Showing papers in "Archives of Virology in 1990"
TL;DR: Findings suggesting that the H CMV particle rapidly stimulates AA metabolism are consistent with the view that the interaction of a HCMV virion component(s) with the cell surface may initiate membrane-associated events similar to those induced by growth factors.
Abstract: Exposure of human lung fibroblasts to human cytomegalovirus (HCMV) stimulated a rapid increase in the release of [3H] from cells prelabelled with radiolabelled arachidonic acid ([3H]AA). Maximum stimulation of [3H] release was observed at 20 min postinfection and was quantitatively similar to that induced by the tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA: 10 nM) or fetal calf serum (5%). The level of [3H] release was dependent on the multiplicity of infection, and appeared to be mediated by a component(s) of the virion, since the findings from three series of experiments suggested that neither infectious virus, nor HCMV-specific macromolecular synthesis was required for stimulation of [3H] release. (1) Inactivation of HCMV infectivity with ultra-violet (UV) light (approximately 254 nm, 4.80 x 10(4) ergs/mm2) did not diminish the stimulation of [3H] release. (2) Significant reduction in the level of [3H] release was not observed when infected cells were maintained in the presence of a protein synthesis inhibitor, cycloheximide (50 micrograms/ml), or an inhibitor of mRNA synthesis, 3'-deoxyadenosine (cordycepin, 50 micrograms/ml). (3) No correlation was established between the expression of HCMV immediate early (IE) antigens and the induction of [3H] release, since there was little, if any, synthesis of HCMV IE antigen detectable by anticomplement immunofluorescence through the first 30 min postinfection. These findings suggesting that the HCMV particle rapidly stimulates AA metabolism are consistent with the view that the interaction of a HCMV virion component(s) with the cell surface may initiate membrane-associated events similar to those induced by growth factors.
359 citations
TL;DR: A double antibody sandwich blocking ELISA, using a monoclonal antibody (MAb) against influenza A nucleoprotein (NP) was developed to detect antibodies against influenza, and is suited for influenza A antibody screening, especially in species which harbor several influenza subtypes.
Abstract: A double antibody sandwich blocking ELISA, using a monoclonal antibody (MAb) against influenza A nucleoprotein (NP) was developed to detect antibodies against influenza. Collections of serum samples were obtained from human and various animal species. All influenza A subtypes induced antibodies against hemagglutinins and NP. A close correlation between titers of the hemagglutination inhibition (HI) test and the NP-ELISA was seen. Antibodies against influenza NP were demonstrated in serum samples from humans, ferrets, swine, horses, chickens, ducks, guinea pigs, mice, and seals. The serum samples were collected at intervals during prospective epidemiological studies, from experimental and natural infections, and vaccination studies. The decline of maternal antibodies was studied in swine and horses. The NP-ELISA enables rapid serological diagnosis and is suited for influenza A antibody screening, especially in species which harbor several influenza subtypes. The HI and neuraminidase inhibition tests, however, must still be used for subtyping.
128 citations
TL;DR: The in vitro demonstration of the susceptibility of endothelial cells to hantaviruses corroborates in vivo findings, and suggests that endothelial Cells may serve as target cells in hemorrhagic fever with renal syndrome.
Abstract: To investigate whether the hantaviruses replicate in endothelial cells, we inoculated human umbilical vein endothelial cells with several pathogenic and nonpathogenic strains of hantavirus. Intracytoplasmic, virus-specific granular fluorescence was detected initially at three days postinoculation and nearly 100% of cells contained viral antigen at 10 days. Cytopathic effect or inclusion bodies were not observed. The in vitro demonstration of the susceptibility of endothelial cells to hantaviruses corroborates in vivo findings, and suggests that endothelial cells may serve as target cells in hemorrhagic fever with renal syndrome.
121 citations
TL;DR: Conditions for the growth of human faecal astrovirus in a continuous colonic carcinoma cell line (CaCo-2) are reported and three polypeptides appeared loosely held on the exterior.
Abstract: We report conditions for the growth of human faecal astrovirus in a continuous colonic carcinoma cell line (CaCo-2). Purified particles contained three polypeptides, one of which (24k) appeared loosely held on the exterior.
