- Volume 70, Issue 12, 1989
Volume 70, Issue 12, 1989
- Animal
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Mutation of Host Cell Determinants which Discriminate between Lytic and Persistent Mouse Hepatitis Virus Infection Results in a Fusion-resistant Phenotype
SUMMARYThe expression of mouse hepatitis virus (MHV) E2-specific mRNA, the E2 polypeptide and its associated cell fusing activity was monitored in various cell types inoculated with a recombinant vaccinia virus, designated vMS containing the E2 gene. The results suggest that host cell permissiveness to MHV infection correlates with cellular susceptibility to membrane fusion mediated by the MHV E2 glycoprotein. In addition, we utilized a genetic approach to the analysis of host cell functions involved in determining permissiveness to MHV. By using the chemical mutagen ethyl methanesulphonate, mouse fibroblast cell mutants were generated and selected for their resistance to cell killing by MHV. When challenged with MHV, all five mutants examined gave rise to persistent infections, in contrast to wild-type L-2 cells which were rapidly killed by the virus. The results provide genetic evidence in support of a previous correlation proposed between MHV permissiveness and two host determinants, namely susceptibility to MHV infection and to MHV-mediated cell fusion. Fusion resistance was specific to fusion mediated by the MHV E2 glycoprotein as shown in contact fusion assays between uninfected cells and cells infected either with MHV or with an E2-expressing recombinant vaccinia virus. In contrast, mutant cells were not resistant to fusion after treatment with polyethylene glycol. The observed high rate of generation of these mutants suggests that the conversion of a fully MHV-susceptible cell to a semi-resistant one is a fairly common event, possibly involving a single mutation. In this case, resistance to MHV infection and to E2-mediated membrane fusion may depend on a common host function. This result provides prospects for the precise genetic and biochemical characterization of the steps involved in host cell permissiveness to MHV infection.
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The Site of Bluetongue Virus Attachment to Glycophorins from a Number of Animal Erythrocytes
More LessSUMMARYBluetongue virus (BTV) was shown to agglutinate human, ovine and porcine erythrocytes. Removal of neuraminic acid (NA) from erythrocytes by Vibrio cholerae neuraminidase prevented their agglutination. Haemagglutination was also inhibited by N-acetyl neuraminic acid (NANA), N-glycolyl neuraminic acid (NGNA) and N-acetyl neuramin-lactose. The ability of BTV to agglutinate trypsin-treated human erythrocytes, which lack the amino-terminal domain and the single N-linked oligosaccharide of glycophorin A, suggests that the virus bound to human erythrocytes via NANA-containing, O-linked oligosaccharides. Glycoproteins with NA-containing oligosaccharides of known structure such as mucin, fetuin, alpha 1-acid glycoprotein, ovomucoid and ovine, porcine, human and equine glycophorin were examined for their ability to inhibit BTV-mediated agglutination of human, ovine and porcine erythrocytes. All glycoproteins containing NANA- or NGNAα2-6GalNAc were capable of inhibiting the agglutination of human and porcine erythrocytes. Treatment of human erythrocytes with Newcastle disease virus neuraminidase and of porcine erythrocytes with Clostridium perfringens neuraminidase to cleave preferentially the NANA- and NGNAα2-3Gal linkages respectively, were shown to have little effect on the ability of the erythrocytes to be agglutinated by BTV. The results suggested that BTV binds to NANA- and NGNAα2-6GalNAc residues in the O-linked oligosaccharides of human and porcine glycophorins respectively and indicated the presence of different binding sites on the virus for erythrocytes from other species.
