.) or intraperitoneally (i.p.) with dengue virus type 2 (DEN2). This resulted in leakage of protein-bound Evans blue dye and 51Cr-labelled erythrocytes into the brain tissue. The leakage increased with time after infection and coincided with an increase of a DEN2-induced cytokine, the cytotoxic factor (CF), in the spleens of such mice. The titres of virus in the brain increased exponentially in i.c. inoculated mice but the virus was not detected in brains of mice given DEN2 by the i.p. route. Similar breakdown of the blood-brain barrier also occurred in mice inoculated intravenously with CF; the damage was dose-dependent and the vascular integrity was restored during the 3 h period after inoculation. Treatment of mice with antihistamine drugs, blocking H1 or H2 receptors, decreased the DEN2-induced protein leakage by up to 50% in i.c. inoculated mice and up to 92% in those inoculated i.p. Indomethacin, a prostaglandin synthetase inhibitor, had no effect. In i.c. inoculated mice protein leakage was inhibited by about 60% by treatment with CF-specific (CFA) or DEN2-specific antisera (DEN2A) whereas protection was complete with the combined treatment with both antisera. On the other hand, in i.p. inoculated mice the inhibition of protein leakage was 80 to 89% with CFA. These findings show a breakdown of the blood-brain barrier leading to cerebral oedema during DEN2 infection which is mediated via the release of histamine by a virus-induced cytokine.
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Construction and nucleotide sequence analysis of an infectious DNA clone of the autonomous parvovirus, mink enteritis virus
We have cloned the replicative form (RF-) DNA of mink enteritis virus (MEV), constructed an infectious recombinant plasmid containing MEV DNA and determined the nucleotide sequence of the cloned MEV DNA. RF-DNAs were detected and infectious virus was generated when the recombinant plasmid containing the entire MEV genome was introduced into feline kidney cell cultures. The MEV genome was 5094 nucleotides (nt) in length; the 3′ end of the virion strand contained a 205 nt palindromic sequence and the 5′ end a 62 nt palindromic sequence that could assume Y- and U-shaped configurations, respectively. The 5′ end of the virion strand had a direct repeat of 61 nt at the carboxyl terminus of the capsid protein gene. The organization of the MEV genome is similar to those of canine parvovirus (CPV) and feline panleukopenia virus (FPLV); there are two large open reading frames (ORFs), one in the 3′ half and the other in the 5′ half of the genome, with coding capacities of 668 and 722 amino acid residues, respectively. Both are in the same reading frame and no significant ORFs are apparent in the virion strand (negative-sense strand). Possible functional promoter motifs are located at map unit (m.u.) 4.5 and m.u. 40, and a possible functional poly(A) signal is located at m.u. 96. The nucleotide and amino acid sequence homology with CPV and FPLV is greater than 98%, consistent with the hypothesis that MEV and CPV are host-range variants of FPLV.
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Positive and negative E2-independent regulatory elements in the long control region of bovine papillomavirus type 4
More LessThe long control region (LCR) of bovine papilloma-virus type 4 demonstrated enhancer activity when cloned upstream of a bacterial chloramphenicol acetyl-transferase reporter gene under thymidine kinase promoter control. Deletion analysis of the LCR revealed the presence of several positive and negative control elements, all of which could function independently of the viral E2 trans-activator. Each of the three positive elements present appeared to be paired with a negative element which modulated its activity. DNase I footprinting was used to identify protein binding sites within the LCR, which might represent these control elements. The results suggest a highly complex and finely tuned control of viral gene expression.
