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Biomedical subjects

M J Levin

Publications and source records attributed to M J Levin.

At least 109 records · Page 6Linked to original sources
PubMed1991

Trypanosoma cruzi: antibodies to a MAP-like protein in chronic Chagas' disease cross-react with mammalian cytoskeleton.

Trypanosoma cruzi lambda gt 11 library from epimastogote derived mRNA was screened with human chagasic sera or sera from chronically infected mice. Strong reactive recombinants were detected with both sera. Two recombinant clones were studied in more detail and shown to be composed of the same 114-bp repetitive sequence coding for a 38 amino acid repetition. This repetition is the same size and shares greater than 60% homology with the reported T. brucei microtubule associated protein (MAP) p320. The insert of one of these clones, K1-7 (228 bp), was subcloned into pMSgt11 and the soluble recombinant polypeptide expressed. Antibodies against the K1-7 fusion polypeptide recognized a major 110-kDa band from cytoskeleton. Anti K1-7 monospecific antibodies detected several cytoskeletal proteins from 3T3 fibroblasts and bovine brain microtubule preparations. Reciprocally, anti-MAP1b monoclonal antibodies raised against bovine brain microtubule reacted with the K1-7 polypeptide on Western blots. The protein identified by K1-7 antibodies may be one of the parasite molecules associated to molecular mimicry.

Amino Acid Sequence↗
PubMed1991

Evolution of the placental barrier to fetal infection by murine enteroviruses.

A murine model that demonstrated a placental barrier to fetal enterovirus infection in late pregnancy was extended to middle and early gestation. Inoculation with Theiler's murine encephalomyelitis virus (TMEV) in middle and early gestation infected 73% and 90% of placentas and 7% and 78% of fetuses, respectively. In situ hybridization (ISH) of tissues obtained after middle-gestation inoculation revealed TMEV in the placental decidua and spongiotrophoblast layers but generally not in the labyrinth (the layer adjacent to the fetus) or fetus (similar to late gestation). In contrast, ISH of placentas harvested after early-gestation inoculation identified TMEV predominantly in the labyrinth, in which vasculature was often replaced by hyalinized hemorrhagic tissue and small cell infiltrates; fetuses contained virus in heart, pericardium, great vessels, lung, pleura, brain, and liver. The placental barrier to enterovirus transmission appears to develop between early and middle gestation. Enterovirus infection before this time may induce placental damage, fetal infection, or both.

Animals↗
PubMed1991

Humoral autoimmune response to ribosomal P proteins in chronic Chagas heart disease.

The C terminal region of a Trypanosoma cruzi ribosomal P protein, encoded by the lambda gt11 JL5 recombinant, defined a major antigenic determinant in chronic Chagas heart disease. Immunopurified anti-JL5 antibodies were tested for anti-human ribosome reactivity by immunoblotting. They recognized the parasite ribosomal P proteins and clearly reacted with the corresponding human P proteins. The peptide R-13, that comprises the 13 C terminal residues of the JL5 recombinant and defines the specificity shared between chronic Chagas heart disease anti-JL5 antibodies and the systemic lupus erythematosus (SLE) anti-P antibodies, was used to study the specificity and the IgG subclass distribution of the anti-R-13 response by ELISA. The R-13 autoepitope is recognized mainly by sera from chagasic patients, but not by sera from malaria patients. Moreover, there was a significant correlation between anti-R-13 antibody levels and anti-T. cruzi antibody titres. The anti-R-13 response was mainly restricted to the IgG1 heavy chain isotype and correlated with the anti-T. cruzi isotype distribution.

Antibodies, Protozoan↗
PubMed1991

Recombinant Trypanosoma cruzi antigens and Chagas' disease diagnosis: analysis of a workshop.

A workshop organized by the Ibero-American Project of Biotechnology evaluated the diagnostic potential of several cloned Trypanosoma cruzi recombinant antigens for Chagas' disease serodiagnosis. A set of recombinants, Antigen 2, Antigen 13, SAPA, H49, A13, JL5, JL7, JL8, JL9, and RA1 provided by three different South American laboratories were probed with a panel of 236 South American serum samples. Antigens JL7, H49, Antigen 2, and A13 scored as the best diagnostic recombinant reagents. The results suggested that the main advantage of using cloned peptides for chronic Chagas' disease diagnosis resided in their highly specific immunoreactive properties.

Animals↗
PubMed1991

Use of intravenous gamma globulin to passively immunize high-risk children against respiratory syncytial virus: safety and pharmacokinetics. The RSVIG Study Group.