119 citations
TL;DR: PDV-1 should be considered a newly recognized member of the genusMorbillivirus, whereas PDV-2 proved to be quite similar if not identical to CDV.
Abstract: Recently morbilliviruses were isolated from harbour seals (Phoca vitulina) in North West Europe (phocid distemper virus-1: PDV-1) and from Baikal seals (Phoca sibirica) in Siberia (phocid distemper virus-2:PDV-2) during outbreaks of severe disease which resembled distemper in dogs. PDV-1 and PDV-2 were passaged in SPF dogs, in which they caused distemper-like disease symptoms, and were subsequently passaged in Vero cells in which they caused cytopathic changes. PDV-1, PDV-2, and canine distemper virus (CDV) were compared with respect to their biological, morphological, physical, protein chemical, and antigenic properties. It was concluded that PDV-1 should be considered a newly recognized member of the genusMorbillivirus, whereas PDV-2 proved to be quite similar if not identical to CDV.
116 citations
TL;DR: Although virus administered intranasally to young calves with maternal antibodies does not evoke antibody responses, it can prime these calves for a protective memory response upon reinfection, and protection appears to be associated with the capacity to mount a mucosal memory IgA response.
Abstract: Human and bovine respiratory syncytial viruses resemble each other closely During annual winter outbreaks, they cause similar respiratory tract disease in infants and calves The disease is most severe in children and calves between 1 and 3 months old, when maternal antibodies against the virus are usually present Reinfections, which are common, are accompanied by progressively milder illnesses in children, but are symptomless in calves Because maternal antibodies suppress serum and mucosal antibody responses of all isotypes, the development of a vaccine that is effective in young children and calves with high levels of maternal antibodies has been severely hampered Although virus administered intranasally to young calves with maternal antibodies does not evoke antibody responses, it can prime these calves for a protective memory response upon reinfection Protection appears to be associated with the capacity to mount a mucosal memory IgA response There are several indications that one or more immunopathologic mechanisms contribute to the disease An Arthus reaction (type III) may have a role in the pathogenesis, because activated complement may cause most of the pathologic lesions, including edema and emphysema in uninfected parts of the lung Lungs from calves with severe or fatal disease have depositions of complement component C3 and a low histamine content The most immunogenic and protective antigen of the virus is the fusion (F) glycoprotein, which evokes a strong antibody response and is a target for cytotoxic T cells On the F protein, epitopes that induce neutralizing and non-neutralizing antibodies, both of which may enhance complement activation, were identified Immunity to the F protein may have beneficial and harmful effects
86 citations
TL;DR: Eight monoclonal antibodies directed against the hog cholera virus (HCV) strain Alfort/187 and displaying broad cross-reactivity with other HCV strains were characterized and showed the mapping of two distinct conserved antigenic domains on this protein.
Abstract: Eight monoclonal antibodies directed against the hog cholera virus (HCV) strain Alfort/187 and displaying broad cross-reactivity with other HCV strains were characterized. An enzyme immunoassay on fixed monolayers of porcine or bovine cells infected with 14 different strains and isolates of HCV and 12 bovine viral diarrhea viruses (BVDV), respectively, showed that all antibodies reacted with HCV only. Seven antibodies recognized all HCV tested, thus indicating that they were directed against conserved epitopes. All antibodies neutralized the homologous strain and different patterns of the other HCV tested. Radioimmunoprecipitation analysis showed that the monoclonal antibodies were directed against a doublet of 56–60 kDa, presumably representing the major envelope glycoprotein of HCV. The results of reciprocal antibody blocking assays allowed the mapping of two distinct conserved antigenic domains on this protein.
83 citations
TL;DR: Rhesus monkeys inoculated intravenously with Rift Valley fever (RVF) virus presented clinical disease syndromes similar to human cases of RVF, and there was a significant correlation between a delayed interferon response and mortality, suggesting that the early appearance of interfer on was influential in limiting the severity of disease.