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Asynchronous Mixed Infection of Culicoides variipennis with Bluetongue Virus Serotypes 10 and 17
More LessSUMMARYCulicoides variipennis (Diptera: Ceratopogonidae) the primary vector of bluetongue virus (BTV) in the U.S.A. were asynchronously mixedly infected with two BTV serotypes (BTV-10 and BTV-17); flies first ingested a blood meal that contained BTV-17 and 1, 3, 5, 7, and 9 days later selected flies ingested a second blood meal that contained BTV-10. Control flies ingested each parental virus separately, or both viruses simultaneously, in a single blood meal. Electrophoretic analysis of progeny virus clones indicated that superinfection with BTV-10 occurred when the flies ingested the second virus 1, 3 and 5 days post-initial infection. Parental BTV-17 and reassortant virus clones were isolated from these flies, but parental BTV-10 virus was not isolated from any flies. Reassortant clone frequencies were 67%, 71% and 17% when superinfection occurred on days 1, 3 and 5 after initial infection, respectively, as compared to 48% for simultaneously infected flies. Only parental BTV-17 clones were isolated from flies that ingested the second virus on days 7 and 9 after initial BTV-17 infection. The results indicated that interference to superinfection occurred in C. variipennis by 5 days and flies were refractory to superinfection by 7 days post-initial infection. Analysis of segregation of the parental origin of genome segments in the reassortant clones indicated selection against most segments of BTV-10 parental origin. This occurred both in individual flies and in individual groups. The fact that C. variipennis readily fed on a second blood meal and their ability to produce new viral genotypes suggested that these vectors are highly permissive hosts for evolution of BTV by genome reassortment.
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Identification and Primary Structure of the Gene Encoding the Berne Virus Nucleocapsid Protein
SUMMARYThe nucleotide sequence of the nucleocapsid (N) protein gene of Berne virus (BEV; proposed family Toroviridae) was determined from two independent clones of a cDNA library. From the deduced amino acid sequence a basic protein of 18.3K was predicted. In vitro transcription and translation, followed by immunoprecipitation, were used to identify the gene. The identification was confirmed by metabolic labelling, using the knowledge that cysteine residues are absent from the amino acid sequence of the N protein. Smaller N-related polypeptides encountered in BEV-infected cell lysates were shown to be probable products of aberrant translation, due to initiation on AUG codons further downstream in the N protein gene.
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Organ Distribution of Proteinase-resistant Prion Protein in Humans and Mice with Creutzfeldt-Jakob Disease
More LessSUMMARYWe attempted to clarify the organ distribution of human and murine proteinase-resistant prion protein (PrPCJD)in Creutzfeldt-Jakob disease (CJD), and to measure the concentration of PrPCJD, using a semi-quantitative Western blot analysis. Human PrPCJD was restricted to the central nervous system, whereas murine PrPCJD was present in the central nervous system and in the lymphoreticular system at the end stage of CJD. PrPCJD concentration in the central nervous system of mice was almost identical to that of humans. The minimum wet weight of an organ with a positive reaction was 0·3 mg for brain, 1 to 3 mg for spleen, 3 mg for spinal cord, 3 mg for lymph node, 10 mg for thymus and 10 to 30 mg for intestine of the CJD-infected mice. There were no immunoreactions in purified PrPCJD fractions from 300 mg of spleen, lymph node, liver or peripheral nervous systems of humans, nor in 300 mg of liver, lung or kidney of CJD-infected mice. Within the limits of our method, the distribution of murine PrPCJD differed from that of human PrPCJD. Antibodies on the Western blot membrane from murine spleen PrPCJD fractions stained the kuru plaques in the CJD-infected mouse brain. Therefore, PrPCJD in the murine spleen probably shares the epitopes of the antigen in the murine kuru plaques. Although the immunological detection of PrPCJD does have limits of sensitivity, PrPCJD concentrations did correlate with infectivity titres in scrapie-infected or CJD-infected mice.
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Detection of Defective Genomes in Hepatitis A Virus Particles Present in Clinical Specimens
More LessSUMMARYHepatitis A virus (HAV) particles harbouring a physically defective RNA genome have been reported to occur in all HAV-infected cell culture systems analysed so far. The most prominent defects consist of three distinct overlapping deletions in the region of the HAV genome encoding the structural proteins. By probing for the endpoints of these deletions in RNA samples using S1 nuclease and exonuclease VII mapping, we obtained suggestive evidence for the existence also of defective genomes in HAV particles present in faecal specimens, in viraemic blood collected in the course of hepatitis A virus infection in man, as well as in the liver of an experimentally infected marmoset monkey. The deletions identified extend from nucleotide (nt) 1200 to nt 3820 and from nt 1200 to nt 3240 of the HAV genome. They are compatible with two of the deletions detected in particles grown in vitro in cell cultures and shown to interfere with the replication of standard hepatitis A virions.