Infants with cardiopulmonary disease develop severe illness from respiratory syncytial virus (RSV) infection. Safety, feasibility, and pharmacokinetics of intravenous gamma globulin (IVIG) to prevent RSV illness were studied in 23 high-risk infants in a phase I trial. IVIG with an RSV neutralizing antibody titer of 1:1,100 in 5% solution was given monthly over a 2- to 4-h period in a clinical setting during the RSV season. The first group (n = 7) received 500 mg/kg of body weight, the second group (n = 9) received 600 mg/kg, and the third group (n =7) received 750 mg/kg. Serum was drawn prior to infusion and 2, 14, and 30 days after infusion. Total immunoglobulin G and RSV A2 and RSV B neutralizing antibody levels were obtained after the first IVIG infusion. Two children developed mild reversible pulmonary edema (group receiving 600 mg/kg per dose), and one developed hives and wheezing during one infusion (group receiving 500 mg/kg per dose). Twelve children developed subsequent RSV infection during two RSV seasons (November to April) over a 2-year follow-up period; 9 of 12 developed infection during the infusion year. Eleven illnesses were mild; one child died of progressive RSV illness (group receiving 500 mg/kg per dose). A cumulative infusion effect was not observed. IVIG appears safe and feasible in an outpatient setting, and at 750 mg/kg per dose, a target RSV antibody level of greater than or equal to 1:100 was achieved.

Child, Preschool↗
PubMed1991

Incidence of nonbacterial intraamniotic infections in abnormal pregnancies.

Amniotic fluids from 41 abnormal and 47 control pregnancies were examined for viruses, Chlamydia trachomatis, Ureaplasma urealyticum and Mycoplasma hominis. Abnormal pregnancies included those with fetal abnormalities, maternal complications, suspected chorioamnionitis and premature labor. Two percent of cultures were positive, including cytomegalovirus from one case of fetal growth retardation and U urealyticum from two patients with chorioamnionitis and from two controls. The abnormal pregnancies studied generally were not associated with nonbacterial intraamniotic infections.

Amniocentesis↗
PubMed1991

Immunization of high-risk infants younger than 18 months of age with split-product influenza vaccine.

Influenza is an important cause of serious illness in very young children with cardiopulmonary disease. A 4-year study was conducted at two centers to assess immunogenicity and safety of influenza split-product vaccine in children aged 3 to 18 months with bronchopulmonary dysplasia and congenital heart disease. A total of 113 children were studied: 62 children 3 to 5 months of age and 51 children 6 to 18 months of age. Sera were drawn prior to first and second immunization and 3 weeks after second immunization and were tested by hemagglutination inhibition; protection was defined as greater than 1:32. Ninety-five children were surveyed for adverse reactions. Seroresponses were age and antigen specific. Best responses for all ages were to A/Mississippi (H3N2) (97%). Children older than 6 months of age had better seroresponses to A/Leningrad (H3N2) (73%, P less than .03) and B/Victoria (62%, P less than .02) than did children younger than 6 months of age. Seroconversion rates to the remaining antigens were low. Only 9% of children experienced adverse reactions; all but one were mild. The immunologic mechanisms responsible for preventing serious influenzal disease and more effective immunization strategies need to be defined for very young high-risk children.

Aging↗
PubMed1991

Neonatal adenovirus infection: four patients and review of the literature.

Four newborns with adenovirus infection are described, and the profile of neonatal adenovirus disease is outlined based on the cases of these newborns and nine previously described. Characteristic historical features included prolonged rupture of membranes, maternal illness, vaginal delivery, and onset of illness within the first 10 days of life. Clinical findings included lethargy, fever or hypothermia, anorexia, apnea, hepatomegaly, bleeding, and progressive pneumonia. Thrombocytopenia, coagulopathy, and hepatitis were typical laboratory manifestations. Illness was severe and generally unremitting; only two survivors have been reported. Pathologic changes were prominent in lung, liver, and brain. Virus isolates, predominantly serotypes 3, 7, 21, and 30 were obtained from multiple sites and organs. Epidemiologic evidence suggests that viral acquisition from the mother, perhaps via the birth canal, is a major mode of transmission. Neonatal adenovirus infection, which is frequently disseminated and generally fatal, should be considered in the differential diagnosis of neonatal sepsis and pneumonia.

Adenovirus Infections, Human↗
PubMed1990

Varicella-zoster virus infection of human astrocytes, Schwann cells, and neurons.

Human fetal cell cultures enriched for astrocytes, Schwann cells, or dorsal root ganglia neurons were infected with cell-free varicella-zoster virus (VZV), and the course of these infections was compared with that in fetal fibroblasts. Virus replication was detected in each neural cell type as early as 10-16 hr postinfection. Permissiveness of each cell type was confirmed by electron microscopy. However, the kinetics of virus spread varied between the neural cell types. Moreover, the accumulation, progression, and localization of VZV putative immediate early (IE), early (E), and late proteins was neural cell-type specific. VZV replication was slower in Schwann cells and neurons than in astrocytes. In Schwann cells and neurons VZV E proteins could be detected before IE proteins, a reversal of the order of accumulation noted with astrocytes and fibroblasts. There was also relatively more VZV IE protein in the perinuclear cytoplasm of Schwann cells and neurons, suggesting a delay in the transport of this antigen to its nuclear site. The permissiveness of non-neuronal cell types suggests that they could play a role in the pathogenesis of herpes zoster.

Antigens, Viral↗
PubMed1990

Viral pneumonia in the first month of life.

