A serological relationship between mumps and sendai viruses
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Abstract:
Sixty-six paired sera from patients suffering from mumps were examined with Sendai and mumps virus particle antigen: 50% showed a rise of complementfixing antibodies to mumps virus particle antigen only and the rest to both antigens. This relationship was further substantiated by the occurrence of both antibodies in a proportion of the sera of 362 blood transfusion donors and 978 sera from antenatal patients. The occurrence of both antibodies in patients' sera is discussed and the conclusion is reached that one of the components of the mumps antigen complex is indistinguishable from the essential components of the Sendai virus. I am indebted to the Maternity Department of the Edgware General Hospital for supplying the antenatal sera, and to Dr Preston of the Regional Transfusion Centre, Oxford, for the blood donor sera.Keywords:
Sendai virus
Mumps virus
De Meio and Walker were the first who recognized the antibody elevation against Sendai virus with mumps infections. The work to be reported here was conducted one to confirm their results and another to test the usefulness of soluble antigens of respective virus in serodiagnosis, in an effort to differentiate these two kind of infections.The results obtained so far will be summarized as follows:1) From 19 mumps children living in Sendai, paired serum specimens were obtained and tested for their antibody titer by means of hemagglutination inhibition (HAT) and complement fixation tests (CFT) with both viral and soluble antigens of respective virus. Antibody elevation in HAI as well as in CFT-V and-S was evident with all of these pairs, when mumps virus (Habel strain) was used as antigen.2) When these paired specimens were tested with antigens of Sendai virus, significant elevation of HAI titer was shown with 7 pairs (37%). However total 13 pairs among 19 (68%) revealed the positive HAI titer against Sendai virus including the pairs with a little or no elevation. The fact may suggest the possibility that mumps virus antigen is highly related to that of Sendai virus, particularly in HAI test. The fact that even in acute phase, some patients revealed HAI antibody titer against Sendai virus comparative to or higher than the titer against mumps virus was the main interest here evoked. Parallel elevation against heterologus antigen here pointed out, however, did not hold true with all of the tested pairs. Elucidation of this fact was left in a future.3) With complement fixation test using antigens derived from Sendai virus, some cross reaction was also observed at least when V antigen was used. But the correlation rate with mumps antigen was rather low when compared to the result obtained in HAT test.4) Any specimens examined here did not reveal antibody titer against soluble antigen of Sendai virus. This fact was thought to be useful, in differentiating mumps patients from infection of Sendai virus.
Sendai virus
Mumps virus
Complement fixation test
Antibody titer
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Summary Cultured spinal ganglia and cord from mice and hamsters were infected with mumps virus or Sendai virus. Expression of five structural proteins, the haemagglutinin-neuraminidase, fusion, nucleocapsid (NP), phospho (P) and matrix proteins was examined with monoclonal antibodies to each protein. In Sendai virus-infected mouse neurons all five viral proteins were detected. In hamster neurons infected with mumps virus all viral proteins were also expressed, but in mouse neurons only the NP and P proteins were seen. This suggests a species-specific cellular restriction of viral protein synthesis in mumps virus-infected mouse neurons. There was no, or only a slight, reduction in the number of neurons between days 4 and 20 after infection of mouse cultures with mumps virus, but the proportion of infected neurons diminished from 68% to 15% during this time.
Mumps virus
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The wild mumps virus which had been isolated from a patient suffering from mumps meningitis propagated biphasically in human lung cancer cell lines (Pc-3, Pc-10), while attenuated Urabe strain propagated monophasically. The early virus was detected in these cell lines when the cells were inoculated with the wild mumps virus at any multiplicity of infection but rapidly disappeared. The infectious virus, thereafter, could not be detected for about 20 days. However, the infectious virus appeared again and the titer of the virus in the culture fluid gradually increased. The late virus rapidly propagated in Pc-3 cells, while the early virus replicated in the same way as the original wild virus did. All of ten clones obtained from the original wild virus represented the biphasic growth in Pc-3 cells and the late virus was detected on the 25th-30th day after infection. The viral antigens in Pc-3 cells infected with wild virus did not disappear after cultivating under the presence of anti-mumps virus antibody for over 50 days. Furthermore, treatment of anti-mumps virus serum in the early period did not affect the appearance of the late virus. It is quite conceivable that the wild mumps virus might be able to persist in completely latent state and the adaptation of the virus to Pc-3 cells might progress during the latent period.