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Presence and distribution of human papillomavirus sense and antisense RNA transcripts in genital cancers
More LessRNA transcription in eight human papillomavirus (HPV) type 16-positive genital carcinomas and in two cervical squamous cell carcinoma (SCC)-derived cell lines was analysed by in situ hybridization using 125I-labelled subgenomic riboprobes. Transcripts corresponding to the E6 and E7 open reading frames were always present, except within the keratinizing layers of differentiated SCCs. Intranuclear E1 gene transcripts were detectable in both cell lines and some tumours whereas E2/E4 transcripts were absent from five of seven assessable tumours, suggesting transcription from integrated viral DNA. When mRNA sense riboprobes were used as controls, no signal was seen in the two cell lines; however, three tumours contained a focal, intense nuclear RNase-sensitive signal using mRNA sense riboprobes. This antisense RNA signal mapped across the whole genome including the non-coding region. In one tumour, the presence of antisense RNA was independently confirmed by using E7 and E2/E4 RNA probes of both orientations in RNase protection assays. Transcription of antisense RNA may be a natural feature of some HPV-positive genital tumours and its possible role in modulating cell behaviour in vivo requires further investigation.
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Investigation of herpes simplex virus type 1 genes encoding multiply inserted membrane proteins
The herpes simplex virus type 1 genome contains four open reading frames (ORFs) which are predicted to encode hydrophobic proteins with the potential to cross a membrane several times. The products of these genes (genes UL10, UL20, UL43 and UL53) have not previously been identified. To investigate the role of these proteins in the virus life cycle, we attempted to inactivate the genes individually by inserting the lacZ gene from Escherichia coli within the ORFs. Using this approach we have isolated insertion mutants for UL10 and UL43, as well as a deletion mutant lacking the majority of the UL43 ORF. The growth of the UL10-lacZ virus was slightly impaired in tissue culture compared to that of the wild-type virus parent, whereas the growth of the UL43 mutants was indistinguishable from that of wild-type virus. Furthermore, deletion of the majority of the UL43 ORF did not impair the ability of the virus to replicate in vivo at the periphery, or to spread to and replicate within the nervous system, in a mouse ear model. Repeated attempts to isolate lacZ insertion mutants for UL20 and UL53 were unsuccessful, suggesting that these genes may be essential for virus growth, at least in tissue culture. Using antipeptide sera, the products of genes UL10 and UL20 have been detected.
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Establishment of latency in vitro by the herpes simplex virus type 1 mutant in 1814
More LessThe herpes simplex virus type 1 (HSV-1) mutant in1814 possesses an insertion mutation that abolishes trans-activation of immediate early (IE) transcription by the virion protein Vmw65. Interactions between in1814 and the host cell were examined by use of an in vitro latency system which relies on infection of human foetal lung (HFL) cells at 42 °C to prevent lytic growth of virus. Mutant in1814 was retained in HFL cells after infection at low m.o.i. and incubation at 42 °C, and was reactivated by superinfection of monolayers with viruses that express the HSV-1 IE protein Vmw110. Moreover, latency was established by in1814 in an analogous manner at 37 °C. The low cytotoxicity of in1814 enabled an investigation of latency after infection at high m.o.i. (five particles per cell) to be undertaken. At 42 °C, or at 37 °C in the presence of an inhibitor of DNA synthesis, in1814 DNA was maintained at low abundance (one to eight copies per infected cell) in a non-linear configuration. The absence of trans-activation by Vmw65 therefore predisposes HSV to latency, as opposed to lytic growth, in HFL cells, resulting in the retention of the genome in a form resembling that found in vivo.
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Glycoprotein C of herpes simplex virus type 1 is essential for the virus to evade antibody-independent complement-mediated virus inactivation and lysis of virus-infected cells
More LessGlycoprotein C (gC) of herpes simplex virus type 1 (HSV-1) is a receptor for the complement component C3B. We have previously isolated HSV-1 gC− strains (TN1, TN2 and TN3) from a patient with recurrent keratitis at three different times. These are very rare isolates because gC was thought to be essential for the virus in vivo. To determine whether gC modifies the interaction of complement with cell-free virus or virus-infected cells, we constructed gC+ recombinant viruses in which the intact gC gene of strain KOS was inserted into the TN1 virus genome. TN1 virus was inactivated by complement and TN1 virus-infected cells were lysed by complement; however, gC+ recombinant viruses became resistant to these effects of complement. These results suggest a role for gC in protection of both the virion envelope and the infected cell surface against damage by complement. TN1 virus was inactivated by complement from rats (Wistar, WKA, F344 and SD), guinea-pigs (Hartley) and humans, but not by complement from mice (C3H, DDD and BALB/c), which indicates that mice seem to be inappropriate as an experimental model for the study of HSV infection in which complement factors need to be considered.
