- Volume 59, Issue 2, 1982
Volume 59, Issue 2, 1982
- Bacterial
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Analysis of Proteins Induced by the Salmonella typhimurium Phage P221, a Hybrid between Serologically and Morphologically Unrelated Phages P22 and Fels 1
More LessSUMMARYThe Salmonella phage P221 is a hybrid between the morphologically and serologically unrelated Salmonella phages P22 and Fels 1. P221 carries about 30% of P22 DNA containing a number of the early genes. Head and tail proteins are morphologically and serologically indistinguishable from those of Fels 1. The early proteins synthesized in Salmonella typhimurium strain Q1 after P221 infection were pulse-labelled with 35S and analysed by gel electrophoresis and autoradiography. These P221 early proteins were compared with early P22 proteins in an effort to detect proteins specified by the homologous region between P22 and P221. This analysis showed that nine P221 protein bands correspond to P22 protein bands. Seven of these protein bands appeared early, about 6 min after infection, and two additional protein bands appeared about 18 min after infection. The origin of these nine protein bands was also determined by protein synthesis patterns of P22 amber mutants. A large number of previously isolated P22 amber mutants were subdivided as to their location within the homologous or non-homologous region by complementation and marker rescue experiments. Four P22 amber mutants located within the homologous region were chosen for analysis of their early proteins. When the non-permissive host Q1 was infected with a P22 amber mutant in gene 24 (the gene which initiates the transcription of the P22 phage genome) no phage protein bands were observed. Similarly, when two P22 amber mutants located in gene 12 and gene 23 infected the non-permissive host Q1 no phage protein bands were detected. Mutants of the gene for endolysin showed that one specific protein band was lacking in the non-permissive host. When the amber suppressor host Qsu + was infected with any of the above amber mutants all protein bands were found. By the use of an amber mutant in gene 3 of the P22 late gene region located outside the P22–P221 homologous region, we showed that mutations in the non-homologous region did not affect the synthesis of these nine proteins. The genetic origin of proteins found in mature P221 particles was determined by subjecting proteins of purified P221, P22 and Fels 1 phage particles to analysis by SDS-gel electrophoresis. It was concluded that P221 and Fels 1 share the same head, tail and internal proteins in mature phage particles, whereas none of the protein components of these mature phage particles is the same as those of P22 particles.
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- Animal
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Aspects of Thymidine Metabolism and Function in Cultured Mammalian Cells Infected with Herpes Simplex Virus Type 1
More LessSUMMARYWe have investigated aspects of thymidine metabolism and function in cultured mammalian cells infected with herpes simplex virus under conditions in which virus DNA synthesis was either permitted, or was prevented by inhibiting the virus-induced DNA polymerase with phosphonoacetate. In 30 min pulse-labelling experiments the rates of [3H]thymidine transport into cells and its subsequent phosphorylation both reached maximum values about 6 h after infection. During the next 17 h these rates remained relatively constant in the absence of phosphonoacetate but declined to about 50% of the 6 h value in the presence of this inhibitor. When the radioactive thymidine was present continuously throughout the infection the accumulated intracellular acid-soluble radioactivity reached maximum values at about 9 h. In the absence of phosphonoacetate this declined thereafter, but it remained relatively constant when virus DNA synthesis was prevented. This suggests some established equilibrium between the continuing entry of thymidine into cells and its subsequent removal by excretion. Excretion of thymidine-derived radioactivity was initially established by determining the fate of isotopically labelled host cell DNA. During 24 h of infection about 50% of the host cell DNA was rendered acid-soluble and of this 60 to 70% was excreted from the cells. High pressure liquid chromatographic analysis of the intracellular acid-soluble radioactivity showed only phosphorylated thymidine derivatives, whereas the excreted radioactivity was exclusively in thymidine. Excretion of intracellular radioactive molecules derived directly from [3H]thymidine in the medium was also observed, but only when virus DNA synthesis was inhibited with phosphonoacetate.
Simple kinetic studies with the purified virus-induced DNA polymerase showed that a straight line double-reciprocal plot was obtained when dGTP was used as the limiting substrate (K m = 0.8 µm, V max = 330 nmol dGTP incorporated/10 min) but that a biphasic plot was obtained when dTTP was limiting (K m1 = 0.5 µm, V max1 = 208 nmol dTTP incorporated/10 min; K m2 = 5 µm, V max2 = 370 nmol dTTP incorporated/10 min).
