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Biomedical subjects

J V Hallum

Publications and source records attributed to J V Hallum.

At least 19 recordsLinked to original sources
PubMed1990

Due process protection.

Explore the source record for details and available documents.

National Institutes of Health (U.S.)↗
PubMed1984

Bluetongue virus type 17 can exist in a latent state in MDBK cells.

An infection with bluetongue virus type 17 can be regulated by the temperature of incubation to be either persistent, producing low levels of virus; lytic, producing a high titer of released virus; or latent, producing no detectable virus. The persistent and latent states are reversible.

Animals↗
PubMed1981

Role of the host cell in persistent viral infection: coevolution of L cells and reovoirus during persistent infection.

Mutant L cells, designated LR cells, were isolated after "curing" a persistently infected cell line (L/C) with antireovirus serum. The LR cells were shown to be virus-free; no reovirus was detectable by infectious center assays, plaque assays, presence of viral proteins, presence of viral dsRNA and immunofluorescence studies. Persistent infections were readily established n LR cells following infection with either cloned, low passage wild-type reovirus or cloned, low passage reovirus isolated from carrier cultures. Reovirus isolated from carrier cultures, however, grew much better than wild-type reovirus in LR cells and showed complete dominance over wild-type reovirus in coinfection experiments. Infection of LR cells with wild-type reovirus resulted in a low-level persistent infection with inefficient viral replication; these mutant L cells were partially resistant to infection with wild-type reovirus. In contrast, infection of the mutant L cells with virus isolated from the persistently infected cells resulted in a persistent infection accompanied with efficient viral replication. Infection of the original L cells with either wild-type reovirus or reovirus isolated from the persistently infected cells resulted in a lytic infection with no surviving cells. Thus the host cell plays a crucial role in the maintenance of persistent reovirus infection. Our results show that there is a coevolution of both mutant L cells and mutant reovirus during persistent infection.

Animals↗
PubMed1979

Myelin basic protein binding cells in active multiple sclerosis.

A sensitive, antigen-specific rosetting technique was used to enumerate blood cells that bind myelin basic protein (BP) in MS patients and controls. Sixteen of 23 MS patients in exacerbation but only 7 of 48 in remission formed elevated numbers of rosettes. Five of the latter 7 patients had recovered from an exacerbation within four months of the laboratory evaluation. Eight of 20 patients with progressive MS, all of whom had had disease for more than four years, had BP rosette-forming cells. None of the 16 normal volunteers and 1 of 8 neurological controls had BP rosette-forming cells. These results suggest that BP-binding cells in MS are confined to patients in acute exacerbation or within four months of activity, and those who have had progressive disease for at least four years.

Antigen-Antibody Reactions↗
PubMed1978

Immunoglobulin class distribution of measles virus antibodies in serum and spinal fluids of patients with subacute sclerosing panencephalitis.

Sera and cerebrospinal fluids (CSF) from patients with subacute sclerosing panencephalitis (SSPE) were tested by indirect immunofluorescence for the presence of measles virus specific antibodies of the various heavy chain classes. IgG and IgA antibodies were detected in the CSF while IgG, IgM, IgA, IgD and IgE measles virus antibodies were found in a significant number of the patient sera. Sera from SSPE patients had slightly elevated levels of IgG, IgM, IgD and IgE while IgA was decreased. The heterogeneous heavy chain class distribution of measles antibodies suggests the possibility that non-complement fixing antibodies serve as blocking antibodies which aid in the persistence of intracellular measles virus infection in patients with SSPE.

Antibodies, Viral↗
PubMed1977

A persistent infection of baby hamster kidney-21 cells with mumps virus and the role of temperature-sensitive variants.

A persistent infection of baby hamster kidney-21 (BHK-21) cells with mumps virus (BHKpi) was maintained for over 60 cell passages in the absence of antiserum. Viral persistence was demonstrated in the cultures by hemadsorption, immunofluorescence, multinucleate syncytia, and released mumps virus at the level of 10(2)--10(3) fluorescent focus-forming units/ml. No detectable levels of interferon were found in cultures persistently infected with mumps virus. Approximately 85--95% of the cells contained viral antigens. Nuclear fluorescence was observed in the persistently infected cells. Mumps virus from persistently infected clutures (MuVpi) was more heat-labile than wild-type mumps (MuVo) when subjected to 40 degrees C. BHKpi cells had a more rapid doubling time and a higher cloning efficiency in soft agar in comparison to BHK-21 cells. MuVpi was also found to be temperature-sensitive. The temperature-sensitivity of MuVpi was determined by the efficiency of plating at 33 degrees and 39 degrees C. MuVpi readily established a persistent infection in BHK-21 cells with less cytopathology than MuVo, and released temperature-sensitive virus.

Animals↗
PubMed1977

Temperature-sensitive mutants of measles virus produced from persistently infected HeLa cells.