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Studies on glycoprotein 13 (gp13) of equid herpesvirus 1 using affinity-purified gp13, glycoprotein-specific monoclonal antibodies and synthetic peptides in a hamster model
Hamsters were immunized with either an affinity-purified preparation of equid herpesvirus 1 (EHV-1) glycoprotein 13 (gp13) or synthetic peptides representing three sequences within the homologous glycoprotein of EHV-4, resulting in the production of anti-peptide (in the case of peptide-immunized animals) or antivirus antibodies. The sera from gp13-immunized hamsters contained antibodies which showed virus-neutralizing activity and complement-mediated antibody lysis of EHV-1-infected target cells. These hamsters were protected from EHV-1 challenge. The characteristics of a panel of anti-gp13 monoclonal antibodies (P28, P17, 14H7, 16E4 and 16H9) were assessed both in vivo and in vitro. 16E4 and P28 showed high levels of complement-mediated neutralization of virus, complement-mediated lysis of virus-infected target cells and passive protection of hamsters. Furthermore, epitope mapping studies demonstrated that this glycoprotein contains a neutralizing epitope recognized by EHV-1-immune horse serum. The data imply that gp13 has potential as a candidate antigen for a molecular vaccine.
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The influence of porcine recombinant interferon-α1 on pseudorabies virus infection of porcine nasal mucosa in vitro
More LessTo determine the effect of interferon (IFN) on the pathogenesis of pseudorabies virus (PRV), porcine nasal mucosal explants were first treated with recombinant porcine methionyl-IFN-α1 and then infected with one of three strains of PRV. The stroma of treated mucosal explants were protected against infection with virulent PRV or PRV of intermediate virulence because the infection was restricted to the epithelial cells. In contrast, untreated mucosal explants were readily infected by virulent PRV or PRV of intermediate virulence; the infection spread from epithelial cells to stromal fibroblasts. Avirulent PRV infection was restricted to the epithelial cells of treated and untreated mucosal explants. IFN treatment limited the extent of all three PRV infections in the epithelial cells. Cultured porcine fibroblasts and porcine kidney cells were also treated with IFN and subsequently infected with PRV; infection was prevented in most porcine fibroblasts and the virus yield from porcine kidney cells was reduced. Budding of virulent PRV nucleocapsids through the inner nuclear membrane was observed more frequently in treated than in untreated mucosal explants and enveloped virus particles accumulated between the inner and outer nuclear membranes, indicating that the membrane-associated events of PRV replication had been affected. We conclude that IFN-α protects stromal fibroblasts against PRV infection and reduces virus replication in epithelial cells.
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Properties and evolutionary relationships of the Marek’s disease virus homologues of protein kinase, glycoprotein D and glycoprotein I of herpes simplex virus
More LessThe deduced amino acid sequences of the open reading frames (ORFs) mapping in the short unique segment (US) of Marek’s disease virus (MDV) reported in the accompanying paper have been analysed using computer programs to determine their relationships to herpesvirus proteins. Analysis of the catalytic domains of protein kinases showed that the MDV kinase (MDV PK) was closely related to the alphaherpesvirus protein kinase mapping in US. The results also showed that the MDV PK was more closely related to the cellular kinases that control cell division than to the proto-oncogenes c-src and c-mos and it was predicted that the MDV PK would phosphorylate serine/threonine. The MDV homologue of herpes simplex virus (HSV) glycoprotein D (gD) contained several residues that were conserved in mammalian herpesviruses. In particular, six cysteines were perfectly aligned in all the gDs and there were numerous conservative substitutions. Although only approximately 65% of the MDV homologue of glycoprotein I (gI) of HSV has been sequenced, it was clear that a significant number of amino acid residues including four cysteines were conserved in the gI homologues of MDV and mammalian herpesviruses. Further analysis suggested that MDV gD was more closely related to the gDs of pseudorabies virus (PRV) and equine herpesvirus 1 than to the gD of HSV-1 and HSV-2. It was noted that HSV-2 glycoprotein G (gG), PRV gX and MDV gD were related and that MDV ORF4 was related to MDV gD and probably to HSV-1 gG. The results have shown a clear relationship between the genes of MDV and their counterparts in mammalian alphaherpesviruses and are consistent with the idea that MDV glycoprotein genes in US might have arisen by a process of gene duplication and independent evolution.