Abstract: Rhesus monkeys inoculated intravenously with Rift Valley fever (RVF) virus presented clinical disease syndromes similar to human cases of RVF. All 17 infected monkeys had high-titered viremias but disease ranged from clinically inapparent to death. Three (18%) RVF virus-infected monkeys developed signs of hemorrhagic fever characterized by epistaxis, petechial to purpuric cutaneous lesions, anorexia, and vomiting prior to death. The 14 remaining monkeys survived RVF viral infection but, 7 showed clinical signs of illness characterized by diminished food intake, cutaneous petechiae, and occasional vomiting. The other 7 monkeys showed no evidence of clinical disease. All monkeys had detectable serum interferon 24–30 h after infection, but 4 of 7 monkeys that did not develop clinical illness had serum interferon titers within 12h after infection. In lethally infected macaques, indices of hepatic function and blood coagulation were abnormal within 2 days, implicating early pathogenetic events as critical determinants of survival. Serum transferase values were elevated in proportion to severity of clinical disease and outcome of infection. Both myocardial damage and laboratory evidence consistent with disseminated intravascular coagulation were present in fatal infections. All surviving monkeys developed neutralizing antibodies to RVF virus 4–7 days after infection, and this coincided with termination of viremia. Two fatally infected monkeys were viremic until death on days 6 and 8, and the third cleared viremia on day 5 and developed antibody on day 6 but died on day 15. There was a significant correlation between a delayed interferon response and mortality, suggesting that the early appearance of interferon was influential in limiting the severity of disease.
82 citations
TL;DR: It is demonstrated that a variety of human mononuclear cell lines can be infected with d Dengue-2 virus and may be useful as models for the analysis of dengue virus-human cell interactions in dengued virus infections.
Abstract: Twenty three human mononuclear cell lines including ten myelomonocytic cell lines, eight B cell lines and five T cell lines, were examined to determine whether they could be infected with dengue-2 virus. All the cell lines were infected with dengue-2 virus as determined by immunofluorescent staining and by virus titration of culture supernatant fluids. K 562, Jiyoye and Jurkat, respectively, showed the highest percentage of infected cells of these myelomonocytic, B and T cell lines. Antibody to dengue-2 virus at subneutralizing concentrations augmented dengue-2 virus infection of myelomonocytic cell lines, but not of B cell lines or of T cell lines.
80 citations
TL;DR: An experimental rat model to study acute cytomegalovirus infections is described, appropriate for studies on the pathogenesis and antiviral therapy of CMV infections in the immunocompromised host.
Abstract: An experimental rat model to study acute cytomegalovirus infections is described. Eight-week old male Brown Norway rats, immunosuppressed by total body irradiation, were infected with rat cytomegalovirus (RCMV). The effects of infection were determined by survival rates and the presence of virus or viral components in different organs was assayed by plaque test, immunoperoxidase staining, dot-blot DNA hyridization and in situ DNA hybridization. At days 10-post infection nearly 90% of the animals had died. Spleen, liver and bone marrow were heavily infected. Interstitial pneumonia was observed. Pathological findings strongly resembled the full scale of lesions in human CMV infections. Anti-RCMV hyperimmune serum was effective against mortality from RCMV infection and viral spread to lungs and liver was prevented. This model is appropriate for studies on the pathogenesis and antiviral therapy of CMV infections in the immunocompromised host.
79 citations
TL;DR: It is confirmed that fibrillar structures are not essential for the morphogenesis of polyhedron envelopes and demonstrated that the association of anti pp 34 serum with these structures is specific but fortuitous.
Abstract: Using immuno-electron microscopy the 34 kDa polyhedron envelope (PE) phosphoprotein (pp 34) was localized in cells infected withAutographa californica multiple-nucleocapsid nuclear polyhedrosis virus (AcMNPV) In wild-type AcMNPV-infected cells this protein was found associated with electron-dense “spacers” and the polyhedron envelopes demonstrating their structural relationship In these cells pp 34 was also found associated with fibrillar structures present in the nucleus and cytoplasm of infected cells However, when cells were infected with an AcMNPV mutant with an inactivated pp 34 gene, antiserum against pp 34 still localized in fibrillar structures In cells infected with AcMNPV mutants lacking p 10, and thus devoid of fibrillar structures, pp 34 localized normally with both electron-dense “spacers” and polyhedron envelopes These data confirm that fibrillar structures are not essential for the morphogenesis of polyhedron envelopes and demonstrate that the association of anti pp 34 serum with these structures is specific but fortuitous
TL;DR: Structural and antigenic alterations were observed in the envelope glycoproteins gp90 and gp45, with greatest variation in gp90, and neutralizing activity of sera collected later in the infection was broadly reactive regardless of the number of clinical episodes the donor had suffered.