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Fine Structure of Virus Chromatin in Thin Sections of SV40-infected Cells: A Cytochemical and Autoradiographical Study
More LessSUMMARYThe ultrastructural organization of virus chromatin was studied within nuclei prepared from CV1 cells (cultured monkey kidney cells) lytically infected with SV40 virus (simian virus 40) by a procedure which allows a mild loosening of nucleoproteins. In addition to dispersed host components, DNA-containing nucleoplasmic structures could be identified as virus chromatin. Both standard staining for structure and specific staining for DNA clearly revealed in thin sections the nucleosomal structure of well-extended virus chromatin as well as alignments of virions on host chromatin. In addition, replicating and transcribing virus chromatins were abundant as revealed by high-resolution authoradiography. Therefore, the procedure of loosening of nucleoproteins used in this report also preserves the active SV40 chromatin and allows the in situ visualization in Epon sections of transcription and replication of the virus genome.
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Replication of Lactate Dehydrogenase-elevating Virus in Macrophages
SUMMARYCultures of starch-elicited peritoneal mouse macrophages in medium containing macrophage growth factor (MGF) were infected with lactate dehydrogenase-elevating virus (LDV) and, after various times in culture, LDV production was monitored as a function of time by infectivity titrations in mice, by measuring [3H]uridine incorporation into LDV RNA and extracellular LDV, by autoradiographic analysis of the proportion of productively infected cells and by electron microscopy. Regardless of the age of the cultures when infected with LDV, only a small proportion of the macrophages (generally between 3 and 20% of the total) became productively infected after a primary infection; maximum virus RNA synthesis and virus production occurred during the first 24 h after infection and then decreased precipitously. Productively infected macrophages could be readily recognized in electron micrographs of 24-h infected macrophage cultures and in sections of spleens from 24-h infected mice by characteristic morphological alterations. These consisted of formation of clusters of double-membrane vesicles with a diameter of 100 to 300 µm, budding of nucleocapsids into vesicles with single membranes and accumulation of mature virions in these vesicles. One to 4 days later, however, such cells were no longer found in infected cultures or spleens of infected mice and superinfection did not restimulate LDV replication. Cultures established with macrophages from 1-day LDV-infected mice also did not support LDV replication. We conclude that LDV replication in cultures or mice is limited to a single cycle in a subpopulation of macrophages and that infection leads to cell death and rapid phagocytosis of the dead cells by the resistant, uninfected macrophages.
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Replication of Lactate Dehydrogenase-elevating Virus in Macrophages
SUMMARYA primary infection of peritoneal macrophage cultures with the lactate dehydrogenase-elevating virus (LDV) results in productive infection of 3 to 20% of the cells. When cultures were incubated in the absence of macrophage growth factor (MGF), LDV production ceased after a single cycle, but in cultures in which macrophage replication was stimulated by the presence of MGF LDV production continued for several weeks at a low level, representing not more than 1% of that observed during the acute phase. Significant amounts of interferon were not present in either acutely or persistently infected cultures, and treatment of persistently infected cultures with anti-interferon globulin or superinfection with LDV did not significantly stimulate LDV replication. Macrophage cultures established with peritoneal macrophages from LDV-infected mice also showed only a low level of LDV replication and were resistant to superinfection by LDV. Mouse hepatitis virus, Semliki Forest virus and vesicular stomatitis virus, on the other hand, replicated normally in LDV-persistently infected macrophage cultures. LDV replication was relatively resistant to interferon whether added to the cultures or generated endogenously by infection with Newcastle disease virus or defective-interfering (DI) particles of vesicular stomatitis virus. Temperature-sensitive mutants or DI particles of LDV were not detected in LDV-persistently infected cultures or chronically infected mice. The results support our hypothesis that the decrease in LDV production in mice or macrophage cultures at the end of the acute phase results from the destruction of the subpopulation of macrophages that is permissive for LDV, and that the low level persistent infection involves the passage of the virus to new permissive cells that are generated continuously, although at a low rate, from non-permissive precursor cells.
