PubMed Health⌕ Search

Biomedical subjects

J S Wolinsky

Publications and source records attributed to J S Wolinsky.

At least 19 recordsLinked to original sources
PubMed1992

Antibody response to rubella virus antigen and structural proteins in retinitis pigmentosa.

Elevated serum ELISA IgG antibodies to rubella virus (RV) were found by three independent determinations in 41 (72%) of 57 adults with the retinal degeneration retinitis pigmentosa, while antibody responses to five other common neurotropic viruses were normal. However, these patients lacked clinical signs of active RV infection or known recent RV exposure, and 56 lacked IgM anti-RV antibody. Unusual relative percentages of IgG antibody to RV structural proteins compared with those of controls were found in patients' sera by radioimmunoprecipitation assay. For retinitis pigmentosa patients, percentage of RV envelope glycoprotein E1 antibody was similar to, of RV envelope glycoprotein E2 antibody was greater than, and of antibody to RV nucleocapsid C protein was lower than control percentages. Abnormal immunity to RV was also suggested by a lack of increased proliferation of lymphocytes to RV antigen despite elevated anti-RV antibody in patients with retinitis pigmentosa. Not associated with age or particular genetic pattern, these divergences from normal immunity suggest an unusual association between RV proteins and retinitis pigmentosa.

Adolescent↗
PubMed1991

Monoclonal antibody-defined epitope map of expressed rubella virus protein domains.

An expanded library of murine monoclonal antibodies (MAbs) was generated by infecting BALB/C mice with the Therien strain of rubella virus (RV) and selecting secreting hybrids by enzyme-linked immunosorbent assay (ELISA) using purified virion targets. A panel of plasmids containing specified RV cDNA fragments was also constructed by using a variety of strategies with pGE374- and pGE374-derived expression vectors. Hybrid RecA-RV-beta-galactosidase (LacZ)- or RecA-RV-truncated LacZ-containing proteins collectively representing the entire open reading frame of the structural proteins of RV were overexpressed in Escherichia coli. Bacterial lysates were then probed by ELISA with selected MAbs and by immunoblot following separation by electrophoresis under denaturing conditions. With this approach, MAbs that appeared to react with linear determinants defined epitopes localized within the following domains: MAbs C-1, C-2, and C-8 bind epitopes within the predicted amino-terminal 21 amino acids of the capsid region C9 to C29; MAb C-9 binds to a domain bounded by C64 and C97; MAbs E2-1 through E2-6 bind to the E2 glycoprotein backbone region from E2(1) to E2(115); MAbs E1-18 and E1-20 bind to the E1 glycoprotein region from E1(202) to E1(283). MAb E1-18 neutralizes RV infectivity; MAb E1-20 neutralizes infectivity and modestly inhibits hemagglutination. Analyses with selected synthetic peptides have confirmed several of the molecular domains deduced with the expressed proteins. These plasmid constructions and peptides have proven useful in beginning to unravel the molecular organization of several antigenic sites of this human pathogen.

Animals↗
PubMed1990

Antibody response to rubella virus structural proteins in multiple sclerosis.

The antibody response to the structural proteins of rubella virus was studied in patients with multiple sclerosis (MS). Irrespective of the antibody titer to whole rubella virus, the relative proportion of the IgG response to the surface glycoprotein E1 was diminished, and that to the surface glycoprotein E2 was elevated in MS patients when compared to a matched control population of normal health individuals or a group of patients with systemic lupus erythematosus and other collagen vascular diseases. No difference was observed in the response to the core protein of rubella virus on comparing the MS and normal control groups. This divergence in the relative antibody response to the viral surface proteins suggests that the vigorous antibody response to rubella virus reported in MS is not simply an expression of a nonspecific polyvalent B-cell response.

Adult↗
PubMed1990

Proton magnetic resonance spectroscopy in multiple sclerosis.

Regional in vivo proton magnetic resonance spectroscopy provides quantitative data on selected chemical constituents of brain. We imaged 16 volunteers with clinically definite multiple sclerosis on a 1.5 tesla magnetic resonance scanner to define plaque-containing volumes of interest, and obtained localized water-suppressed proton spectra using a stimulated echo sequence. Twenty-five of 40 plaque-containing regions provided spectra of adequate quality. Of these, 8 spectra from 6 subjects were consistent with the presence of cholesterol or fatty acids; the remainder were similar to those obtained from white matter of normal volunteers. This early experience with regional proton spectroscopy suggests that individual plaques are distinct. These differences likely reflect dynamic stages of the evolution of the demyelinative process not previously accessible to in vivo investigation.

Adult↗
PubMed1990

Immune studies in human immunodeficiency virus infection with myasthenia gravis: a case report.

