Publications by authors named "Oldstone M"

The host-directed cleavage of measles virus fusion protein on infected lymphoid cells was studied to understand the mechanism of viral persistence in lymphoid cells in vivo. Several lymphoblastoid cell lines were infected with measles virus, and the viral glycoproteins expressed on the cell's surface were radiolabeled and analyzed for cleavage of fusion (F(0)) to F(1) by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Daudi and Ramos lymphoblastoid cells were deficient in their ability to cleave measles virus fusion protein and correspondingly produced low titers of infectious measles virus, Daudi cells being more defective than Ramos cells.

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Murine cytomegalovirus (MCMV) does not productively infect OTT6050AF1 BrdU, F9, or PCC4 undifferentiated murine teratocarcinoma cell lines, as shown by immunofluorescence assays for viral antigens and by plaque assays for infectious virus. However, these cells were infected by a variety of other viruses. MCMV does productively infect PYS2 and OTT F12 differentiated murine teratocarcinoma cell lines.

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At different times of exposure, interferon (IFN) enhanced and suppressed pokeweed mitogen- (PWM) induced IgG synthesis by human peripheral blood lymphocytes (PBL). Pretreatment of PBL and IFN frequently increased antibody production by more than 100% when compared with that by untreated PBL. Results of experiments in which PBL were separated into T and B subpopulations indicated that IFN preparations acted directly on B cells.

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Purified hemagglutinin and fusion glycoproteins of measles virus either in soluble form or inserted in artifical membranes bind to human peripheral blood lymphocytes and induce cell-mediated cytotoxicity (CMC) in a dose-response fashion. Both autologous and heterologous noninfected target cells are lysed in vitro. The expression of CMC is not inhibited by anti-measles virus antibody added to lymphocytes previously exposed to viral glycoproteins.

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To better understand the mechanism(s) whereby antibody and complement and cytotoxic lymphocytes lyse infected cells, we studied the structure, interrelationship and turnover of measles virus polypeptides expressed on the cell's surface. Of the 6 major viral structural polypeptides, L, HA, P, NC, F, and M, found in purified virions or infected cells, only 2, the HA and F, resided on the surface of infected cells. The HA was present primarily in the form of a 160k dimer, and F was identified as a 64k polypeptide migrating distinct from other viral polypeptides.

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Among Guamanian natives, serum IgA and IgG levels were found to be higher than normal in amyotrophic lateral sclerosis (ALS); serum IgA was higher and IgM lower than normal in parkinsonism-dementia (PD). IgA levels increased with age in ALS, PD, and normal subjects; IgG increased with age in ALS and IgM decreased with age in PD. Serum immunoglobulin (Ig) levels did not correlate with the duration of either disease.

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We report a simple method for the isolation of the measles virus glycoproteins, and their subsequent incorporation into artificial lipid bilayers. The two viral glycoproteins, HA and F, were isolated in preparative amounts from disrupted purified virus by lentil lectin affinity chromatography. The proteins were reconstituted into single bilayer lipid vesicles by: (i) exchanging the non-dialysable detergent Nonidet P40 (NP40) for a dialysable one, octylglucoside, while the proteins were immobilized on the lectin column and (ii) co-dialysis of the eluted glycoproteins in octylglucoside with phosphatidylcholine.

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Mouse hepatitis virus (JHM strain) type 4 induces acute encephalitis followed by death in many strains of laboratory mice. Immunohistochemical study in vivo and analysis of mouse neuronal cells in vitro both indicate that the target cells in this infection is the neuron. Further, examination of several inbred mouse strains and neuronal cells from them shows that disease expression is controlled by a single autosomal gene action at the level of the neuronal cell.

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Demyelination may be induced by several different pathogenetic mechanisms. We have been utilizing mouse hepatitis virus (MHV) to study virus-induced demyelination in the central nervous system (CNS). To learn whether the different disease phenotypes in 4-week-old mice, caused by wild type (a model for fatal encephalomyelitis) or mutant ts8 (a model for primary demyelination), is due to an altered cellular tropism, we have developed an immunolabeling technique to evaluate critically the localization of MHV antigens in the unique cells of the CNS.

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Many strains of mice, when injected at birth with an ordinarily lethal dose of lymphocytic choriomeningitis virus (LCMV), grow to adulthood despite maintaining a persistent virus infection and chronic virus-induced immune complex disease. Because the susceptibility to LCMV infection changed over several years of observation, a number of murine strains with different histocompatibiity gene loci and genetic backgrounds were compared. Neonatal mice with H-2b, H-2d, and H-2q backgrounds were relatively insensitive to the effects of LCMV infection compared to mice with H-2k backgrounds, which had a high mortality rate in this situation.

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Six hours after measles virus antibodies bind to the surface of HeLa cells acutely infected with measles virus, the expression of an external polypeptide F1, as well as internal polypeptides P and M are altered. The loss of F1 molecules during antibody-induced antigenic modulation explains the lack of cell-cell fusion and giant cell formation of infected cells cultured in the presence of antibody. The decrease in F1, P, and M viral polypeptides is specific, since the effect is only seen with antibodies directed against measles virus antigens expressed on the cell's surface and not with antibodies directed against nonviral antigens expressed on the surfaces of virus-infected cells.

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Murine F9 and PCC4 teratoma cells do not express H-2 major transplantation antigens according to virus-specific T-lymphocyte cytotoxic or serological assays. However, such cells can be infected with and readily replicate many types of viruses (coxsackie B 3, mouse hepatitis, Sindbis, Semliki Forest [SFV], lymphocytic choriomeningitis, Pichinde, vesicular stomatitis, herpes simplex type 1) to the same extent as do murine F12 teratoma cells and mouse embryo fibroblasts, all of which express the H-2 determinants. In contrast, F9 and PCC4 cells are not productively infected with murine cytomegalovirus, whereas F12 and mouse embryo fibroblast cells are.

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Mice of several strains persistently infected with lymphocytic choriomeningitis virus (LCMV) mount continuous anti-LCMV immune responses leading to the formation and tissue deposition of immune complexes. Such mice carry infectious virus-immunoglobulin (presumably anti-LCMV antibody) complexes in the circulation. We have now determined that anti-LCMV antibody both complexed and free is found in the circulation of mice persistently infected with LCMV.

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When HeLa cells acutely infected with measles virus were incubated in a mixture containing only the six proteins of the alternative pathway of complement activation (C3, factors B and D, beta 1H, C3b inactivator, and native properdin) without antibody, there was activation of the alternative pathway as shown by progressive uptake of 125I-labeled C3b onto the cell surface. This C3b uptake was blocked by EDTA and was not shown by uninfected cells. The rate of 125I-labeled C3 uptake by infected cells was the same in the absence and presence of properdin; however, when antiviral IgG was bound to the cell surface, the rate of C3 uptake was increased in the presence of properdin.

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This chapter describes the effect of antibody on virus-infected cells with special reference to the human system. The destruction by antibody of the infected cells through the mediation of complement is described in detail based in considerable part on the contributions of the authors. Activation of the alternative pathway by the various infected cells is of special interest.

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Murine cytomegalovirus (MCMV) was found in preproductive tissues of newborn mice acutely infected with this virus. Using 3H-labeled complementary RNA (cRNA) probe made from MCMV DNA, viral genetic material clearly occupied ovarian stromal cells surrounding the follicular region but not cells of the follicle or cells in the outer tunic layers. In the testes, squamous epithelial cells external to the tunica albuginea harbored viral genetic material.

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