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Demonstration of Interference between Dengue Virus Types in Cultured Mosquito Cells using Monoclonal Antibody Probes
D. Dittmar, A. Castro and H. HainesSUMMARYCultured Aedes albopictus cells (clone C6/36), persistently infected (PI) with dengue virus type 1 (dengue-1) were found resistant to superinfection with dengue virus type 3 (dengue-3). This was determined by indirect immunofluorescent (IF) staining of cultures using monoclonal antibody against a dengue-3 type-specific antigen. Dengue-1 PI cultures stained with this antibody 3 days after superinfection with dengue-3 virus (m.o.i. of 2) had dengue-3 antigen in 0.1 to 1.0% of the cells. Control cultures infected with dengue-3 at the same multiplicity contained dengue-3 antigen in greater than 90% of the cells. The resistance to superinfection was not interferon-mediated, and occurred within 20 h after primary infection. In cultures simultaneously infected with two dengue virus types, one virus type was excluded from replication in most cells. A small population of cells was also found (about 1%) that contained type-specific antigen of both dengue virus types.
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Three Strains of European Foot-and-Mouth Disease Virus are Highly Conserved in the 3′-Termini and Highly Variable in the Genes of Two Capsid Proteins
More LessSUMMARYRestriction enzyme-generated subgenomic fragments of cloned cDNA prepared from RNA of the strain O1 Kaufbeuren (O1K) of foot-and-mouth disease virus (FMDV) were compared qualitatively and quantitatively for sequence complementarity with radioactive RNA from strains C Oberbayern (CObb) and A2 Spain (A2S) in hybridization experiments on nitrocellulose membranes. Quantitative comparison of nucleic acid sequences neighbouring (CObb/O1K) or including (A2S/O1K) the 3′ end of the virus genomes demonstrated more than 80% homology. In contrast, sequences coding for the capsid proteins VP1 (10%, CObb/O1K; 16 to 21%, A2S/O1K) and VP3 (12%, A2S/O1K) were remarkably heterologous. Sequences downstream from the gene for VP1, i.e. those coding for non-structural proteins, showed 23 to 51% homology to both RNAs except for the area coding for protein P56a. Here, the observed homology was 82% to CObb and 39 to 46% to A2S.
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Location and Characterization of the Antigenic Portion of the FMDV Immunizing Protein
More LessSUMMARYPurified foot-and-mouth disease virus (FMDV) of type O1K was treated with several endopeptidases of differing specificity. The immunizing protein VPThr was cleaved into two detectable fragments by all enzymes except for glutamic acid-specific Staphylococcus aureus V8 protease. The longest fragments were generated by mouse submaxillary gland protease and the shortest by trypsin treatment of the intact virion. Several fragments, including the peptides resulting from the cyanogen bromide (CNBr) cleavage of the isolated protein VPThr, were characterized in terms of their molecular weights, N- and C-terminal amino acids, and ability to induce virus-specific antibodies. The order of the fragments along the protein was determined, and then located on the amino acid sequence of the protein. Two enzyme-sensitive areas of the protein were found on the surface of the virion: between sequence positions 138 and 154 and between portion 200 and the C terminus. Peptides containing these sections were able to induce neutralizing antibodies against the homologous FMDV. When the virus was treated with trypsin or with chymotrypsin, several amino acids between the detectable fragments were lost and the infectivity of the virus was reduced. The infectivity was retained, however, when the enzyme treatment resulted in cleavage of protein with no loss of amino acids or only the cutting away of the C-terminal section. These results suggest that the property of cell attachment is restricted to small regions of the surface of the virus particle.
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Characterization of Strains of Type 3 Poliovirus by Oligonucleotide Mapping
More LessSUMMARYT1 RNase oligonucleotide maps of RNA prepared from type 3 poliovirus were shown to be highly characteristic of the strain from which they were prepared. Strains isolated from paralytic cases of poliomyelitis temporally associated with live poliovirus vaccination were shown to be very closely related to the Sabin vaccine strain. Comparison of strains isolated in 1962, and strains isolated between 1973 and 1975 indicated that strains derived from the Sabin vaccine strain have displaced other circulating strains of type 3 poliovirus in the U.K. as a result of the use of live polio vaccine.
