[Virus and abnormality of immuno-system].
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Abnormality
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Superinfection
Viral Interference
Viral transformation
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To investigate biological characteristics of the IVpi-189 progeny virus derived from the culture of influenza A virus as a live-attenuated vaccine candidate. Persistent infection of a cultured cell line with influenza A virus (MDCK-IVpi) was established by incubating continuously influenza virus-infected cells at a lower temperature. The infectious progeny virus derived from MDCK-IVpi cells at the 189rd subculture was designated as the IVpi-189 strain of influenza virus. The cytopathic effect induced by IVpi-189 virus was observed under different temperature conditions. The production of infectious progeny virus was examined at 38 and 32 degrees C by plaque titration of cell-associated and released virus. IVpi-189 virus showed cytopathic effect as strong as that of IVwt in infected cell line of MDCK at 32 degrees C. However, when culture temperature was raised to 38 degrees C, the cytopathic effect induced by IVpi-189 virus was delayed and less pronounced. Virus growth in IVpi-189 virus-infected cells at 38 degrees C was significantly reduced as compared with that of IVwt virus, although both viruses yielded nearly equivalent high titers of cell-associated and released virus at 32 degrees C. The reasons of the decreased proliferative ability of IVpi-189 virus at high culture temperature were unrelated with virus inactivation or the release of progeny virus, but associated with the decreased replication of infectious progeny virus in the infected cells. IVpi-189 virus derived from MDCK cells infected persistently with influenza A virus showed biological characteristics as a potential live-attenuated vaccine candidate.
Cytopathic effect
Subculture (biology)
Viral culture
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The investigated 16th and 45th in vitro passages of non-pathogenic variant 83 of the Kekava strain Marek's disease virus have led in chickens to resistance to Marek's disease by introduction of the above-mentioned virus 14 days before application of pathogenic variant 55 of the Kekava strain Marek's disease virus. Simultaneous administration of both variants of the Kekava strains Marek's disease virus did not protect chickens from the disease. Presence in those variants of the Kekava strain Marek's disease virus of genetic markers manifesting themselves on passaging the virus in chicken fibroblast cultures created the possibility to investigate interrelations between them in the organism of chickens, utilizing in isolation of the virus the method of infecting cultures with chicken fibroblasts. The results of isolation of the virus from the blood cells of vaccinated chickens have shown that in their organism there is interference between those virus variants since the frequency of isolation of the pathogenic virus variant was 3-times lower than that of the apathogenic Kekava strain Marek's disease virus, and both virus variants persisted in various cells. After simultaneous administration of both virus variants to chickens equal amounts of the pathogenic and of the apathogenic Kekava strain Marek's disease virus were isolated from their blood cells. In that case also persistance of both virus variants in one cell may occur.
Marek's disease
Strain (injury)
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The potential of live, attenuated influenza A virus vaccine strain (ts-1[E]) to safely evoke immunity in man was studied. Virus grown in eggs, like virus grown in bovine kidney culture, exhibited an acceptable balance between attenuation and immunogenicity. The attenuation of this virus was evident by its large 50% infectious dose for man (105tcid50) and by the failure of a large quantity of virus (107tcid50) to cause influenzal illness. The ts-1[E] virus replicated well in the nasopharynx and was genetically stable in man. Moderate levels of neutralizing antibodies were induced in serum and nasal wash, and there was a suggestion that the latter antibody was associated with resistance to wild-type influenza A virus. However, the ts-1[E] virus was a poor stimulator of antibody to neuraminidase. Overall the pattern of infection produced by the ts-1[E] recombinant virus was comparable to that seen with wild-type virus but was of shorter duration and lesser magnitude. These features make the ts-1[E] virus suitable for use as a live influenza A vaccine in man.
Attenuated vaccine
Recombinant virus
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Infectivity
Feline calicivirus
Strain (injury)
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Newcastle Disease
Veterinary virology
Viral culture
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Abstract The hemagglutinin (HA) protein of influenza virus mediates essential viral functions including the binding to host receptor and virus entry. It also has the antigenic sites required for virus neutralization by host antibodies. Here, we characterized an H3N2 triple reassortant (TR) influenza virus (A/turkey/Ohio/313053/04) with a mutation at the receptor binding domain (Asp190Ala) that occurred upon virus transmission from turkeys to pigs in an experimental infection study. The mutant virus replicated less efficiently than the parental virus in human, pig and turkey primary tracheal/bronchial epithelial cells, with more than 3-log 10 difference in virus titer at 72 hours post infection. In addition, the mutant virus demonstrated lower binding efficiency to plasma membrane preparations from all three cell types compared to the parental virus. Antisera raised against the parental virus reacted equally to both homologous and heterlogous viruses, however, antisera raised against the mutant virus showed 4-8 folds lower reactivity to the parental virus.