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Persistent Infection of MDCK Cells by Influenza C Virus: Initiation and Characterization
More LessSUMMARYPersistent influenza C virus infection was readily initiated in Madin-Darby canine kidney (MDCK) cells at low m.o.i. and has been maintained for over 1 year. The persistently infected (p.i.) cultures were characterized by the following properties: virus infection was limited to a minority of cells, small amounts of infectious virus were produced together with low levels of interferon (IFN) and the cultures were resistant to superinfection by homologous virus and vesicular stomatitis virus, but not by influenza A and B viruses. These properties fluctuated cyclically with passage of the p.i. culture. When p.i. cultures were cured by cultivation in the presence of antiserum, the cultures lost their IFN-producing activity and became as susceptible to homologous virus as normal MDCK cell culture. The results suggest that persistent influenza C virus infection may be regulated by endogenously produced IFN. Under the condition of high m.o.i. a persistent influenza C virus infection could not be initiated in MDCK cells due to the development of cytopathic effects.
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Immunological Response of Monkeys Infected Intranasally with Human Parainfluenza Virus Type 4
SUMMARYThis report describes our attempt to establish an experimental animal model for human parainfluenza virus type 4A (HPIV-4A) and 4B (HPIV-4B) infection, which was used to study the immune response to the viruses. Monkeys were inoculated intranasally with the viruses, and at 10 weeks post-infection they were re-infected with homologous subtype viruses. Virus-specific IgM and IgG serum antibodies were measured by ELISA. A small peak of IgM antibody was detected in the monkeys re-infected with HPIV-4B, whereas this response was not detected after re-infection with HPIV-4A. Virus-specific IgA and IgE antibodies were not detected in sera following infection and re-infection with HPIV-4. However virus-specific IgA and IgE antibodies were found in the saliva and nasal exudates of monkeys infected with either HPIV-4A or -4B. Re-infection of monkeys with HPIV-4B also stimulated an IgA and IgE response. To our knowledge this is the first description of a virus-specific IgE antibody response generated by a paramyxovirus infection of an experimental animal. The kinetics of haemagglutinin-inhibition and neutralization (NT) antibodies were similar to that of virus-specific IgG antibodies. The NT titres of sera from HPIV-4A-infected monkeys were enhanced by the addition of complement, whereas complement did not affect the NT activity of sera obtained from HPIV-4B-infected animals. Antigenic specificities of IgG antibody induced by HPIV-4 infection were analysed with radioimmunoprecipitation followed by SDS–PAGE. Anti-NP, -HN and -F antibodies appeared 2 weeks after infection, and the highest titres were found 2 weeks after re-infection. Anti-F antibody production followed a biphasic pattern previously observed in mumps virus infection.
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Na+ and K+ Concentration and Regulation of Protein Synthesis in L-A9 and Aedes albopictus Cells Infected with Marituba Virus (Bunyaviridae)
More LessSUMMARYInfection of L-A9 cells with Marituba virus produces a severe inhibition of protein synthesis. This inhibition is temporally correlated with an increase in the intracellular Na+ concentration and a decrease in the intracellular K+ concentration. However in Marituba virus-infected Aedes albopictus cells the intracellular level of Na+ and K+ ions and protein synthesis remained unaltered. Incubation of both cell types at high NaCl concentration facilitated the translation of viral RNA whereas the cellular protein synthesis was inhibited. Using a hypotonic medium, the opposite was found. Results are discussed in terms of a possible involvement of these ions in the viral translational process.
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Efficient Transfection of Insect Cells with Baculovirus DNA Using Electroporation
More LessSUMMARYEfficient transfection of Spodoptera frugiperda cells with Autographa californica nuclear polyhedrosis virus (AcNPV) DNA has been carried out using the technique of electroporation. The efficiency of transfection was monitored by assaying the extracellular virus in cell culture supernatants 3 days post-electroporation. Maximum titres of 2 × 109 p.f.u./ml AcNPV were obtained when using a pulse length of 7·7 ms and a field strength of 500 V/cm. This compared with a titre of 2 × 106 p.f.u./ml AcNPV using the standard calcium phosphate transfection method. Cotransfections of wild-type AcNPV DNA and the transfer plasmid pAcRP23-lacZ were also performed using electroporation and gave β-galactosidase recombinant virus titres of 5 × 104 p.f.u./ml; this compared with 5 × 102 p.f.u./ml using the calcium phosphate method. The maximum proportion of recombinant virus, 2·9%, was obtained by harvesting the transfection medium after 2 days, and using a pulse length of 2·8 ms and a field strength of 750 V/cm. We therefore conclude that electroporation provides a very efficient method for the transfection of insect cells with baculovirus DNA.