Abstract: Three ponies were inoculated with plasma containing 104.8 TCID50 of equine infectious anemia virus (EIAV) and observed for 165 to 440 days. Each pony developed a febrile response within 3 weeks of infection during which a plasma viremia ⩾103.5 TCID50/ml was observed. Analyses of four isolates from sequential febrile episodes in a single pony were conducted by two-dimensional tryptic peptide maps and with monoclonal antibodies in immunoblots. Structural and antigenic alterations were observed in the envelope glycoproteins gp90 and gp45, with greatest variation in gp90. Specific IgG to EIAV gp90, gp45, and p26 of homologous and heterologous isolates was detectable by immunoblots within one month after infection although IgG levels to gp45 at this time were relatively low. The group-specific determinants of gp90 and gp45 were more antigenic than those of p26; however, binding of IgG to these determinants did not correlate with neutralization of EIAV as assayed in fetal equine kidney cells. Neutralizing antibodies were first detectable within two months of infection and only neutralized viruses isolated prior to serum collection. Neutralizing activity of sera collected later in the infection was broadly reactive regardless of the number of clinical episodes the donor had suffered.
TL;DR: Four group A human rotaviruses having antigenic specificity of subgroup I and ‘long’ RNA electropherotype were isolated in MA104 cell cultures and cross-neutralization tests with hyperimmune antisera suggested that they are serologically distinct from the six previously recognized humanrotavirus serotypes.
Abstract: Four group A human rotaviruses having antigenic specificity of subgroup I and ‘long’ RNA electropherotype were isolated in MA104 cell cultures. Cross-neutralization tests with hyperimmune antisera suggested that they are serologically distinct from the six previously recognized human rotavirus serotypes.
TL;DR: Seven 69 M-like (serotype 8) strains circulating in Europe are detected, six from Finland and one from Italy, which appeared to be closely related to serotype 8 HRV strain 69 M by neutralization, but showed partial homology with several human and animal strains by hybridization.
Abstract: During an epidemiological study on the prevalence of human rotavirus (HRV) serotypes 1–4 in Europe, we found that some strains could not be typed. However, when a monoclonal antibody directed to serotype 8 HRV was included in the typing assay, we detected seven 69 M-like (serotype 8) strains, six from Finland and one from Italy. The previously reported serotype 8 HRV strains, 69 M, B 37, and B 38 isolated in Indonesia, were of subgroup I specificity and presented a peculiar “super short” RNA electropherotype. In contrast, all the seven European strains possessed a long RNA pattern, and one of them had subgroup II specificity. Three of these strains were adapted to growth in cell cultures and were further characterized by neutralization and by Northern blot hybridization. They appeared to be closely related to serotype 8 HRV strain 69 M by neutralization, but showed partial homology with several human and animal strains by hybridization. The epidemiological importance of these serotype 8 strains circulating in Europe should be investigated, in view of their possible inclusion in a rotavirus vaccine.
TL;DR: A neutralization escape mutant (A/1 E) of equine infectious anemia virus was isolated after 13 passages in cell culture in the presence of serum containing antibodies to type-and group-specific determinants of EIAV envelope glycoproteins as mentioned in this paper.
Abstract: A neutralization escape mutant (A/1 E) of equine infectious anemia virus was isolated after 13 passages in cell culture in the presence of serum containing antibodies to type- and group-specific determinants of EIAV envelope glycoproteins. Loss of neutralization by the selecting serum correlated with loss of two epitopes in the major envelope glycoprotein gp90 of A/1 E which were present in a parallel variant isolated from a persistently infected pony.
TL;DR: Southern blot analysis using32P-labelled BEHV DNA as probe indicated that bovine herpesvirus 1 (BHV1), buffalo herpesv Virus 1 (BuHV 1) and caprine herpesv virus 1 (CaHV3) were similar and that the similarity occurred throughout the entire length of the genomes; CaHV2 was more distantly related to the other 3 viruses.