A patient with human immunodeficiency virus infection had cellular and humoral immune responses studied longitudinally from the onset of generalized myasthenia gravis. Progressive decline in CD4+, CD45R+ and CD4+, CDw29+ T-cells, cellular immune responses to alloantigen and mitogen stimulation, and acetylcholine receptor antibody titers were associated with clinical improvement of all myasthenic symptoms.

Adult↗
PubMed1985

A quantitation of myelin-associated glycoprotein and myelin basic protein loss in different demyelinating diseases.

The loss of myelin-associated glycoprotein (MAG) and myelin basic protein (MBP) was compared by quantitative immunocytochemistry in demyelinating lesions of measles encephalomyelitis (ME), multiple sclerosis (MS), and progressive multifocal leukoencephalopathy (PML). Serial sections from paraffin-embedded tissue were reacted with antisera for MAG and MBP, and areas of staining loss were compared morphometrically. Lesions in ME showed MAG loss equal to that of MBP, lesions of PML showed MAG loss greater than that of MBP, and MS lesions showed a mixture of patterns. These data demonstrate distinctive patterns of MAG and MBP loss in these three diseases.

Central Nervous System↗
PubMed1985

Detailed immunologic analysis of the structural polypeptides of rubella virus using monoclonal antibodies.

A panel of murine monoclonal antibodies prepared against rubella virus is described. Fourteen of these monoclonal antibodies react with the E1 glycoprotein of rubella virus and define a total of six spacially separate epitopes in competitive inhibition assays. Antibodies binding to epitopes E1(a), E1(b), E1(c), or E1(e) inhibit the hemagglutinin function of the virus, while antibodies binding to epitopes E1(d) or E1(f) do not. Monoclonal antibodies binding to epitopes E1(c) or E1(d) prevent virus infectivity and identify antigen in distinct intracytoplasmic vacuoles of rubella virus-infected Vero cells by indirect immunofluorescence. Monoclonal antibody to epitope E1(f) localizes antigen primarily to the plasma membrane of infected cells, while antibodies binding to epitopes E1(a), E1(b), or E1(e) localize antigen throughout the infected cell's cytoplasm. A single monoclonal antibody is described which only reacts with the mature form of the virion E2 glycoprotein after rubella virus is treated with a disulfide-bond reducing agent. This antibody immunoprecipitates a 43,000 MW precursor to the E2 glycoprotein from lysates of infected cells and localizes its antigen throughout the cytoplasm of infected cells. The five remaining monoclonal antibodies react with the rubella virus C polypeptide. They define four topographically separate epitopes on the C polypeptide, C(a), C(b), C(c), and C(d), each of which is diffusely distributed throughout the cytoplasm of rubella virus-infected cells.

Animals↗
PubMed1979

Neuronal and oligodendroglial infection by the WW strain of Theiler's virus.

Newborn ICR mice were infected by intracerebral inoculation of 10(5.3) LD50 of the WW strain of Theiler's virus and examined serially by virologic and ultrastructural methods. Maximal titers of 10(6) LD50 developed in the brain by day 8 when 90 per cent of the animals were dead or moribund. The virus first appeared and was most prominent in the thalamus, basal ganglia, and midbrain. It spread from these areas throughout the cortex, brainstem, and spinal cord but spared the cerebellar cortex. Both neurons and oligodendroglia were infected. Infected cells first showed dispersion of polyribosomes, accumulation of vesicles, and widening of perinuclear cisternae. Normal cytoplasmic organelles and the nucleus were displaced by an accumulation of viral crystals, membranous profiles, and fibrillar material. Within degenerating cells the nuclear chromatin became clumped and marginated and the cytoplasm was filled either with vesicles or masses of paracrystalline viral arrays. These changes were accompanied by a vigorous inflammatory response of lymphocytes, plasma cells, macrophages, neutrophils, and eosinophils. Lysis of oligodendroglia during acute infection with the WW strain of Theiler's virus may provide a stimulus for the late autoimmune demyelination that has been described in animals that survive the acute encephalitis.

Animals↗
PubMed1979

Progressive rubella panencephalitis: immunovirological studies and results of isoprinosine therapy.

Two patients with progressive rubella panencephalitis, one with and one without stigmata of congenital rubella, were treated for 9 months with isoprinosine and showed continued clinical deterioration. Immunoviorological studies performed before, during and after treatment were unaffected by drug therapy. The virus was recovered on one occasion from the lymphocytes of one of these cases. Neither patient showed any major defects in cellular or humoral immunity. However, the lymphocytes of the patient with stigmata of congenital rubella failed to respond to rubella virus in vitro and had a heat stable, non-dialysable serum inhibitor of in vitro protein A stimulated proliferative responses. Both patients' serum interfered with the production of interferon by normal donor lymphocytes following stimulation with rubella and varicella virus antigen. Increasing serum titres of interferon which did not appear to be lymphoid or immune-specific in origin were found in these two cases.

