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At least 19 recordsLinked to original sources
PubMed1978

Synthesis and packaging of herpes simplex virus DNA in the course of virus passages at high multiplicity.

Herpes simplex virus type 1 (HSV-1), strain ANG, was passaged serially at high MOI or undiluted on RC-37 cells. The yields of infectious virus decreased and increased periodically with a maximum of about 3 log units variation in titer. The amount of newly synthesized HSV-1 DNA, however, did not vary by more than a factor of 2. On the other hand, the fraction of total HSV-1 DNA associated with virions was reduced at passage numbers coinciding with the minima in the yields of infectious progeny virus. Apparently, low yields of infectious virus mainly reflected a reduced efficiency of packaging of viral DNA into mature virus particles. One step in the process of virus maturation which appeared to be impaired was the assembly of nucleocapsids. HSV-1 ang was shown to be capable of generating different classes of defective particle in independent series of virus passages at high MOI.

Capsid↗
PubMed1978

Modification of Trichoplusia ni nuclear polyhedrosis virus passaged in vivo.

A designated strain of plaque-purified Trichoplusia ni nuclear polyhedrosis virus (NPV) was used to initiate a serial passage series in vivo. The virulence of polyhedra inclusion bodies (PIB) and the distribution of MP (many PIB) and FP (few PIB) strains in hemolymph were monitored. When virus was passaged per os as PIB, there was no major change in virulence after 15 passes in insects. Plaque analysis of hemolymph from the infected insects indicated that there was no selection for the FP strain of virus. There was little overall change in the infectivity of nonoccluded virus (NOV) after 16 passes by injection into T. ni larvae; however, plaque analysis of the hemolymph from the infected insects indicated progressive selection of FP virus. It is postulated that when PIB are the vehicles of virus transmission, there is no progressive accumulation of noninfectious FP PIB; however, when NOV are the vehicles of virus transmission, FP NOV production displaces MP virus synthesis. This may result from a growth advantage of the FP NOV over the MP NOV as shown in vitro and from the noninfectious nature of FP PIB.

Animals↗
PubMed1978

Excess of interfering over infectious particles in herpes simplex virus passaged at high m.o.i. and their effect on single-cell survival.

The capacity of herpes simplex virus to kill cells and to form both infectious centres and progeny virus was studied in cell culture. Two virus stocks were compared at various m.o.i.: (i) a standard virus stock and (ii) a stock which contained interfering virus particles (I particles). The formation of infectious progeny virus as well as of infectious centres appeared to be reduced by the action of I particles. In the examined virus stock I particles exceeded infectious particles by at least a factor of 5 to 10. More than 50% of cells which could be demonstrated to be hit by I particles survived and formed colonies.

Cell Line↗
PubMedDate not supplied

[Study of formation of amantidine and rimantidine resistant variants of influenza A2 subtype virus].

Passages of influenza A2/Hong Kong/68 in developing chick embryos in the presence of amantadine and rimantadine were carried out and demonstrated rapid development of a resistant virus line under these conditions. Changes in the sensitivity of the virus to the drug were due to selection of resistant particles from genetically inhomogenous original virus strain. The rate of formation of the resistant population was shown to be clearly dependent upon the amount of amantadine inoculated into embryos. The resulting resistant lines retained this property throughout multiple virus passages in embryos without the drug. These biological and antigenic properties of the resulting variants did not differ from those of the initial A2/Hong Kong/68 strain.

Animals↗
PubMed1977

Effects of low- and high-passage influenza virus infection in normal and nude mice.

A human isolate of type A Hong Kong influenza virus (H3N2) was adapted to mice by serial passage. Lung homogenates from mice who received low passage levels contained about the same quantity of virus (10(6.2-6.95) 50% tissue culture infective doses/ml) as those from mice who received high passage levels (10(5.95-6.45) 50% tissue culture infective doses/ml); however, death occurred only in animals given high-passage virus. Passage 3 (P3) and passage 9 (P9) viruses were selected as representative of low-passage and high-passage viruses, respectively. Although minimal differences were detected in infectivity for rhesus monkey kidney tissue cultures and mice, P9 virus was at least 10,000 times more lethal for mice (mean lethal dose = 10(4.2)). Infection with P3 virus was accompanied by minimal bronchitis and bronchiolitis only, whereas P9-infected animals exhibited marked bronchitis, bronchiolitis, and pneumonia. Striking thymic cortical atrophy was also demonstrable in the P9-infected animals and, although virus was more commonly recovered from thymuses from these animals, immunofluorescent studies revealed only a few cells containing influenza virus antigens. To further explore the participation of thymus-derived lymphocytes in influenza, athymic nude mice and furred immunocompetent littermates were given 500 50% mouse infectious doses of P9 virus. Nude mice exhibited an increased survival time and, in contrast to the extensive lung pathology seen in furred littermates, manifested minimal cellular infiltration and no tissue destruction in lungs. Brains from nude mice exhibited encephalomalacia with lymphocytic perivascular cuffing, which was not seen in furred animals. Virus was recovered from brains of 6 of 13 nude mice and 1 of 10 furred animals. The contrasting models suggest that thymus-dependent cells play a significant role in the inflammatory response to influenza virus infection and should prove useful for probing host-virus interactions which characterize influenza virus virulence.