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Structural Study of Vesicular Stomatitis Virus G Protein in the Virion Envelope
More LessSUMMARYSome structural properties of the vesicular stomatitis virus (VSV) G protein were examined in virions and isolated envelope fragments. We have shown that in the virion a portion of the G protein extends through the lipid envelope and that this part of the molecule can be cleaved by chymotrypsin. Envelope fragments isolated from VSV without the use of detergents maintained the structural characteristics of the G protein found in intact virions. In addition, we provide evidence that at least some of the isolated envelope fragments have both sides of the bilayer exposed to added reagents, suggesting that this preparation would be useful for in vitro reassociation experiments.
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Processing of the env Gene Products of Moloney Murine Leukaemia Virus
More LessSUMMARYThe initial env gene polyproteins present in Moloney murine leukaemia virus (M-MuLV)-infected NIH/3T3 cells were examined to determine their relationship to each other as well as their role in generating env gene products gp70, p15(E) and p12(E). Steady-state labelling with [3H]glucosamine revealed anti-gp69/71 immunoprecipitable proteins of mol. wt. 93000 (gPr93env), 83000 (gPr83env) and 70000 (gp70), whereas similar labelling with [3H]fucose showed only two bands of anti-gp69/71 immunoprecipitable radioactivity migrating in SDS-polyacrylamide gels with gPr93env and gp70. Pulse-chase experiments employing [3H]leucine labelling instead of labelled sugars failed to detect gPr93env using similar techniques. The gPr83env was the only polypeptide detected in 15 min [3H]leucine pulselabellings, whereas gPr83env, gp70, p15(E) and p12(E) were detected in chase experiments using appropriate antisera in immunoprecipitation experiments. Pretreatment of infected cells with tunicamycin, an inhibitor of glycosylation, allowed the synthesis of a major band at mol. wt. 62000 (Pr62env) and a minor band of 73000 mol. wt. at the expense of gPr83env. In pulse-chase experiments conducted in the presence of tunicamycin, Pr62env increased during the early chase period but disappeared during the later stages of the chase. No product of Pr62env was detected. Cation-exchange chromatography of tryptic digests of radioactive tyrosine-labelled gPr83env, Pr62env and gp70 showed sequence relationships among the three proteins. Comparison of the two-dimensional fingerprints of [3H]leucine-labelled gPr83env and the mature proteins gp70 and p12(E) support their precursor-product relationship. Of interest is the observation that gp70 and p12(E) seemed to share a few leucine-containing tryptic peptides. These results provide strong evidence that gPr83env is the primary product of the env gene which, upon tunicamycin treatment, is synthesized as a subglycosylated protein, Pr62env. It appears that gPr83env undergoes further modification of its core oligosaccharide structure as detected by fucosylation to yield gPr93env. Our inability to detect gPr93env by [3H]leucine labellings suggests a close chronological relationship between fucosylation and cleavage of the precursor polyprotein, suggesting that cleavage of gPr93env yields gp70 and p15(E). The latter is further cleaved to yield p12(E) plus a polypeptide containing the C-terminal end of p15(E).
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Slow Virus Replication: the Role of Macrophages in the Persistence and Expression of Visna Viruses of Sheep and Goats
SUMMARYLentiviruses of sheep and goats cause slowly progressive diseases of the central nervous system (visna), lungs (maedi) and joints (arthritis) in their natural hosts. However, the virus target cell(s) in these diseases are still unknown. In this report, using laboratory-adapted Icelandic visna virus and several field strains recently obtained from sheep and goats with natural disease in the U.S.A., we show that macrophages became persistently infected when inoculated in culture. Furthermore, macrophages were an invariable source of virus from experimentally and naturally infected animals. Virus-producing macrophages developed minimal cytopathic changes and virus assembly occurred mainly intracellularly, accumulating in cytoplasmic vacuoles. In contrast to macrophages, sheep choroid plexus fibroblasts developed syncytial cytopathic changes after inoculation and virus maturation occurred at the cell surfaces. Replication of the Icelandic virus was highly productive in this system but that of the field viruses was very inefficient. In some cases these agents failed to replicate in the fibroblasts and no cytopathic effect occurred. This block in the field virus replication was, however, overcome when infected nonproducer fibroblasts were co-cultivated with macrophages. In these cases, virus production with attendant cytopathic effect in the fibroblasts required the continuous presence of macrophages because the cells reverted to a non-productive state when separated from macrophages and became productive again when subcultures were added to new macrophages. The roles of the macrophage as a virus target cell and virus inducer in the virus-macrophage-fibroblast interactions are discussed with inferences to the well-known phenomenon of restricted virus replication in infected animals and the immunopathological aspects of the diseases.