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Preliminary Studies on the Biology of Borna Disease Virus
More LessSUMMARYBorna disease virus (BDV) is an unclassified agent that causes neurological disease in a wide range of animal species and possibly in humans. The infectious nature of BDV has been long established but, despite extensive progress on the pathogenesis of the infection, the aetiological agent is still uncharacterized. Recent studies have shown that BDV replicates productively in cultures of foetal rabbit glial cells (FRG) which produce a virus-specific protein that is easily detected immunocytochemically. This provides a marker for BDV infectivity. This cell culture system was used to investigate the replication cycle of BDV. The agent required at least 1 h to bind to and penetrate the cells and the antigen was detected 24 h later. Cycloheximide and actinomycin D inhibited production of the antigen in inoculated cells, indicating that both protein synthesis and a DNA-dependent function were required for the production of viral antigen. Cocultivation of BDV-infected FRG cells with Vero cells resulted in a persistent productive infection in the latter. Use of these cells showed that the infectious agent matured exclusively in the cytoplasm and within the plasma membrane of the cell. Antigen-laden nuclei did not have infectivity. These studies showed that BDV has the physical and replicative properties typical of conventional viruses but its mechanism of replication and site of morphogenesis may be unique.
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- Plant
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Evidence that Beet Necrotic Yellow Vein Virus RNA-4 Is Essential for Efficient Transmission by the Fungus Polymyxa betae
More LessSUMMARYThe efficiency of transmission by Polymyxa betae of beet necrotic yellow vein virus (BNYVV) isolates containing different RNA components was compared using sugar-beet seedlings as test plants. Isolate S-4, containing RNA-1 +2 + 4, was transmitted by P. betae about 100 times more efficiently than isolate S-3 (RNA-1 +2 + 3) and about 1000 times more efficiently than isolate S-0 (RNA-1 + 2). Isolate S-34 (RNA-1 + 2 + 3 + 4) was transmitted even more efficiently than isolate S-4. Each isolate retained its characteristic RNA composition after transmission by P. betae. The virus content, measured by ELISA, of infected rootlets was S-34 > S-3 > S-4 > S-0. In inoculated leaves of Tetragonia expansa and Beta macrocarpa, isolates S-3 and S-34 multiplied more extensively than did S-4 and S-0. The inefficient transmission of isolate S-3 by P. betae, as compared with S-4, cannot be attributed to a poorer ability to spread in root tissue, but the difference in transmissibility of S-3 and S-0 may be explained in this way. These results show that RNA-4 of BNYVV is essential for efficient transmission by P. betae, and suggest that RNA-3 may influence the ability of the virus to spread in root tissue. RNA-4 and RNA-3 therefore seem to play important, but different, roles in virus survival and spread in nature.