Adolescent↗
PubMed1978

Varicella-zoster virus infection of human brain cells and ganglion cells in tissue culture.

The growth of varicella-zoster virus (VZV) in cultures of human brain (HB) and human ganglion (HG) cells was compared to VZV growth in human fibroblasts. Infected cultures were monitored by histologic, electron microscopic (EM), and virologic techniques. Two to three days after VZV infection of all cell cultures at a multiplicity of infection (MOI) of 0.1, a multifocal cytopathic effect (CPE) developed. CPE was characterized by multinucleated cells and virus-specific intranuclear inclusions as determined by immunofluorescence and EM. In VZV- infected HB and HG cells only, large vacuoles were also seen in the cytoplasm of dying cells. Some vacuoles were almost devoid of structures. Within and at the limiting membranes of other vacuoles, aggregates of VZV particles (measuring 210--230 nm) were seen enveloped in osmiophilic material. VZV infection of HB and HG cultures was strongly cell-associated. Clarified tissue culture medium removed at maximum CPE failed to infect homologous HB or HG cells. When an inoculum of VZV-infected HB or HG cells was transferred to homologous uninfected cultures for 10--15 passages, the incubation period for CPE remained constant, and the titer of VZV in cells sampled randomly corresponded to the amount of virus that was used for original infection.

Brain↗
PubMed1978

Virulence and persistence of three prototype strains of mumps virus in newborn hamsters.

Neuroadapted mumps virus (NMV) produces widespread central nervous system (CNS) disease and death after intracerebral (i.c.) inoculation of newborn hamsters. After intraperitoneal (i.p.) inoculation, NMV causes disseminated disease, moderate mortality and it persists in CNS tissues. Low tissue culture passage isolates of wild mumps virus do not establish CNS infection after i.p. inoculation; after i.c. inoculation they cause limited though persistent infection with little acute mortality. The biological behavior of a highly passaged vaccine strain of mumps virus (Jeryl-Lynn) is more similar to NMV than to the wild strain in its behavior in the newborn hamster.

Adaptation, Biological↗
PubMed1977

Subacute measles encephalitis complicating Hodgkin's disease in an adult.

A progressive neurological illness characterized by myoclonus, motor and sensory deficits, and lethargy occurred in a patient with Hodgkin's disease and was fatal within two months. A focal inclusion cell encephalitis was demonstrated by immunohistological means to be due to measles virus. Measles encephalitis must be considered a potential opportunistic agent in the immune-compromised host.

Antibodies, Viral↗
PubMed1977

Adenine arabinoside in the treatment of progressive multifocal leukoencephalopathy: use of virus-containing cells in the urine to assess response to therapy.

Two patients with biopsy-proved progressive multifocal leukoencephalopathy (PML) were treated with near-maximal doses of adenine arabinoside (Ara-A), 18.6 and 20 mg per kilogram of body weight per day for 14 days. In both patients, clinical progression of the disease was correlated with an increase in the size of low-density lesions seen by computerized tomography. One of the patients was observed to excrete abnormal epithelial cells into the urine. These cells contained papovaviruslike particles, and JC virus was cultured from the urine sediment. The relative number of these abnormal cells declined during Ara-A treatment. Both patients died shortly after the conclusion of therapy without a change in the progression of the central nervous system disease. Systemic administration of Ara-A did not offer significant clinical benefit in the treatment of these 2 advanced cases of PML.

Aged↗
PubMed1977

Experimental infection of human leukocytes with parainfluenza 1 (6/94) virus.

Parainfluenza 1 (6/94) virus replicated in both unstimulated and phytohemagglutinin (PHA)-stimulated human peripheral blood leukocytes (PBL). After exposure of PBL to 6/94 virus at a multiplicity of infection of 1, the presence of viral antigen was demonstrated by immunofluorescence in the cytoplasm of less than 1% of unstimulated PBL and 1 to 5% of macrophages. Small amounts (less than 50 mean egg infective doses per ml in most instances) of cell-free virus were present in 18 of 30 (60%) cell cultures tested from 3 to 8 days postinfection. Cell-free virus peaked 6 days postinfection. Virus replication was enhanced in PHA-stimulated cells. Approximately 1 to 10% of PHA-stimulated PBL contained viral antigen as evidenced by immunofluorescence, and cell-free virus was present in 19 of 25 (76%) of the cell cultures tested from 3 to 8 days postinfection. Paramyxovirus nucleocapsids and tubular aggregates were seen in the cytoplasm of approximately 5% of PHA-stimulated PBL and were visualized only in lymphocytes. No other unusual intracytoplasmic or intranuclear structures were seen.

Capsid↗