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Virus-specific Proteins in Adenovirus Type 12-transformed and Tumour Cells as Detected by Immunoprecipitation
More LessSUMMARYAdenovirus type 12 (Ad12)-specific proteins were determined in nine well-characterized Ad12-transformed hamster cell lines and in Ad12-induced hamster and rat tumour lines by immunoprecipitation, gel electrophoresis and autoradiography. All cell lines expressed a 60K mol. wt. polypeptide. In several cell lines, the presence of a 58K mol. wt. protein could also be demonstrated by these techniques. Smaller Ad12-specific proteins could be detected only in the Ad12-transformed hamster cell lines HA12/7 and A2497-3, and in the Ad12-induced hamster tumour line CLAC3. The quality of the immunoprecipitation tests performed depended primarily on the sera used; their antibody titres varied widely. For at least one of the Ad12-transformed hamster cell lines (HA12/7), there was good agreement in the number and mol. wt. of Ad12-specific proteins detected by both immunoprecipitation and in vitro translation of hybrid-selected cytoplasmic RNA. There was no clear-cut correlation between the number and the nature of Ad12-specific proteins and the way in which the cell lines or tumours were obtained. Cell lines with the least number of copies of Ad12 DNA persisting appeared to express the largest number of Ad12-specific proteins.
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Synthesis of Prematurely Terminated Late Transcripts of Polyoma Virus DNA is Resistant to Inhibition by 5,6-Dichloro-1-β-d-ribofuranosylbenzimidazole
More LessSUMMARYExposure of mouse kidney cells to 5,6-dichloro-1-β-d-ribofuranosylbenzimidazole (DRB) (75 to 300 µm) during the late phase of infection by polyoma virus resulted in nearly complete (90 to 98%) inhibition of virus RNA synthesis. Sedimentation analysis revealed that, although the synthesis of high mol. wt. (> 10S) virus RNA was inhibited in a manner parallel to that of total virus RNA, the synthesis of small (3S to 7S) virus RNA was inhibited by only 40 to 50% in the presence of DRB. As a result, virus RNA synthesized in the presence of DRB contained a peak at 3S to 7S in addition to residual high mol. wt. virus RNA. Small virus RNA from either untreated or DRB-treated cells contained three- to sixfold higher levels of transcripts from the DNA fragment which lies between the BamHI and BglI sites (58.0 to 72.2 map units) than from DNA fragments covering the rest of the virus genome. Furthermore, 80% of the small RNA which hybridized to this fragment was complementary to the L strand of virus DNA. These results suggest that L strand transcripts are initiated within the BglI-BamHI DNA fragment and that a portion of these transcripts is prematurely terminated within several hundred nucleotides of the site(s) of initiation. DRB had little effect on the synthesis of these prematurely terminated RNAs.
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The Presence of α-Interferon in Human Amniotic Fluid
More LessSUMMARYAlmost all the samples of amniotic fluid from 62 pregnant women from the 16th week to the end of the pregnancy contained detectable amounts of α-type interferon. The presence of this substance in amniotic fluid during pregnancy raises the question of the physiological significance of this finding. It is postulated that the amniotic type of α-interferon might be a product of a constitutive gene, rather than induced by latent virus infection.
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Specific Cross-linking of Capsid Proteins to Virus RNA by Ultraviolet Irradiation of Poliovirus
More LessSUMMARYPoliovirus was irradiated with u.v. light under conditions causing approx. 5% cross-linking of capsid protein to virus RNA. Cross-linked RNA-protein complexes, freed from unbound protein, were treated with nuclease, and then analysed on SDS-polyacrylamide gels. The smallest capsid polypeptide VP4 was found to be associated with the RNA to the greatest degree, followed by VP2 and VP1, while VP3 was attached only in trace amounts. Low radiation doses, which produced cross-linking of RNA to protein, did not cause breakdown of the virus particles or conformational changes of the capsid as examined physically and serologically. However, higher doses caused structural alterations of the virus capsid.