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Production and Pathogenicity of Isolates of Beet Necrotic Yellow Vein Virus with Different Numbers of RNA Components
T. Tamada, Y. Shirako, H. Abe, M. Saito, T. Kiguchi and T. HaradaSUMMARYTen Japanese field isolates of beet necrotic yellow vein virus (BNYVV) were transmitted to Tetragonia expansa by inoculation with sap from rootlets of sugar-beet seedlings, to which the virus had been transmitted by the fungus Polymyxa betae. RNA extracted from BNYVV particles obtained from the T. expansa leaves was analysed by agarose gel electrophoresis. Some isolates contained RNA-1 (7·1 kb), RNA-2 (4·8 kb), RNA-3 (1·85 kb) and RNA-4 (1·5 kb) and the others contained, in addition, RNA-5 (1·4 kb). Further isolates, derived from single lesions produced by these isolates, had a variety of RNA compositions. Some contained only RNA-1 and RNA-2. Others contained, in addition, RNA-3, RNA-4, RNA-5 or RNA-6 (1·0 kb), or combinations of two or three of these components. Such isolates generally maintained their RNA composition on further subculture, and their particles had length distributions corresponding to their RNA components. Isolates containing RNA-1 + 2 + 3 caused yellow or strongly chlorotic local lesions in T. expansa, Beta vulgaris, B. macrocarpa and Chenopodium quinoa, and caused systemic stunting and yellow mosaic in B. macrocarpa and, occasionally, in B. vulgaris. In contrast, isolates containing RNA-1 + 2 + 4 or 1 + 2 + 5 induced chlorotic lesions, those containing RNA-1 + 2 + 6 or 1 + 2 induced faint chlorotic lesions, and none of these isolates easily infected B. macrocarpa systemically. Isolates containing different combinations of RNA-3,-4 and -5 induced more severe symptoms than those containing a single RNA. Such synergistic effects occurred between RNA-3 and RNA-4 or RNA-5, or between RNA-4 and RNA-5 or RNA-6, but not between RNA-3 and RNA-6, or between RNA-5 and RNA-6. These small RNA species therefore contain the genetic determinant(s) for lesion type and for ability to infect B. vulgaris and B. macrocarpa systemically. RNA-1 and RNA-2 are viral genome components. The other RNA components have some characteristics of viral satellite nucleic acids but they may not all be dispensable if the BNYVV isolates are to survive in nature.
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Two Related Viroids Cause Grapevine Yellow Speckle Disease Independently
More LessSUMMARYWe have confirmed that two closely related circular RNA molecules previously named grapevine yellow speckle viroid (GYSV) and grapevine viroid 1B (GV1B) are indeed viroids. Electron microscopy after spreading under non-denaturing conditions revealed that GYSV has a rod-like structure typical of viroids. Purified GYSV and GV1B replicated independently in inoculated grapevine seedlings and some of the infected plants developed yellow speckle symptoms indicating that both viroids can cause grapevine yellow speckle disease. Plus-sense RNA transcripts derived from a dimeric GYSV cDNA clone induced yellow speckle symptoms in a grapevine seedling confirming the role of GYSV in the yellow speckle disease. Two oligonucleotide probes were synthesized for the detection of the two related viroids. The probes which could detect each viroid individually were used to assess correlations between the occurrence of these viroids and the incidence of the disease.
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Host-dependent Suppression of Temperature-sensitive Mutations in Tobacco Mosaic Virus Transport Gene
More LessSUMMARYTobacco mosaic virus (TMV) mutants Lsl and Ni2519, temperature-sensitive (ts) in transport function in tobacco plants, were able to spread at high temperature (33 °C) in Amaranthus caudatus L. plants. On the other hand, TMV ts coat protein mutants retained the ts phenotype in both host plants. The ability of Lsl and Ni2519 to spread systemically in A. caudatus at high temperature is probably due to the functional stabilization of the transport proteins by a factor(s) provided by the host plant. In accordance with this, Lsl complemented the transport function of cucumber green mottle mosaic tobamovirus and red clover mottle comovirus; they acquired the ability to spread systemically at 33 °C in the A. caudatus plants preinfected with Lsl.
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Competition between Isolates and Variants of Cauliflower Mosaic Virus in Infected Turnip Plants
More LessSUMMARYThe Cabb S isolate of cauliflower mosaic virus (CaMV) is the only isolate that can be recovered from turnip plants mixedly infected with Cabb S and an infectious variant of Cabb S. Analysis of the progeny resulting from mixed infections of turnip plants was done for a better understanding of this dominance. Cabb S DNA was the dominant DNA recovered from plants after a mixed infection with Cabb S and D/H or W isolates of CaMV, whereas UM130 (derived from Cabb S by the insertion of a short oligonucleotide in open reading frame III) coexisted in turnip plants with D/H, NY8153, CM4-184 and W isolates. To determine whether there are additional sequences responsible for the ability of Cabb S to dominate over UM130, co-inoculation experiments were done using chimeric DNAs, obtained by in vivo recombination (IC141, IC143 and VR246) and by in vitro construction (W/CS and CS/W). Chimeras IC141, IC143 and VR246 coexisted in turnip plants with UM130. Chimera CS/W dominated over UM 130, whereas UM 130 dominated over W/CS. The location of Cabb S sequences in these chimeras suggests that more than one region is responsible for the competitive advantage of Cabb S DNA. A different modification of Cabb S DNA in open reading frame III also destroyed the ability of the DNA to dominate over the W isolate. In DNA from virions obtained after co-infection with UM130 and CS/W, more molecules were recovered with U M 130-specific sequences at position 1364 than with those at position 2040. This and similar results with progeny from W/CS and UM 130 co-infection suggest that genetic exchanges had occurred. However, exchanges were not detected in progeny from other mixed infections. Thus the dominance of the Cabb S isolate in mixed infections was due primarily to a better competitive ability of the Cabb S DNA. Plants inoculated first with UM130 and 2 to 8 days later with Cabb S contained only UM130 CaMV DNA, indicating that dominance was unable to overcome cross-protection.