H5N1 genetic structure
Antibody-dependent enhancement
Veterinary virology
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Summary Six caprine arthritis-encephalitis virus (CAEV)-free goats kept in strict isolation were inoculated intravenously with a cloned CAEV isolate (virus 020). At 78 weeks post-infection a virus (virus 095) isolated from one of the goats was shown to have the characteristics of CAEV, but was antigenically distinct from virus 020 and two other CAEV isolates by serum neutralization tests. Serum from the goat that had the variant virus neutralized the inoculum virus and the variant virus but serum from other inoculated goats neutralized only the inoculum virus. The variant virus and the inoculum virus were shown to co-exist in the infected goat, but the presence of the antigenic variant did not appear to be associated with an increase in severity of lesions compared with other inoculated goats.
Antigenic variation
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A defective interfering (DI) virus differs from the infectious virus from which it originated in having at least one major deletion in its genome. Such DI genomes are replicated only in cells infected in trans with homologous infectious virus and, as their name implies, they interfere with infectious virus replication and reduce the yield of progeny virus. This potent antiviral activity has been abundantly demonstrated in cell culture with many different DI animal viruses, but few in vivo examples have been reported, with the notable exception of DI Influenza A virus. A clue to this general lack of success arose recently when an anomaly was discovered in which DI Influenza A virus solidly protected mice from lethal disease caused by A/PR/8/34 (H1N1) and A/WSN/40 (H1N1) viruses, but protected only marginally from disease caused by A/Japan/305/57 (A/Jap, H2N2). The problem was not any incompatibility between the DI and infectious genomes, as A/Jap replicated the DI RNA in vivo. However, A/Jap required 300-fold more mouse infectious units to cause clinical disease than A/PR8 and it was hypothesized that it was this excess of infectivity that abrogated the protective activity of the DI virus. This conclusion was verified by varying the proportions of DI and challenge virus and showing that increasing the DI virus : infectious virus ratio in infected mice resulted in interference. Thus, counter-intuitively, DI virus is most effective against viruses that cause disease with low numbers of particles, i.e. virulent viruses.
Infectivity
Viral Interference
Infectious dose
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SummarySpider monkeys and chimpanzees were given a series of three injections consisting of 17D yellow fever virus, followed by living West Nile virus, followed by a third injection which consisted of formalin-inactivated Russian spring-summer virus vaccine. On the basis of neutralizing antibody responses, the limitation of viremia, or both, developing when the animals were challenged with virulent viruses, these primates were judged to be protected to a considerable extent against Japanese B encephalitis, West Nile virus, St. Louis encephalitis, Murray Valley encephalitis virus, dengue types 1, 2, 3, and 4, two antigenic types of the Russian spring-summer virus complex, and Wesselsbron virus.An isolate of West Nile virus was passed a number of times in chick embryo tissue cultures and purified by the plaque technique. The progeny of two virus plaques, in a concentration of 106 mouse intracerebral lethal doses, did not produce encephalitis in intracerebrally inoculated rhesus monkeys. These attenuated viral preparations, on the basis of intracerebral titrations in mice, had at least 1,000 times the virus concentration that was necessary to produce encephalitis with the parent type. One of these attenuated isolates still produced homologous and heterologous neutralizing antibodies comparable to those of the parent strain. The data indicate that this attenuated West Nile virus did not revert to a more virulent form after alternate intracerebral passages in rhesus monkeys and suckling mice.The TP-21 strain of the Russian spring-summer virus complex was passed a number of times in chick embryo tissue cultures and purified by the plaque technique. The progeny from one of the virus plaques, in a concentration of approximately 300,000 mouse i.c. LD50, did not produce encephalitis when inoculated intracerebrally into rhesus monkeys. When this purified virus isolate of TP-21 was substituted for the formalin-inactivated Russian spring-summer vaccine in the triple vaccination procedure, considerable protection was noted in spider monkeys challenged with four members of the Russian spring-summer group of viruses.
Viremia
Flavivirus
Attenuated vaccine
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