Abstract: A clone library of 11 of 15 BamHI fragments representing 81% of the 140 kilobase DNA genome of the prototype bovine encephalitis herpesvirus strain N569 (BEHV.N569) was constructed. The clones were used to verify the BamHI, BstEII, EcoRI, and HindIII genomic maps for BEHV.N569 published by Engels et al. [Virus Res 6: 57-73 (1986)] for the same virus although some amendments/variations to the BamHI map were found in that 3 previously unidentified restriction sites were identified. Restriction site maps for BglII and KpnI were also derived for BEHV.N569. Southern blot analysis using 32P-labelled BEHV DNA as probe indicated that bovine herpesvirus 1 (BHV1), buffalo herpesvirus 1 (BuHV1) and caprine herpesvirus 1 (CaHV1) were similar and that the similarity occurred throughout the entire length of the genomes; CaHV1 was more distantly related to the other 3 viruses. Because of the similarities BEHV.N569 and BHV1. Cooper cloned DNA fragments were used to construct BamHI, BglII, BstEII, EcoRI, KpnI, and HindIII restriction site maps for the genome of BuHV1 and BamHI, BglII, and KpnI maps for the genome of BHV1.V155, a genital strain.
TL;DR: Cross neutralization tests with a panel of rotavirus strains representing previously described nine VP7 (G) serotypes revealed that KK-3, a prototype Japanese bovine serotype 2, belonged to a new serotype (G10), confirming and extending the recent report of Snodgrass et al.
Abstract: Cross neutralization tests with a panel of rotavirus strains representing previously described nine VP7 (G) serotypes revealed that bovine rotavirus strain KK-3, a prototype Japanese bovine serotype 2, belonged to a new serotype (G10), confirming and extending the recent report of Snodgrass et al. [J. Clin. Microbiol. 28: 504–507 (1990)] which showed that hyperimmune serum to the KK-3 strain neutralized the B223 strain, a proposed type strain of G10. Further antigenic characteristics of the KK-3 strain, as well as the 0510 strain (a G6 strain isolated in Japan), were examined in terms of their VP4 (P) specificity. For the characterization of P types, we employed genetic reassortants that possess VP4 gene for UK and VP7 gene for D (G1), VP4 gene for NCDV and VP7 gene for SA11 (G3), or VP4 gene for SA11 and VP7 gene for NCDV (G6) in the plaque reduction neutralization assay with hyperimmune sera against these two Japanese strains and the prototype bovine rotavirus NCDV strain. While the 0510 strain had UK-like P and NCDV-like G types, the KK-3 strain had a distinct set of P and G types. Thus, at least three P types (NCDV-, UK-, and KK-3-like) and two G types (G6 and G10) are present among bovine rotavirus strains.
TL;DR: Data is presented suggesting that human polyomaviruses BKV and JCV, widely distributed throughout human populations, are able to induce gene mutations in cultured cells and that the mutagenic effects of the three viruses do not appear to be essentially different.
Abstract: We present data suggesting that human polyomaviruses BKV and JCV, widely distributed throughout human populations, are able to induce gene mutations in cultured cells. In this study, using different infecting agents, cell lines to be infected, mutation expression periods, and selection systems, we observed mutagenic effects of varying extent with values of spontaneous mutant frequencies being increased after BKV infection up to 100-fold in BHK cells (6-thioguanine resistance) and nearly 35-fold in virus-transformed human Lesch-Nyhan cells (ouabain resistance). In experiments with BKV the viral mutagenic potential was found to be raised both in moderately uv-irradiated cells, or when wild-type virus was replaced by the variant BKV-IR isolated from a human tumor [27]. Since BKV-IR is defective in the expression of small-t antigen, the viral mutagenicity does not require this protein to be active. BKV was shown to mutate, besides different established cell lines, human peripheral blood lymphocytes. Moreover, as demonstrated by comparing mutagenicities of DNAs from BKV, JCV, and the related polyomavirus SV40, the mutagenic effects of the three viruses do not appear to be essentially different. Implications of these findings are discussed.
TL;DR: The most promising method for genetic engineering of plants for virus resistance has been the expression of coat-protein coding sequences in plants transformed with a coat protein gene.