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Further Evidence that Viroplasms Are the Site of Cauliflower Mosaic Virus Genome Replication by Reverse Transcription during Viral Infection
More LessSUMMARYCauliflower mosaic virus (CaMV) is a DNA plant virus that replicates its genome through an RNA intermediate. The cytoplasmic step of CaMV DNA replication was studied using a fraction consisting of purified viroplasms, which are virus-specific inclusion bodies accumulating in the infected plant cells. The isolated viroplasms retain a DNA polymerase activity able to synthesize CaMV DNA from endogenous templates. A further characterization of the viral DNA sequences produced in the isolated inclusion bodies indicates that newly synthesized DNA, mostly of polarity opposite to that of viral RNA, is single-stranded and partly associated with RNA by base-pairing. In addition to an RNA-dependent DNA polymerase activity, RNA molecules, which presumably originate from the viral RNA template used for reverse transcription, are found to accumulate in the purified inclusion bodies. Furthermore, a small DNA molecule strongly labelled in the purified fraction has been characterized and corresponds to the CaMV reverse transcription intermediate sa-DNA. These results provide further evidence that the reverse transcription of CaMV RNA occurs in the viroplasms. Additional data are presented which suggest that CaMV replication could occur in virion-related particles.
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Reaction of Coat Proteins of Two Comoviruses in Different Aggregation States with Monoclonal Antibodies
More LessSUMMARYMonoclonal antibodies were produced against two comoviruses, cowpea mosaic virus and cowpea severe mosaic virus. The antibodies were tested for their recognition of coat proteins of each virus in various conformational states by enzyme-linked immunosorbent assays. Three groups of epitopes were identified on the basis of antibody binding to native or denatured virions. Antibodies specific for epitopes exposed only after virus denaturation were cross-reactive, recognizing both viruses. Antibodies binding epitopes of the other two groups recognized intact virions and varied in their degree of cross-reactivity.
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Serological Differentiation between Top Component and Nucleoprotein Components of Comoviruses
More LessSUMMARYRabbit antisera produced against two comoviruses (cowpea mosaic virus and cowpea severe mosaic virus) were used in plate-trapped ELISA and liquid phase competition ELISA. In the latter, the top component competed against bound unfractionated virus more effectively than did nucleoprotein components. One murine monoclonal antibody elicited to cowpea mosaic virus and three monoclonal antibodies to cowpea severe mosaic virus exhibited differential binding to top component, relative to either middle or bottom components in plate-trapped or antibody-trapped ELISAs. Differential binding to centrifugal components of virus by two of these monoclonal antibodies was maintained in liquid phase competition assays. These data suggest that the encapsidation of RNA alters the configuration of the virion surface in the vicinity of the antibody epitopes. Ribonuclease digestion of intact or denatured virus did not affect the binding of monoclonal antibodies.
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Morphological Characteristics of Rice Stripe Virus
More LessSUMMARYThe morphological characteristics of particles of rice stripe virus (RSV) were examined. Each of four components (M1, M2, B and nB) of RSV, isolated by repeated cycles of sucrose density gradient centrifugation, contained circular filaments; the modal lengths were 510 nm for the M1 component, 610 nm for the M2 component, 840 nm for the B component and 2110 nm for the nB component. Each component was associated with a single-stranded species and a double-stranded species of RNA although a fifth component (the T component) did not form a distinct band after the density gradient centrifugation and was associated with circular filaments of 290 nm in length and a ssRNA species.
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