Location and abundance of poly (A) sequences in Sendai virus messenger RNA molecules.
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Adenine-rich sequences from 18S Sendai virus messenger RNA species were 99% adenylate, 3'-OH terminal, and were present in at least 50% of the RNA molecules. Intact virus messenger RNA molecules were resistant to exonucleolytic attack by polynucleotide phosphorylase, suggesting that their 3'-termini are masked. (+info)
Protein synthesis in Sendai virus-infected cells.
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The rate of protein synthesis in chicken embryo cells infected with Sendai virus 18 to 20 h previously was about two times greater than in mock-infected controls. At this time of infection six stable virus-induced proteins, four major structural proteins (P, NH, NP and M) and two non-structural proteins (28K and 61K), were identified by electrophoresis in SDS-polyacrylamide gel of total cell extracts. The structural glycopeptide F was not detected in the infected cell extracts. Pulse-chase experiments showed that PN NP, M and 28K proteins either did not undergo any post-translational processing or the processing occurred very rapidly. By contrast, a glycopeptide NH was apparently derived from one of two unstable precursons, 69K or 63K, which were revealed only after a short pulse. The synthesis of virus-specific proteins appeared to be regulated since its rate varied for individual classes of proteins. In nucleocapsid-particles isolated from infected cells two major structural proteins (P and NP) were found. A minor component with a very large mol. wt. was revealed in these particles as well as in the virus particle. (+info)
Attenuating mutations in the P/C gene of human parainfluenza virus type 1 (HPIV1) vaccine candidates abrogate the inhibition of both induction and signaling of type I interferon (IFN) by wild-type HPIV1.
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Recombinant human parainfluenza virus type 1 (HPIV1) and mutants containing point and deletion (Delta) mutations in the P/C gene (r-CDelta10-15HNT553A, r-CR84G, r-CF170S and r-CDelta170), which have previously been evaluated as HPIV1 vaccine candidates, were evaluated for their effect on the type I interferon (IFN) response in vitro. HPIV1 wt infection inhibited the IFN response by inhibiting IFN regulatory factor-3 (IRF-3) activation and IFN production in A549 cells and IFN signaling in Vero cells. In contrast, r-CR84G, r-CF170S and r-CDelta170 were defective for inhibition of IRF-3 activation and IFN production and r-CF170S and r-CDelta170 did not inhibit IFN signaling. Thus, HPIV1 antagonizes the IFN response at both the level of induction and signaling, and antagonism at both levels was disrupted by mutations in the P/C gene. Because CF170S affects C and not P, the anti-IFN function can be attributed to the C proteins. These data, in the context of previous in vivo studies, suggest that the loss of antagonism of the IFN response at both the level of induction and signaling, observed with the P/C mutants, r-CF170S and r-CDelta170, was necessary for significant attenuation in African green monkeys (AGMs). (+info)
Experimental parainfluenza-type-1-virus-induced encephalopathy in the adult mouse. An ultrastructural study of early lesions.
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The adult mouse inoculated intracerebrally with 6/94 strain of parainfluenza type 1 virus developed selective degenerative lesions in cerebral white matter. Ultrastrucrally, the infiltration of mononuclear cells, mostly lymphoid cells, apparently preceded the alterations of white matter parenchyma. The prominent feature of the white matter lesion was a lytic degeneration of both axon and myelin that seemed to be triggered by the mononuclear cell infiltration. Nucleocapsids of paramyxovirus were found only in ependymal cells and the very early stages of the infection. It is suggested that the mechanism of the white matter degeneration might be that of a virus-induced cell-mediated immune response directed at both the axon and myelin. (+info)
Inhibition of the growth of hemadsorption 2 virus by three acyl derivatives of amino acids.
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Three acyl derivatives of amino acids, dicarbobenzoxy-l-lysine sodium, carbobenzoxy-l-aspartic acid-beta-benzyl ester potassium, and N-3-phenylpropionyl-S-benzyl-l-cysteine potassium inhibit the growth of parainfluenza 1 (hemadsorption 2) virus. The growth of simian virus 40, vaccinia, poliomyelitis type 1, Semliki Forest, Eastern equine encephalitis, and Western equine encephalitis viruses was not affected by these compounds. Four other acyl derivatives of amino acids did not inhibit the growth of any of the viruses tested. (+info)
Specific macrophage immunity to Sendai virus: macrophage aggregation in vitro with Sendai virus by cytophilic antibodies.