Acute Disease↗
PubMed1979

Duck virus hepatitis: serial passage of attenuated virus in ducklings.

The safety of three attenuated virus vaccines of proven efficacy against duck virus hepatitis was assessed by controlled laboratory studies which involved the serial transmission of the virus through groups of two-day-old ducklings known to be susceptible to the disease. Each vaccine was initially derived from a different source. Enhancement of virulence which resulted in deaths from the disease in test groups of ducklings occurred in each instance.

Animals↗
PubMed1976

Further observations on subacute sclerosing encephalitis in adult hamsters: the effects of intranasal infections with Langat virus, measles virus and SSPE-measles virus.

Passage by i.c. inoculations of suckling hamsters enhanced the virulence for adult hamsters of Langat virus (TP21), neurotropic strain of measles virus (HNT) and SSPE-measles virus (HBS), not only for i.c. infections but also for intranasal instillations. The various viral strains passaged in hamsters showed a great similarity of behaviour including the ability of producing in a proportion of apparently unaffected survivors a subacute sclerosing encephalitis, leading to atrophy of parts of the brain especially the rhinencephalon. When large groups of animals were used for transmission experiments it became obvious that within one week after intranasal exposure, all the hamsters either died or became clinically affected, or did not show signs of disease but developed acute inflammatory brain lessions. tlater on, between 2-6 weeks following inoculations only 90% of hamsters were affected with either overt signs of disease or subacute brain lesions, suggesting that in about 10% of hamsters the initial infection did not progress further and that in these animals the early brain lesions disappeared. Passage levels, irrespective of the virus used, did not influence the total numbers of infected hamsters but showed a significant effect on the mortality in TP21 and HNT infections where the number of dead and clinically affected increased in the higher passes. In these higher passes the number of survivors with subacute brain lesions decreased. In SSPE-measles virus the number of clinically affected hamsters and those surviving but developing brain lesions remained constant throughout. Vacuolated neurons were present in the brains of hamsters that survived one of the above 3 viral infections. They were seen beginning from 6 weeks after infection only in animals that developed subacute sclerosing lesions and were most commonly found in the amygdaloid nuclei and in the pyriform cortex. There was a dramatic increase in the number of brains with vacuolated neurons in hamsters infected with the high viral passes; however, in the 36th hamster passage of TP21 no vacuolated neurons were present but the total number of survivors was small, the majority had no brain lesions and none had subacute sclerosing changes.

Age Factors↗
PubMed1977

Virus-induced diabetes mellitus: VIII. Passage of encephalomyocarditis virus and severity of diabetes in susceptible and resistant strains of mice.

The diabetogenic capacity of the M-variant of encephalomyocarditis (EMC) virus was markedly diminished after passage in mouse kidney cell cultures. One passage in mice fully restored this capacity. Virus harvested after five passages in either susceptible (SWR/J) or resistant (C57BL/6J) strains of mice was capable of producing diabetes in susceptible SWR/J mice but not in resistant C57BL/6J mice. Resistance was not overcome by inoculating mice with high concentrations of virus. Immunofluorescence studies showed that islets from strains of mice (i.e. CBA, AKR, C57BL/6J, A/J) that did not develop diabetes after infection with EMC virus, nonetheless, contained virus antigens. The percentage of cells in the islets containing virus antigens varied from 3-6% in CBA to 13-5% in A/J. In contrast 38% of the islet cells in susceptible SWR/J mice contained virus antigens. It is concluded that both the genetic background of the host and the passage history of the virus influence the development of diabetes.

Animals↗
PubMed1992

Mutation of the HANA protein of Sendai virus by passage in eggs.

A study was made to elucidate the effect of host cells on the HANA protein of Sendai virus. Two strains of Sendai virus were isolated from an epidemic in an animal laboratory by inoculating the lung homogenate of a moribund mouse either into LLC-MK2 cells (Oh-L) or into the allantoic cavity of embryonated eggs (Oh-E). Oh-E agglutinated chicken red blood cells at 37 degrees (HA37+), while Oh-L did not (HA37-). When Oh-L was passaged in eggs, conversion of the HA37- virus to the HA37+ virus readily occurred. A single point mutation was recognized on the HANA protein of the HA37+ virus either at position 525 (Gln----Arg) or at position 198 (Leu----Phe). Hl test with monoclonal antibody revealed conformational changes around the receptor binding site. Neuraminidase activity was also affected by these mutations. The changes in these biological activities of the HANA protein seemed to allow the HA37+ virus to replicate in eggs. On the contrary, the HA37+ virus replicates as efficiently as the HA37- virus in LLC-MK2 cells and no reversion to the HA37- virus was observed. The overall results indicate that the passage of Sendai virus in eggs resulted in selection of viruses possessing a specific mutation on the HANA protein. The pneumopathogenicity in mice was not significantly different between the HA37- virus and the HA37+ virus, suggesting the existence of genes other than the HANA gene that determine mouse pathogenicity.