A persistent infection with the Edmonston strain of measles virus was established in HeLa cells in the absence of measles virus antibody (HeLaPI cells). By hemadsorption or immunofluoresnce virtually 100 per cent of the cells possessed measles virus components. HeLaPI cells produced no interferon and were not resistant to superinfection with Newcastle disease virus. HeLaPI cells contained both smooth (15--18 nm) and rought (20--35 nm) nucleocapsids as detected by electron microscopy. The virus produced from the HeLaPI cells (MVPI) varied in titer between 1.5 X 10(2) and 5.5 X10(4) PFU/ml, had a smaller plque size and was more heat resistant than wild-type measles virus. MVPI was also found to be temperature-sensitive. The temperature-sensitivity of MVPI was determined by the efficiency of plaquing at 33 degrees and 39 degrees C in Vero cell monolayers. When HeLaPI cells were incubated at 33 degrees C, there was a 50-fold increase in virus production as well as a slight increase in the percentage of cells forming infectious centers compared to HeLaPI cells grown at 37 degrees C. MVPI readily established a persistent infection in HeLa cells which also rleased temperature-sensitive virus.

Antigens, Viral↗
PubMed1976

Measles virus-specific IgD antibodies in patients with subacute sclerosing panencephalitis.

Indirect immunofluorescent analysis revealed that sera from five patients with subacute sclerosing panencephalitis possessed IgD antibodies directed against measles virus components in persistently infected HeLa cells. IgD levels in these sera were within the normal range. Control studies indicated that the reaction was specific for measles virus. The detection of IgD measles antibodies in these patients suggested that IgD may be involved in the pathogenesis of this viral disease.

Antibodies, Viral↗
PubMed1976

Detection of mumps virus antigens in Hodgkin's disease tissues.

Mumps virus antigens were demonstrated in biopsied tissues from Hodgkin's disease patients by indirect immunofluorescence. Impression smears from ten lymph node and two spleen specimens revealed viral antigens in the nucleus, cytoplasm or both. Measles virus antigens were detected in six out of seven Hodgkin's disease tissue (lymph nodes) both in the nucleus and cytoplasm. All tissues tested for the presence of Newcastle disease virus (NDV, an avian paramyxovirus) antigens were negative. Control tissues were obtained from patients with non-Hodgkin's lymphomas, breast cancers, adenocarcinomas and a number of other disease processes. In control tissues mumps antigens were detected in seven out of 31 specimens and measles antigens in nine out of 18 tissues.

Adolescent↗
PubMed1975

Comparison of RNA polymerase associated with Newcastle disease virus and a temperature-sensitive mutant of Newcastle disease virus isolated from persistently infected L cells.

An in vitro comparison was made of the RNA polymerase activity associated with Newcastle disease virus (NDVo) and three clones of the temperature-sensitive mutant (NDVpi) isolated from persistently infected L cells. Less polymerase activity was associated with the NDVpi clones. Also, compared to NDVo, an increase in incubation temperature from 32 to 37 or 42 C resulted in a marked decrease in polymerase activity for the temperature-sensitive mutants which coincided with their inability to replicate at 42 C.

Cell-Free System↗
PubMed1974

Role of interferon in six cell lines persistently infected with rubella virus.

Presistent infections with rubella virus were established in baby hamster kidney, BSC-1, HeLa, RK-13, rabbit embryo chondrocyte, and Vero cell lines. All of the cultures except Vero continually produced rubella virus and interferon to which the virus was sensitive. Concurrently, only the Vero cells did not display interference against superinfection with Newcastle disease and vesicular stomatitis viruses. The addition of 1,000 U of exogenous interferon to the cultures cured only the rabbit embryo and Vero cells of the persistent infection. That the interferon is not required for the initiation and maintenance of rubella viral persistence in vitro is implied by the following. (1) Vero cells were persistently infected in the absence of interferon; (2) actinomycin D or cortisone inhibited interferon synthesis but not the rubella viral infection; and (3) cells continuously cultured in the presence of cortisone maintained a viral persistence without interferon synthesis. On the other hand, interferon seems to be responsible for the viral interference; Vero cells infected with rubella virus and cultures inoculated with rubella virus in the presence of actinomycin D or cortisone did not display interference against Newcastle disease or vesicular stomatitis viruses.

Amnion↗
PubMed1973

Persistent Newcastle disease virus infection in embryonic chicken tracheal organ cultures.

The persistent infection of embryonic chicken tracheal organ cultures with Newcastle disease virus (NDV) is described. Tracheal explants remained morphologically intact and were able to support the replication of NDV for 6 months. Peak titers of released virus occurred at 1 week postinfection, whereas maximal immunofluorescence was not observed until 30 days postinfection. The inoculum titer was not critical, and viral persistence resulted with either of two strains of NDV tested. Serum was not required in the medium for explant viability or to maintain the persistent infection. The presence of a contaminating virus morphologically resembling a leukovirus neither altered the course of infection nor affected the survivability of explants. Although interferon was not detected in the culture medium, persistently infected explants were resistant to heterologous viral challenge, and a similar resistant state could be induced in uninfected explants with exogenous interferon or ultraviolet light-inactivated NDV. No evidence was found to implicate antibody as a regulatory factor in the establishment or maintenance of persistence. The results from electron microscopy and immunofluorescence suggest the cells of the subepithelial connective tissue as the site of NDV persistence.

Animals↗