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When a 24-h tube culture of rabbit alveolar macrophages was infected with Sendai virus, the rate of infected cells was found to be limited. Even at a multiplicity of infection (MOI) of 500 plaque-forming units per cell, an average of 63% cells was found to synthesize viral antigens stainable by direct immunofluorescence. When the macrophages obtained from rabbits hyperimmunized by an intravenous injection of Sendai virus were infected under the same in vitro conditions, the rate of antigen synthesis averaged a low as 23%. At the time of infection of alveolar macrophages from immunized rabbits (immune macrophages), cell aggregation at an MOI 50 and cell fusion at an MOI 500 were found 24 h after infection, and these reactions were never encountered after the infection of nonimmune macrophages. When the immune macrophages were either pretreated by trypsin or incubated in medium at pH 4.0, the infection no longer caused the aggregation. The supernatant fluid obtained after incubation at pH 4.0 contained neutralizing antibody to Sendai virus. Conversely, when nonimmune macrophages were incubated in the presence of rabbit anti-Sendai virus serum or purified immunoglobulin G, the same aggregation reaction occurred after virus infection. Ultraviolet light-killed Sendai virus could be used as the counterpart of alive virus in the same aggregation reaction. These results suggest that the aggregation reaction of the immune macrophages could be attributed to the presence of specific cytophilic antibodies on their surface. (+info)
Haemoglobin synthesis in fused cells.
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When primitive erythroid cells from 5-day-old chick embryos are exposed to inactivated Sendai virus they do not undergo haemolysis but fuse with other cells by the normal process of cytoplasmic coalescence. In this way cells actively engaged in the synthesis of haemoglobin may be fused with others that are not. In heterokaryons formed by the fusion of such erythroid cells with cells from established mouse or hamster lines, haemoglobin synthesis initially continues at a high level, but then declines and ceases altogether within a period of about 60 h. This decline affects the synthesis of both haem and globin and reflects the activity of specific regulatory mechanism, for under these conditions other chick proteins continue to be synthesized. The haemoglobin synthesized in the heterokaryons is entirely chick, and not mouse or hamster, haemoglobin. (+info)
Comparison of real-time PCR assays with fluorescent-antibody assays for diagnosis of respiratory virus infections in children.
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Conventional fluorescent-antibody (FA) methods were compared to real-time PCR assays for detection of respiratory syncytial virus (RSV), influenza virus type A (FluA), parainfluenza virus types 1, 2, and 3 (PIV1, PIV2, and PIV3), human metapneumovirus (MPV), and adenovirus (AdV) in 1,138 specimens from children with respiratory illnesses collected over a 1-year period. At least one virus was detected in 436 (38.3%) specimens by FA and in 608 (53.4%) specimens by PCR (P<0.001). Specimen quality was inadequate for FA in 52 (4.6%) specimens; 13 of these (25%) were positive by PCR. In contrast, 18 (1.6%) specimens could not be analyzed by PCR; 1 of these was positive by FA. The number of specimens positive only by PCR among specimens positive by PCR and/or FA was 18 (7.0%) of 257 for RSV, 18 (13.4%) of 134 for FluA, 25 (64.1%) of 39 for PIV1, 8 (88.9%) of 9 for PIV2, 17 (30.1%) of 55 for PIV3, and 101 (76.5%) of 132 for AdV. MPV was detected in 6.6% of all specimens and in 9.5% of the 702 specimens negative by FA. The mean number of virus copies per milliliter in specimens positive by both PCR and FA was significantly higher, at 6.7x10(7), than that in specimens positive only by PCR, at 4.1x10(4) (P<0.001). The PCR assays were significantly more sensitive than FA assays for detecting respiratory viruses, especially parainfluenza virus and adenovirus. Use of real-time PCR to identify viral respiratory pathogens in children will lead to improved diagnosis of respiratory illness. (+info)