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  • 1
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  PTCOG 48; Meeting of the Particle Therapy Co-Operative Group; 20090928-20091003; Heidelberg; DOC09ptcog146 /20090924/
    Publication Date: 2009-09-25
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 2
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  PTCOG 48; Meeting of the Particle Therapy Co-Operative Group; 20090928-20091003; Heidelberg; DOC09ptcog171 /20090924/
    Publication Date: 2009-09-25
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 3
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    German Medical Science; Düsseldorf, Köln
    In:  International Conference on SARS - one year after the (first) outbreak; 20040508-20040511; Lübeck; DOC04sars8.09 /20040526/
    Publication Date: 2004-05-26
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 4
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary.  A simple and rapid single-step reverse transcriptase-polymerase chain reaction (RT-PCR) was used to investigate the nucleoprotein (N) gene of 11 rabies viruses. A conserved set of RT-PCR primers was designed to amplify the most variable region in the N gene. N gene regions were amplified from 6 fixed laboratory viruses, 4 street viruses from dogs in Thailand, and a horse in Zambia. Sequences of the amplified products, together with the database of 91 additional sequences, were analyzed by using PILEUP program of the GCG package. The rabies viruses grouped into at least 9 distinct clusters by 〈90% nucleotide similarity of the N gene region: I (4 isolates, USA), II (2 isolates, South America), III (3 isolates, Africa), IV (52 strains, Europe, Middle East, Africa and South America), V (16 isolates, North America and Arctic), VI (17 isolates, Africa), VII (1 isolate, Africa), VIII (6 isolates, Thailand and Malaysia) and IX (1 isolate, Sri Lanka). A unique group of rabies viruses from Thailand and clusters of isolates corresponding to their geographic origin also were determined. The simple and rapid single-step RT-PCR proved to be useful for identifying rabies viruses, and for grouping the viruses into clades by sequence analysis.
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  • 5
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary.  Mutations in the fusion, F, protein of Sendai virus resulting in increased cleavability by ubiquitous host protease(s), and mutations in the matrix, M, protein resulting in bipolar budding, are both important determinants for the systemic infection in mice caused by the protease activating pantropic mutant, F1-R. Several mutants of Sendai virus (BY, BF, and KD-M) with phenotypes of bipolar budding and/or increased cleavability of F protein were isolated. Genomic RNA sequence analysis of the F and M genes of the mutants revealed that several deduced amino acids in the F and M proteins were different from those of F1-R, T-5 (a revertant of F1-R), and wild-type viruses. The BF and KD-M mutants that budded bipolarly and were also activated by ubiquitous proteases were examined for replication in tissue culture cells and in mice. All of the mutants exhibited multiple-step replication in MDCK, MDBK, and LLC-MK2 cells without trypsin, but formed plaques only in MDCK cells. One of the mutants, designated KD-52M, was similar to F1-R in that it formed plaques in all three cell lines without addition of exogenous protease. However, none of the mutant viruses, including KD-52M, caused a systemic infection in mice. The mutated M protein of F1-R enhances the disruption of microtubles. However, none of the mutants with a bipolar budding phenotype (BY, BF, and KD-M), disrupted the microtubules to the same extent as F1-R. All of these mutants had mutations in the M protein that were different from those found in F1-R. Taken together, these results suggest that mutations at Ser115 to Pro in the F protein and at Asp 128 to Gly and Ile210 to Thr in the M protein of F1-R are the mutations specifically required for the systemic infection caused by F1-R.
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  • 6
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Influenza virus A/turkey/Ontario/7732/66 (H 5 N 9), which is highly pathogenic to chickens, is nonpathogenic to quails. After intratracheal or intramuscular inoculation of quails, virus replication was limited to the respiratory tract, genital organs, and pancreas. However, aggravation of the pathogenicity was achieved through adaptation only by several passages of lung homogenates in quails. The adapted virus caused a fatal generalized infection in quails as well as in chickens. The pathogenic change of the virus could not be explained by a change in the proteolytic cleavability of the hemagglutinin, because no difference was found in the cleavability between the original and the adapted viruses. The adapted virus formed larger plaques and grew a little faster than the original one in both chicken embryo and quail embryo cells. The faster multiplication of the adapted virus at the site of infection might be the reason for its change in pathogenicity. The original virus could circulate among quails by a direct contact transmission without causing disease. The shed virus, however, caused a fatal infection in chickens when they were kept in contact with the infected quails. The epidemiological significance of this observation is discussed.