Mumps virus
Mumps vaccine
Viral culture
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Common antigens shared by Sendai and mumps viruses was suggested in the former two experiments, where the first observation was made with clinical materials obtained from mumps patients and the second one was obtained in the field serological survey. Then the third experiment was conducted here in experimental animals, where antibody responses of both chicken and guinea pig against both Sendai and mumps viruses were examined every week for 5 weeks. In chicken, single intravenous administration was the choice of immunization procedure and obtained specimens were examined for their antibody titer on hemagglutination inhibition (HAI) and neutralization tests. In guinea pigs, the inoculum virus was given by instillation and the serum drawn every week was tested in HAI and complement fixation tests (CFT) with both viral and soluble antigens of each virus.Obtained results will be summarized as follows:1) In chicken, when mumps virus was used as an immunogen, antibody response against homologous virus was obtained in a uniform fashion with all tested chickens. Whereas one out of three, revealed parallel antibody shift against Sendai virus. In this case antibody titers were proved both in HAI and neutralization tests. When Sendai virus was used as an antigen, HAI titer against mumps virus was elicited with all three chickens examined so far.2) In guinea pigs, when mumps virus was used for intranasal inoculation. HAI titer against Sendai virus as well as against homologous virus was proved with tested 4 guinea pigs. However, in CFT, no heterologous antibody was provable. On the other hand, when Sendai virus was used as an immunogen, any response against mumps virus was not provable.In summary, shared antigenicity was provable between these two viruses not only with human specimens but also in animal experiments.
Sendai virus
Mumps virus
Antibody titer
Immunogen
Complement fixation test
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Murine cells (L929, MC57G, and P815 mastocytoma) defectively infected with the egg-adapted vaccine strain of mumps virus were found to be susceptible to cytotoxic T-lymphocyte (CTL)-mediated lysis. In vitro secondary, but not in vivo primary, generated CTL caused cytolysis of these targets in an H-2-restricted manner. UV-inactivated-mumps virus-coated murine cells were also found to be susceptible to CTL-mediated lysis. Comparisons of murine CTL-mediated lysis by three paramyxoviruses (mumps, Sendai, and Newcastle disease viruses) indicated that no cross-reactivity occurred. The CTL response with mumps virus exhibited specific unresponsiveness patterns, as influenced by the H-2 K/D regions of the mouse strains, that were partially different from those of Sendai virus and Newcastle disease virus.
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CTL*
Mumps virus
Newcastle Disease
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Sendai virus
Mumps virus
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Summary The immunological relationships between mumps virus and parainfluenza viruses were investigated with 74, 78 and 80 previously developed monoclonal antibodies directed against five major structural proteins of mumps virus, Sendai virus (a murine parainfluenza type 1 virus) and parainfluenza type 3 virus. These monoclonal antibodies were reacted with the three viruses, with parainfluenza type 2 virus and with Newcastle disease virus (NDV) in ELISA and immunofluorescence (IF) tests. In addition, immunoprecipitation tests with [35S]methionine-labelled extracellular virions were carried out with cross-reacting monoclonal antibodies. None of all 232 monoclonal antibodies against the three viruses cross-reacted with either parainfluenza type 2 virus or NDV in ELISA and IF tests. In the collection of 74 mumps virus monoclonal antibodies, three directed against the nucleocapsid (NP) protein, polymerase protein, and fusion protein cross-reacted with Sendai virus. Two Sendai virus monoclonal antibodies directed against two different epitopes of the haemagglutinin-neuraminidase (HN) protein cross-reacted with parainfluenza type 3 virus. Six other Sendai virus monoclonal antibodies directed against four different epitopes of the HN protein and one directed against the NP protein cross-reacted with mumps virus. Eight out of 80 monoclonal antibodies directed against parainfluenza type 3 virus cross-reacted with Sendai virus. One was directed against the HN protein, four were directed against a minimum of two epitopes of the matrix protein and three were directed against three different epitopes of the NP protein. The different cross-reactions found show that Sendai virus is antigenically related to both mumps virus and parainfluenza type 3 virus. In contrast, no antigenic relationship could be demonstrated between mumps virus and parainfluenza type 3 virus.