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DNA sequence and organization of genes in a 5.5 kbp EcoRI fragment mapping in the short unique segment of Marek’s disease virus (strain RB1B)
More LessThe DNA sequence of a 5.5 kbp EcoRI fragment located in the short unique region (US) of the ‘highly oncogenic’ strain RB1B of Marek’s disease virus (MDV) was determined. The sequence contained six open reading frames (ORFs), four of which were homologous to proteins mapping in the US region of herpes simplex virus type 1 (HSV-1). These include the homologues of HSV-1 protein kinase, glycoprotein D (gD), glycoprotein I (gI) and US2 which is of unknown function. The MDV ORFs had a marked bias for A or T in the third codon position and analysis of the dinucleotide frequencies showed a marginal deficit in ApG/CpT but no overall deviation of CpG from random expectations. Comparison of genes in the US region of MDV to herpesvirus proteins confirmed and extended our previous observation that MDV is more closely related to alphaherpesviruses than to gamma-herpesviruses. We also showed that MDV possessed a homologue of HSV-1 gD which is lacking in varicellazoster virus (VZV) but that MDV probably lacked homologues of US4 and US5 of HSV-1. These results show that in contrast to the genes in the long unique region which were grossly collinear in HSV, VZV and MDV, those mapping in US show greater diversity.
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The use of β-galactosidase fusion proteins encoding the early region 1 transforming proteins of adenovirus type 12 to examine the humoral response in tumour-bearing animals
More LessSera from 26 rats bearing tumours induced by wild-type (wt) and mutant human adenovirus type 12 (Ad12), or by cells transformed with these viruses, were analysed for antibodies against the early region 1 (E1) transforming proteins. Six Ad12-β-galactosidase fusion proteins encoding different regions of the Ad12 E1 proteins were constructed. The sera from the tumour-bearing animals reacted most strongly with the fusion protein encoding the N terminus of the E1A protein. Tumour-bearing rats exposed to the E1B 54K and 19K proteins showed strong reactions with the N terminus of the 54K protein and the C terminus of the 19K protein. Monospecific polyclonal antisera were raised against five of the fusion proteins by immunization of rats and rabbits; these sera cross-reacted with the purified native protein. No antibodies could be obtained which recognized a fusion protein containing amino acids 136 to 268 of the 54K protein. The fusion proteins were also used to purify monospecific antisera from tumour-bearer sera using affinity chromatography.
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Production of dimer-specific and dengue virus group cross-reactive mouse monoclonal antibodies to the dengue 2 virus non-structural glycoprotein NS1
More LessA panel of mouse monoclonal antibodies (MAbs) raised against the non-structural glycoprotein NS1 of dengue 2 virus (PR159) was studied for cross-reactivity with the NS1 protein of other dengue virus serotypes and other members of the Flaviviridae using immuno-blotting. Most of the 35 anti-NS1 MAbs were found to be specific for dengue 2 virus NS1 (some of which were specific for the native, dimeric form of this protein), but others were found to cross-react within the dengue virus group. This latter group of MAbs, although dominated by MAbs defining a dengue 2 and 4 virus subgroup, also contained some MAbs that were shown to cross-react with both linear (sequential) and conformational epitopes common to the NS1 glycoproteins of all four dengue virus serotypes. Several of these MAbs were also able to cross-react with other flaviviruses, most notably viruses from the Japanese encephalitis antigenic complex. Although cross-reactive epitopes were previously demonstrated on this glycoprotein using polyclonal sera from dengue virus-infected animals and human, this is the first report of the isolation of MAbs which define these determinants and which will allow their further analysis.
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