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  • 7
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The NS 2 messenger RNA (mRNA) of several influenza A viruses was shown to be synthesized in primary transcription. Analysis of in vitro translation products of mRNAs from infected MDCK cells treated with cycloheximide indicated that the NS 2 mRNA in addition to the NS 1 mRNA was synthesized with PR/8, Udorn, and Aichi viruses. The findings indicated that the NS 1 mRNA of these viruses was able to be spliced into the NS 2 mRNA as a primary transcript without viral protein synthesis, although the extent of splicing varied among different virus strains.
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  • 8
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary.  Infection with measles virus induces a transient immunosuppression, which occasionally results in fatal opportunistic infections. To obtain fundamental information about the mechanism, we examined peripheral blood mononuclear cells (PBMC) from acute measles patients aged from infants to 35 years old, obtained at various times from incubation periods to 103 days after onset of rash, for the number of lymphocyte subsets by flowcytometry. The data were analyzed for relationships between aging of the patients and the severity of immunosuppression. In classical measles cases, infected lymphocytes detected as a minor pupulation during the incubation period disappeared soon after onset of rash, whereas in the cases of serious illness, the infected cells persisted longer after the rash. At the onset of rash, remarkable lymphopenia had already occurred in all measles cases with reduction in cell numbers of CD4+T cells, CD8+T cells, B cells, neutrophils, and monocytes. In contrast, natural killer (NK) cells were increased in number and activated, which might be a response compensatory for the lymphopenia. Apoptosis-associated molecules such as CD95(Fas) and TNF-related apoptosis-inducing ligand-receptor (TRAIL-R) were highly expressed on the cell surface of most surviving non-infected lymphocytes, and DNA fragmentation was also observed upon incubation in vitro. These results suggested that the profound lymphopenia was primarily due to extended death of non-infected blood cells caused by apoptosis. The severity and duration of the lumphopenia were age-dependent; less severe in young children whereas much severer in infants under one year of age as well as adolescents and adults. From these results, it was suggested that remarkable lymphopenia due to apoptosis of uninfected cells is one of the principal causes for immunosuppression induced by measles virus infection, and is correlated with the age-dependent severity of the disease.
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  • 9
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The protective effects of the passive administration of convalescent serum from mice infected with Sendai virus were evaluated in mice challenged intranasally with wild-type and a pantropic variant (F1-R) of Sendai virus. Adoptive transfer of the serum efficiently prevented F1-R from infecting the systemic organs, but it failed to protect the mice from infections of the respiratory tracts by either virus. Virus replication in nasal turbinates was not diminished while infection in the lung was suppressed sufficiently for the infected mice to survive the infection. These findings suggest that serum antibody is less effective for the protection against viral infections on the surface of the respiratory tract, but it is effective for inhibition of spread of the virus into the systemic organs.
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  • 10
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The MDBK-R cell line is a variant of the MDBK cell line, which was derived by three consecutive high multiplicity superinfections of MDBK cells with AWBY-140 virus, a mutant of influenza virus A/WSN (H 1N 1). MDBK-R cells are permissive for productive replication of AWBY-140, but resist lysis by the virus and grew normally without producing infectious virus after replication of the mutant occurred there. By polymerase chain reaction (PCR), we demonstrated nucleotide sequences specific to all the 8 genes of AWBY-140 in MDBK-R cells which had been infected with the mutant at a high multiplicity and subsequently received 25 passages. This suggests that the genes of influenza virus mutant persisted in the dividing host cells for a long time after productive infection, when none of the cells was producing virus. We were also able to amplify the M gene related sequence of the mutant from both poly(A)+ and poly(A)− fractions of the RNA extracted from the cells at 27th passage level by PCR, which suggests that the persisting genes were replicated and transcribed, but we failed to demonstrate any viral protein in the cells by Western blotting.
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