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Abstract Rat dorsal root ganglia in tissue culture, which contain an interferon‐γ (IFN‐γ)‐like immunoreactive subpopulation of neurons, were infected with paramyxoviruses. Sendai virus caused a substantial neuronal lysis, while the RW strain of mumps virus caused a much less pronounced nerve cell loss. Early during infection, the subpopulation of IFN‐γ‐like immunoreactive neurons was less susceptible to mumps virus. Virus antigen was rapidly lost from surviving IFN‐γ‐like positive neurons infected with Sendai virus, while this remarkable self‐curing effect occurred in both nerve cell populations at later time points after mumps virus infection. By quantitative enzyme‐linked immunosorbent assay (ELISA) technique, increased levels of “neuronal IFN‐γ” were recorded at 10 hr and 30 hr after infection with Sendai and mumps virus, respectively. This study indicates a role for the neuronal IFN‐y‐like molecule in determining the outcome of a viral infection in sensory ganglia.
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Mumps virus
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A hemagglutinating virus was reported to be frequently isolated from laboratory mice by us in Japan (Fukumi et al, 1954) . This virus was later proposed to be called HVM (hemagglutinating virus of mice) by us, but as several independent names were adopted by several groups of investigators and more confusion was apt to occur, a committee was established by the Society of Japanese Virologists to control such confusion. This committee finally agreed to propose the name HVJ (hemagglutinating virus of Japan) for the virus in question. This virus is however, widely called Sendai virus in countries outside of Japan since Jensenet al.'s publication (Jensenet al., 1956), where they proposed to call it as influenza virus D. Now it seems fairly well accepted that the virus belongs toMyxovirus parainfluenzaetype 1, though there is still some reservation (Fukumi and Nishikawa, 1961) .As this virus has been considerably widely distributed among laboratory mice, it has often caused disturbances in experiments in which intranasal inoculations of laboratory mice are employed, especially experiments dealing with mouse passages of influenza and some other viruses. This situation prompted us to conduct experiments concerned with epidemiology and some other features of Sendai virus infections in laboratory mice.
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Confusion
Virus isolation
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To test the possibility of recent outbreak of Sendai virus infections among the population of Sendai, this serological survey was intended. Proposal of the work was originally made from the result reported in the previous paper, where most sera obtained from mumps patients at acute stag revealed high antibody titer against Sendai virus when tested in hemagglutination inhibition reaction.An explanation of the fact was the shared antigen between these 2 viruses. An alternative idea was the anamestitic elicitation of Sendai virus antibody with mumps virus. However, both possibilities may finally lead to the same conclusion of shared antigen.Serum specimens were obtained from 260 healthy people in Sendai and divided into two groups, i.e. one of children under 15 years, another of adult over 16 years old. The results obtained so far revealed the following conclusion.1) 73% of children and 89% of adult did not have any antibody titer against Sendai virus when examined on hemagglutination inhibition test.2) High distribution of antibody was found only among children between 4 and 10 years old. Antibody titer of these specimens was also high.3) From 71 healthy children of 6 years old, new serum specimen were obtained to test the cross relationship of Sendai virus with mumps virus. 52% of the tested specimens had the titer against Sendai virus and 82% against mumps virus. Among 37 specimens positive against Sendai, 36 specimens (97%) had the significant titer against mumps virus. Whereas among 58 specimens positive agaiast mumps, 36 (62%) was positive against Sendai virus. Taken together, HAI titer revealed here against Sendai virus was anticipated to have the character provoked by mumps virus. However, critical analysis of this observation was left for further studies
Sendai virus
Mumps virus
Antibody titer
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