Amino Acids↗
PubMed1992

Phenotypic properties of 3T3 cells transformed in vitro with polyoma virus and passaged once in syngeneic animals.

Cloned BALB/c 3T3 cells transformed in vitro with polyoma virus (PyV) acquired a higher tumorigenicity phenotype after a single in vivo passage. Some of the in vivo passaged cells (CTC cells) exhibited also a higher metastatic phenotype than cells from the same clones that were maintained only in culture (C cells). A phenotypic comparison between CTC and C cells was performed. It was found that most CTC lines exhibited a higher binding to laminin compared to their clonal C cell ancestors. Some CTC cells were less sensitive to the cytotoxic effects of TNF-alpha than the corresponding C cells. CTC cells originating from tumors which appeared after a long latency period (late tumors) tended to express Fc gamma RII while CTC cells originating from tumors which appeared after a short latency period (early tumors) as well as the corresponding C cells tended not to express Fc gamma RII. The expression of a membrane epitope recognized by a monoclonal antibody expressing specificity towards PyV transformed cells, was down-regulated on late tumor cells compared to early tumor cells. Transfection of cloned PyV-transformed BALB/c 3T3 cells with the beta 1Fc gamma RII gene augmented the tumorigenicity and metastatic phenotype of the transfectants compared to control transfectants.

3T3 Cells↗
PubMed1975

The occurrence of vacuolated neurons in the brains of hamsters affected with subacute sclerosing encephalitis following measles or Langat virus infection.

Hamsters infected by the intranasal route with either hamster adapted Langat virus passaged at least 10 times in hamsters and the HNT strain of measles virus passaged 149 times in hamsters, developed subacute sclerotic lesions in the pyriform cortex, and beginning from 2 months after infection, were accompanied by neuronal vacuolation with ballooning of the cytoplasm, especially in parts of the brain in close proximity of the sclerotic lesions. The vacuolated neurons resembled those seen in scrapie, especially of sheep and goats, suggesting a similarity between the effects of slow and subacute viral infections.

Animals↗
PubMed1978

Characteristics of herpes simplex virus resistance to disodium phosphonoacetate.

Herpes simplex virus (HSV), which was partially resistant to the inhibitory effect of disodium phosphonoacetate (PAA), could be recovered following four virus passages in the presence of 100 microgram/ml PAA. Resistant strains were isolated from both HSV type 1 and HSV type 2. Virus resistance to PAA was not complete, and in most isolations a significant proportion of the virus stock remained susceptible to the drug. Resistance was shown to be heritable and persisted through virus passage and cloning experiments. PAA inhibited the replication of virus-specific DNA in sensitive strains of HSV but not in resistant strains of HSV. In vitro experiments directly demonstrated that PAA inhibited the activity of the virus-specific DNA polymerase 10 times more effectively in PAA-susceptible HSV than in PAA-resistant HSV. The treatment of HSV-infected mice with high levels of PAA did not induce the formation of resistant virus strains.

DNA Replication↗
PubMed1975

Development of a live attenuated varicella vaccine.

The Oka strain of varicella virus, isolated in our labolatory, was serially cultivated in guinea-pig embryo cultures (GPEC), and a considerable amount of cell-free virus was obtained from infected cell. GPEC passage virus at the 6th passage level was used in a small scale field trial. Susceptible children of 1 to 10 years old were injected subcutaneously with 100 to 1,000 PFU of virus. No clinical reactions due to the vaccination were observed in any children, and a high rate of antibody response was obtained with viral doses of more than 200 PFU. Attenuated virus obtained by passage in GPEC was propagated in human diploid (WI-38) cells, and it was also effective in inducing an immune response without clinical reactions. The results show that the Oka strain of varicella virus passaged in GPEC and human diploid (WI-38) cells may be used safely and effectively as a live attenuated vaccine.

Animals↗
PubMed1978

Pancreas-passaged avian encephalomyelitis virus and its immunogenicity.

A serial 34-chicken pancreas passage of avian encephalomyelitis virus by oral administration was successful. Oral inoculation test with 4 passaged viruses showed rapid infection of the duodenal wall and unchangeable infection of pancreas diminishing the viral invasiveness to other organs. The passaged virus caused neither detectable viremia nor clinical avian encephalomyelitis signs and produced neutralizing antibody of high titers.

Animals↗