Abstract: Historically, control of plant virus disease has involved numerous strategies which have often been combined to provide effective durable resistance in the field. In recent years, the dramatic advances obtained in plant molecular virology have enhanced our understanding of viral genome organizations and gene functions. Moreover, genetic engineering of plants for virus resistance has recently provided promising additional strategies for control of virus disease. At present, the most promising of these has been the expression of coat-protein coding sequences in plants transformed with a coat protein gene. Other potential methods include the expression of anti-sense viral transcripts in transgenic plants, the application of artificial anti-sense mediated gene regulation to viral systems, and the expression of viral satellite RNAs, RNAs with endoribonuclease activity, antiviral antibody genes, or human interferon genes in plants.
TL;DR: The relative affinity of the MAbs, in addition to steric constraints, were shown to be important factors in the ability to compete for interaction with HA.
Abstract: Monoclonal antibodies (MAbs) specific for the hemagglutinin (HA) of the H3 subtype of influenza A virus were grouped according to their inability to bind to particular MAb-selected neutralization escape mutants of the virus having an amino acid substitution in one of the five postulated antigenic sites on the molecule. Additional residues critical to the binding of the MAbs were deduced from their patterns of reactivity with a panel of field strains and receptor mutants of the H3 subtype. The relationship of these residues to the actual epitopes recognized by the MAbs was inferred from their location on the three-dimensional structure of the HA molecule. In this way it was generally possible to identify a number of residues that are critical to the integrity of the epitope recognized by each of the MAbs examined. It was found that: (1) Several of these epitopes appear to be discontinuous and some may depend on residues contributed by more than one monomer. For example, residue 205, in the interface between monomers of the HA, was found to affect the integrity of the epitopes for several MAbs, possibly by stabilizing the conformation of residues around the receptor-binding pocket and/or in site B on the adjacent monomer. The activity of these particular MAbs was greatly decreased if the virus was exposed to pH 5. (2) All the MAbs tested neutralized viral infectivity and inhibited hemagglutination, although the single MAb directed to site C, which is the most distant from the receptor-binding site, was the least efficient. (3) Hemagglutination inhibition, and particularly neutralization tests, were more discriminating than ELISA in discerning subtle differences between the corresponding epitopes recognized by MAbs on different field strains. (4) Efficiency of neutralization of infectivity did not correlate consistently with hemagglutination inhibiting efficiency; MAbs postulated to bind to epitopes close to the receptor-binding pocket were very efficient at inhibiting hemagglutination, whereas neutralization efficiency tended to be more influenced by the affinity of binding of the MAb. (5) A MAb binding to any particular epitope could affect the binding of a second MAb directed to an epitope within the same or even a different antigenic site. The observed effect was most commonly inhibition of binding, which was not always reciprocal; enhancement of binding was also observed with certain combinations of MAbs. The relative affinity of the MAbs, in addition to steric constraints, were shown to be important factors in the ability to compete for interaction with HA.
TL;DR: Following oral inoculation, the excretion of a virulent or an attenuated strain of bovine coronavirus in calf feces and their persistence in spiral colon, ileum, and jejunum were studied using hemagglutination and direct fluorescent antibody tests.
Abstract: Following oral inoculation, the excretion of a virulent or an attenuated strain of bovine coronavirus in calf feces and their persistence in spiral colon, ileum, and jejunum were studied using hemagglutination and direct fluorescent antibody tests, respectively The virus was excreted in feces for only 3 days at high titers and then intermittently at low titers However, viral antigen was detected in crypt or Peyer's patches for at least 3 weeks after infection in 1 of 3 calves given virulent virus and 1 of 2 calves given attenuated virus
TL;DR: The ELISA was most precise and most suitable for routine diagnosis in the field, and the dot-blot hybridization, detected several TSWV isolates in different host species equally well.
Abstract: The immunoreactivity of a panel of monoclonal antibodies raised to tomato spotted wilt virus (TSWV) was examined in enzyme-linked immunosorbent assays (ELISA) and dot immunobinding assays (DIBA) procedures. MAbs 6.12.15 and 2.9 were specific for the nucleocapsid protein of TSWV. The sensitivity of the two immunoassays was compared with that of a dot-blot hybridization technique using riboprobes (RNA transcripts) to TSWV M RNA. Using deproteinized plant extracts or purified virus preparations, as little as 1 pg RNA could be detected. Although an ELISA using MAb 6.12.15, a DIBA procedure using MAb 3.22.6 and the dot-blot hybridization, detected several TSWV isolates in different host species equally well, the ELISA was most precise and most suitable for routine diagnosis in the field.