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Kinetics of Synthesis of Influenza Virus Ribonucleoprotein Structures
More LessSUMMARYThe synthesis of influenza virus ribonucleoprotein structures (RNPs) in infected chick embryo cells was analysed by polyacrylamide gel electrophoresis (PAGE) in the presence of sodium deoxycholate which resolves the RNPs into five size classes. A relatively small proportion of total RNPs accumulated in the nucleus but free NP protein was found there in large amounts over the period 1.5 to 4 h post-infection. In contrast, by 4 h post-infection, all cytoplasmic NP was complexed into RNP structures. At early times, during a 15 min pulse of [35S]methionine, nearly all the newly synthesized NP was incorporated into RNPs but by 4 h the majority of pulse-labelled NP was present as free protein. However, the proportion of free NP:NP in RNPs remained constant over the 1.5 to 4 h post-infection period, indicating that there was a delay before the NP synthesized later in infection was assembled into RNP structures. Individual RNP size classes were predominantly cytoplasmic and accumulated at similar rates but were not produced in equimolar amounts. The rates of synthesis of individual RNPs were in general agreement with their rates of accumulation with the remarkable exception of RNP d (containing RNA 7, the matrix protein gene). This was synthesized nearly 10-fold faster but accumulated at the same rate as the other RNPs. Possibly RNP d is more rapidly degraded than the other RNPs.
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Suppression of Fibronectin Synthesis by an Early Function(s) of Human Cytomegalovirus
S. Ihara, S. Saito and Y. WatanabeSUMMARYLabelling of fibronectin with [3H]leucine and its isolation by immunoprecipitation followed by electrophoresis on gels showed that fibronectin synthesis was specifically suppressed in human embryonic cells infected with human cytomegalovirus. Degradation or release of pre-existing fibronectin into the medium was not affected. The inhibition of fibronectin synthesis was also observed when cells were infected with a DNA-minus temperature-sensitive mutant at the non-permissive temperature but not observed in infection with u.v.-irradiated virus, suggesting the involvement of the expression of an early virus function(s). This capacity of the virus may be implicated in the virus-induced early cell rounding.
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In vitro Stimulation of Rabbit T Lymphocytes by Cells Expressing Herpes Simplex Antigens
More LessSUMMARYLymphocyte stimulation responses to herpes antigens were studied using virus-infected X-irradiated cells. Rabbits were immunized with herpes simplex virus type 1 (strain HFEM) grown in RK13 cells. For in vitro stimulation assay BHK21 cells were X-irradiated (15000 rad) and infected with a high m.o.i. of a temperature-sensitive (ts) mutant (N102) of HFEM strain at the non-permissive temperature (38.5 °C) of virus. Virus antigens were expressed on the infected cells and there was no leakage of infectious virus into the medium at 38.5 °C. T lymphocytes from rabbits immunized with herpes simplex virus were specifically activated by herpesvirus-infected X-irradiated cells; lymph node cells from rabbits immunized with RK13 cells and from non-immune rabbits showed no proliferative response.
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Properties of Monoclonal Antibodies Directed Against the Glycoproteins of Sindbis Virus
More LessSUMMARYFour monoclonal antibodies that react with Sindbis virus glycoproteins have been examined for (i) their effects on virus infectivity, (ii) their ability to recognize conformational changes in glycoprotein structure, and (iii) their cross-reaction with several different alphaviruses. Two of the monoclonal antibodies reacted with the native forms of the E1 glycoprotein but did not neutralize virus infectivity. One of the anti-E1 antibodies formed an infectious virus‐antibody complex. The other two monoclonal antibodies reacted with the E2 glycoprotein in both an unfolded as well as a native structure. One of these antibodies was very effective for blocking virus infectivity. None of these antibodies reacted with Semliki Forest virus. The anti-E1, but not the anti-E2, antibodies cross-reacted with three serologically related equine encephalomyelitis viruses.
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