We performed a 5-year review of 40 patients less than or equal to 30 days of age with viral pneumonia. Isolates included respiratory syncytial virus (55%), enteroviruses (15%), rhinoviruses (15%), adenoviruses (10%), parainfluenza virus (7.5%) and herpes simplex virus (5%). Most infants were previously healthy but had ill family members. Nine were born at less than 37 weeks of gestation. Symptoms and signs included tachypnea, decreased feeding, cough, cyanosis, lethargy, retractions, apnea, bradycardia, seizures and depressed consciousness. Seasonality and clinical features, but not radiographic patterns, suggested specific pathogens. Patients were moderately to severely ill. The median duration of hospitalization was 7 days; therapies administered included oxygen (90%), mechanical ventilation (45%), blood transfusions (25%) and supplemental oxygen after discharge (27%). The case fatality rate was 7.5%. Prematurity, ill appearance at presentation, lobar consolidation and adenovirus infection were risk factors for severe disease.

Adenovirus Infections, Human↗
PubMed1990

Major Trypanosoma cruzi antigenic determinant in Chagas' heart disease shares homology with the systemic lupus erythematosus ribosomal P protein epitope.

A Trypanosoma cruzi lambda gt11 cDNA clone, JL5, expressed a recombinant protein which was found to react predominantly with chronic Chagas' heart disease sera. The cloned 35-residue-long peptide was identified as the carboxyl-terminal portion of a T. cruzi ribosomal P protein. The JL5 13 carboxyl-terminal residues shared a high degree of homology with the systemic lupus erythematosus (SLE) ribosomal P protein epitope. Synthetic peptides comprising the 13 (R-13), 10 (R-10), and 7 (R-7) carboxyl-terminal residues of the JL5 protein were used to study, by enzyme-linked immunosorbent assay, the specificity of the Chagas' disease anti-JL5 and SLE anti-P antibodies. The R-13 peptide defined a linear antigenic determinant of the JL5 recombinant protein. As was proved for JL5, R-13 defined antibody specificities which were significantly increased in chronic Chagas' heart disease patients. Only SLE anti-P positive sera were found to react with JL5 and R-13. Fine epitope mapping showed that Chagas' disease anti-JL5 and SLE anti-P antibodies define similar epitopes within the R-13 peptide. The binding of the SLE sera to JL5 was completely blocked by the R-13 peptide, indicating that the shared specificity between anti-JL5 and anti-P autoantibodies was exclusively limited to the conserved linear epitope(s) within the R-13 peptide. The prevalence of high anti-R-13 antibody titers in Chagas' heart disease patients supports the hypothesis that postulates the existence of autoimmune disorders in Chagas' heart disease.

Amino Acid Sequence↗
PubMed1989

Evidence for a novel picornavirus in human dermatomyositis.

We prepared RNA probes from cloned segments of human and murine enteroviruses (EVs) for in situ hybridization of skeletal muscle biopsies from patients with dermatomyositis (DM), polymyositis, other inflammatory myopathies, and noninflammatory muscle diseases, and from normal control subjects. A probe derived from Theiler's murine encephalomyelitis virus (TMEV) detected viral RNA within mononuclear cells of the interstitial connective tissue in 3 of 5 patients with adult-onset DM. None of these patients showed positive hybridization to probes derived from human EVs (poliovirus type 1 and Coxsackie virus B3) applied to subjacent sections of the same biopsies. The remaining 2 adult DM patients, 4 patients with childhood-onset DM, and 24 non-DM patients did not react with either TMEV or human enterovirus probes. Histochemical stains for esterase and immunoperoxidase stains for Mac-1 antigen in the 3 DM patients who reacted positively revealed positive cells in the same distribution as, but in far greater number than, those positive by in situ hybridization. Immunoperoxidase staining for HLA-DR antigens revealed positive cells in the same distribution and number as were seen with the TMEV probe. We conclude that an EV-like agent, more closely related to TMEV than to human EVs, may be associated with DM and that this agent is probably localized within muscle macrophages that express class II major histocompatibility complex antigens.

Adult↗
PubMed1989

Blastocystis hominis gastroenteritis in a hemophiliac with acquired immune deficiency syndrome.

Blastocystis hominis is an enteric protozoan that has occasionally been associated with gastrointestinal illness in man but is not considered an opportunistic pathogen. We describe a 16-year-old hemophiliac with acquired immune deficiency-related complex in whom upper gastrointestinal symptoms in conjunction with high densities of B. hominis in duodenal secretions and stool developed. Furazolidone treatment was associated with eradication of the organism and improvement in clinical symptoms. One month later, the patient had invasive Candida albicans esophagitis and died 2 weeks later of complications of acute pancreatitis. In immunocompetent individuals surveyed in Colorado the frequency of identification of B. hominis in stool concentrates was not different between asymptomatic and symptomatic persons. We suggest that B. hominis may be an opportunistic pathogen in immunocompromised patients and should be sought in duodenal secretions and feces when gastrointestinal symptoms are present.

Acquired Immunodeficiency Syndrome↗