TL;DR: Both the genomic homology and the similarities from the infectivity and pathogenicity studies between the mink virus and the recent avian isolates point to a direct invasion of the minking population by an avian H10N4 virus.
Abstract: Strains of an influenza H10N4 virus have been isolated during an outbreak of a respiratory disease in mink on the south-east coast of Sweden. This was the first example of a disease in mammals caused by the H10 subtype. We compared the A/mink/Sweden/84 strain with two recent avian H10N4 isolates, one from fowl and another from a mallard, both isolated in Great Britain in 1985 as well as the prototype A/chicken/Germany/N/49 (H10N7). The comparison was carried out by genomic analysis of the strains by oligonucleotide fingerprinting and in bioassays on mink. The oligonucleotide fingerprint analysis revealed a high degree of genomic homology of around 98% between the viruses from mink, mallard and fowl. Only the recent avian isolates, that from the mallard and fowl could infect mink by contact, causing similar pathological and clinical signs and inducing seroconversion as did the mink virus. However, the susceptibility of mink to the fowl and mallard viruses by contact was less pronounced than that to the mink virus. Both the genomic homology and the similarities from the infectivity and pathogenicity studies between the mink virus and the recent avian isolates point to a direct invasion of the mink population by an avian H10N4 virus.
TL;DR: Symptom development in tomato plants following whitefly-mediated inoculation with tomato yellow leaf curl virus (TYLCV) was related to the occurrence of viral DNA using a specific DNA probe.
Abstract: Symptom development in tomato plants following whitefly-mediated inoculation with tomato yellow leaf curl virus (TYLCV) was related to the occurrence of viral DNA using a specific DNA probe. Although disease symptoms were first observed 15 days post-inoculation, viral DNA could be detected 7 days earlier. TYLCV-DNA concentrations reached an optimum 4 days before symptoms appeared. The highest concentrations of TYLCV-DNA were found in rapidly growing tissues (shoot apex, young leaves, roots) and in the stems; the lowest concentrations were found in the older leaves and cotyledons. Plants were also inoculated on specific sites. Young leaves and apices were the best targets for virus inoculation. In these tissues, the viral DNA replicated at the site of inoculation and was transported first to the roots, then to the shoot apex and to the neighboring leaves and the flowers. Inoculation through the oldest leaves was inefficient.
TL;DR: The cloning and 3′ sequence determination of feline calicivirus strain F9 enabled the production of strand specific probes for RNA synthesis and it is shown that numbers 1–5 are represented as negative strands which may serve as templates in the synthesis of these RNAs.
Abstract: We report here the cloning and 3' sequence determination of feline calicivirus strain F9. Subcloning the 3' terminus enabled the production of strand specific probes for RNA synthesis. We extend the number of virus specific RNAs detected intracellularly to 8, and show that numbers 1-5 are represented as negative strands which may serve as templates in the synthesis of these RNAs.
TL;DR: The PTV-hamster model shares similarities to Rift Valley fever (phleboviral disease), which causes fatal disease in man and domesticated ruminants, and Lesions in the hamsters had characteristics of disseminated intravascular coagulation (DIC).
Abstract: The hamster,Mesocricetus auratus, was examined as a possible model for investigating the poorly defined pathogenesis of the familyBunyaviridae, genusPhlebovirus. Punta Toro virus (PTV) isolates from Eastern Panama were highly virulent for two outbred and five inbred hamster strains, while isolates from western Panama were of low virulence. The Adames strain (eastern Panama) of PTV (LD50 approximately 1 PFU, sc) caused an acute fatal disease (average survival time, 3.8 days) in 10-week-old Lak: LVG (SYR) hamsters. Severe necrosis of the liver, spleen, and small intestine was associated with extensive expression of viral antigen in these organs. The Balliet strain (western Panama) of PTV (LD50>6log10 PFU, subcutaneously) caused a mild hepatocellular infection with peak viral liver titers of 3–4 log10 PFU/g compared to 8–9 log10 PFU/g for the Adames strain. We observed histological lesions in the red pulp of the spleen or the lamina propria of the small intestine with the Adames strain. Lesions in the hamsters had characteristics of disseminated intravascular coagulation (DIC). The PTV-hamster model shares similarities to Rift Valley fever (phleboviral disease), which causes fatal disease in man and domesticated ruminants.
