Immunofluorescence with respiratory syncytial virus

Kisch, Alexander L.; Johnson, Karl M.; Chanock, Robert M.

doi:10.1016/0042-6822(62)90293-3

Cited by 44 publications

(15 citation statements)

References 6 publications

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“…Immunofluorescence studies by Kisch, Johnson and Chanock (45) confirmed observations of the replicative cycle observed by others (4,68). In their more detailed observations, they noted specific fluorescence only in the cytoplasm throughout the replicative cycle (45).…”

Section: It Was In This Context That the Search For New Viral Agentssupporting

confidence: 67%

“…In their more detailed observations, they noted specific fluorescence only in the cytoplasm throughout the replicative cycle (45). They also found no evidence of hemagglutination or growth in embryonated eggs.…”

Section: It Was In This Context That the Search For New Viral Agentsmentioning

confidence: 97%

“…The recognition of the importance of the virus in human disease stimulated studies of the properties of the virus itself (4,40,45).…”

Section: It Was In This Context That the Search For New Viral Agentsmentioning

confidence: 99%

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Isolation, characterization, and pathogenicity studies of a bovine respiratory syncytial virus

Smith

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Section: It Was In This Context That the Search For New Viral Agentssupporting

confidence: 67%

Section: It Was In This Context That the Search For New Viral Agentsmentioning

confidence: 97%

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Isolation, characterization, and pathogenicity studies of a bovine respiratory syncytial virus

Smith

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“…However, they pointed out that, when Veto cells were used as the host, extensive syncytia production was not seen. Similarly, when the Long strain was used with HEp-2 cells and stained by immunofluoreseenee, the nuclei within syneytia were seen to be free of specific fluorescent staining (3). In the present study, the replication of the A2 strain was seen to take place solely in the cytoplasm.…”

Section: Discussionmentioning

confidence: 75%

Electron microscopic studies of respiratory syneytial temperature-sensitive mutants

Kalica

Wright

Hetrick

et al. 1973

Archiv f Virusforschung

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SummaryThe A2 strain of respiratory syncytial (RS) virus and several temperature sensitive mutants derived from it were grown at the permissive (32 ~ C) and restrictive temperature (39~ in HeLa cells and thin sections of these cells were examined by electron microscopy. The mutants selected for this study were representative of 3 different complementation groups. The parent strain underwent the same sequence of morphogenesis at the permissive and restrictive temperatures. Morphogenesis of each of the mutants at the permissive temperature was similar to that of the parent strain. At the restrictive temperature cells infected with mutants belonging to two of the complementation groups developed a significantly reduced amount of one or more of the recognizable viral structures. In one instance (ts-4, complementation group A) budding and release of virus did not occur, while in another (ts-7, complementation group C) no virus specific structures were seen. Cells infected with the ts-2 mutant of complementation group B exhibited normal viral morphogenesis at restrictive temperature.

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“…The inhibitory effects of the test compounds on the expression of specific RSV antigens and syncytium formation were examined by indirect immunofluorescence following a procedure reported previously (22,28,30 (25,5, and 1 ,ug/ml), 3-deazaguanine (25, 5, and 1 ,ug/ml), or pyrazofurin (0.5, 0.1, and 0.02 ,ug/ml) was added to each of two chambers. After 18, 24, and 48 h of incubation at 35°C, the chambered slides were harvested, stained by immunofluorescence, and evaluated for the number of fluorescent foci (single cells and syncytia) and the number of nuclei per syncytium in 10 microscopic fields (x 100 magnification).…”

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confidence: 99%

Inhibitory effects of antiviral compounds on respiratory syncytial virus replication in vitro

Kawana¹,

Shigeta²,

Suzuki³

et al. 1987

Antimicrob Agents Chemother

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We examined the inhibitory effect of 20 antiviral compounds, including ribavirin, on the replication of respiratory syncytial virus in HeLa and HEp-2 cell cultures. Of the compounds studied, pyrazofurin and 3-deazaguanine emerged as more potent inhibitors of respiratory syncytial virus than ribavirin. Based on their inhibitory effect on the cytopathogenicity of respiratory syncytial virus in HeLa cells, the average 50% effective dose of pyrazofurin and 3-deazaguanine for eight strains was 0.07 and 1.65 ,ug/ml, respectively; that of ribavirin was 5.82 p.g/ml. The cytotoxicity of these compounds for HeLa cells was examined by monitoring the incorporation of radiolabeled uridine into cellular RNA. The selectivity indexes of pyrazofurin and 3-deazaguanine exceeded that of ribavirin by 70-and 11-fold, respectively. Pyrazofurin, 3-deazaguanine, and ribavirin inhibited both viral antigen expression and syncytium formation in HeLa cell cultures, as assessed by an indirect immunofluorescence assay. In these assays, pyrazofurin and 3-deazaguanine again proved more potent than ribavirin. 2,5-Diamidinoindole and carbodine were less potent than ribavirin. Various other compounds, i.e., 3-adenin-9-yl-2-hydroxypropanoic acid isobutyl ester, 3-deazauridine, 3'-C-methyluridine, 5'-deoxy-5-fluorouridine, 5-cyanoimidazole-4-carboxamide, and its ribofuranosyl derivative, did not inhibit the cytopathic effect of the Long strain of respiratory syncytial virus at concentrations -125 pLg/ml. Tubercidin, 5-chlorotubercidin, xylotubercidin, neplanocin A, thiosemicarbazone R, and 3-methylquercetine were too toxic to HeLa cells for their inhibitory effects on respiratory syncytial virus to be examined.Respiratory syncytial virus (RSV) causes lower respiratory tract infections such as bronchiolitis and pneumonia in infancy and early childhood. Most clinicians consider RSV one of the most important agents of acute respiratory disease in children, and almost 50% of infants are expected to suffer from RSV infection during their first winter (15,16,20,32,35). Inactivated RSV vaccine does not protect against natural infection and leads to an unusual immune response and even lung inflammation during the course of a subsequent natural infection (21). Recent research efforts have therefore focused on the development of either potent live RSV vaccines or effective antiviral compounds.Following reports that ribavirin may reduce the severity of illness and amount of virus shed in acute respiratory infections due to RSV or influenza B virus (13,14,23,37), the drug has been approved in aerosol form for the chemotherapy of RSV infections. This has prompted the search for antiviral compounds that may be as effective, if not more effective, against RSV than ribavirin. We have now investigated the inhibitory effects of 20 antiviral compounds, including ribavirin, on the replication of RSV in vitro.MATERIALS AND METHODS Viruses. The Long, S-2, and S-8 strains of RSV were kindly provided by Y. Numazaki, National Sendai Hospital, Sendai, Japan. The 58-8, 58-7,...

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Immunofluorescence with respiratory syncytial virus

Cited by 44 publications

References 6 publications

Isolation, characterization, and pathogenicity studies of a bovine respiratory syncytial virus

Isolation, characterization, and pathogenicity studies of a bovine respiratory syncytial virus

Electron microscopic studies of respiratory syneytial temperature-sensitive mutants

Inhibitory effects of antiviral compounds on respiratory syncytial virus replication in vitro

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