TL;DR: The haemagglutinin genes of the viruses were sequenced and changes were detected indicating amino acid substitutions at position 196–198 in the attenuated egg-grown virus D whereby a potential glycosylation site present in the other viruses was lost.
Abstract: An influenza B virus was passaged in man (virus A) and then in human embryo trachea (C) and into embryonated eggs (D) or directly into eggs (B). Virus A, B, and C had the same (cell-like) haemagglutinin phenotype on reaction with selected monoclonal antibodies while D had an “egg-like” phenotype. The viruses were administered at a dose of 1,000 TCD50 (for MDCK cells) by intranasal inoculation to groups of 27 or 28 volunteers. Viruses A, B, and C all produced disease in six to eight volunteers, whereas D produced no illness and only four volunteers were infected. The viruses shed by the volunteers were indistinguishable from those with which they were inoculated. The haemagglutinin genes of the viruses were sequenced and changes were detected indicating amino acid substitutions at position 196–198 in the attenuated egg-grown virus D whereby a potential glycosylation site present in the other viruses was lost.
TL;DR: A role for the mitochondria as supports and/or energy suppliers for viral RNA synthesis and translation in the infected muscles of G. mellonella and suckling mice is postulated.
Abstract: The replication of Nodamura virus, type species of the familyNodaviridae, takes place principally into the interfibrillar spaces of the sarcoplasm in close association with mitochondria in the infected muscles of bothG. mellonella and suckling mice. The most striking event in infection ofG. mellonella muscle cells was the aggregation and shape modification of numerous mitochondria (elongation, interdigitation, and vesiculation) at an early stage of infection. These clusters of mitochondria were cemented by a thick electrondense material at the periphery of which viral particles undergo maturation process. In a later stage, degenerated and dilated mitochondria showed a clear assembling of virus particles on their outer membrane and occasionally on some inner membranes. These facts and the localization of RNA by RNase-gold technique in the assembling sites of viruses around and inside the mitochondria allowed us to postulate a role for the mitochondria as supports and/or energy suppliers for viral RNA synthesis and translation.
TL;DR: Gangliosides were able to restore the susceptibility of glycosidase-treated Vero cells to BK virus infection and inhibit infectivity by standard preparations of different ganglioside.
Abstract: BK virus infectivity was inhibited by gangliosides extracted from Vero cells and by standard preparations of different gangliosides. Gangliosides were also able to restore the susceptibility of glycosidase-treated Vero cells to BK virus infection.
TL;DR: It was suggested that the morphological maturation of HIV-1 particles was completed just before release from the cell surface in several cell clones producing HIV- 1 particles of different morphology.
Abstract: Three cell clones producing large numbers of infectious or noninfectious particles of human immunodeficiency virus type 1 (HIV-1), designated M 10/LAV-2, M 16/LAV-3, and MT/LAV-17, were isolated from persistently HIV-1-infected MT-4 cells. In M 10/LAV-2, the HIV-1 proteins were defective in the cleavage of gag precursor protein, and the particles were doughnut-shaped with a double-ring structure. These particles were produced by budding at the cell surface from crescentic structures followed by the formation of double-ring structures. The viral proteins in M 16/LAV-3 were defective in the cleavage of env precursor protein. The morphology of the virus particles was intact, and an electron dense bar-shaped core was seen inside a single-ring enveloped structure. The intact particles were released from the cell surface by a budding process in which crescent shape structures first appeared at the cell membrane, then subsequently just before release matured to a complete structure with an electron dense core. In MT/LAV-17, the synthesis of HIV-1 proteins was normal, and the particles were teardrop-shaped with an intact core structure. These particles were produced by budding with an electron dense core at the cell surface. Thus, it was suggested that the morphological maturation of HIV-1 particles was completed just before release from the cell surface in several cell clones producing HIV-1 particles of different morphology.