Search PubMed⌕ Search

Biomedical subjects

M J Levin

Publications and source records attributed to M J Levin.

At least 91 records · Page 5Linked to original sources
PubMed1993

Infection of human fetal dorsal root neurons with wild type varicella virus and the Oka strain varicella vaccine.

The relative ability of a varicella-zoster virus (VZV) clinical isolate and a live attenuated VZV vaccine strain (Oka) to infect human neurons was determined in vitro. VZV infection of neurons prepared in culture from dorsal root ganglia of fetuses was assessed using an infectious center assay. Cultures were infected with 50-5,000 pfu of either VZV and assayed at either 24 or 48 hours post-VZV infection. Cultures infected with the clinical VZV isolate had seven-fold more infected neurons than cultures infected with the vaccine strain VZV.

Cells, Cultured↗
PubMed1993

Impact of herpesvirus infections in the future.

Numerous diverse, often opposing, trends will determine the frequency (and severity) of herpesvirus infections in the future. A major factor is the growing population of iatrogenically immunocompromised patients, accruing especially from large increases in organ and autologous bone marrow transplantation. Of even greater importance is the immense number of human immunodeficiency virus (HIV)-infected patients for whom herpesviruses may: (1) have been a cofactor in acquisition of HIV infection; (2) contribute to in vivo activation of HIV; (3) cause severe infections. Another factor influencing severe herpesvirus infections is the aging of populations in developed countries; this will be associated with a greater prevalence, and more morbid manifestations, of herpes zoster. Sociologic changes will also be important. The consequences of these, such as attempts to influence sexual practices, will be difficult to predict. Other changes, such as more frequent use of early child care facilities, will predictably lead to early acquisition of most herpesviruses, thereby decreasing the incidence of severe disease in adulthood. Factors that will reduce the incidence and/or severity of herpesvirus infections include vaccines (varicella, herpes simplex, cytomegalovirus); prophylactic strategies for immunocompromised hosts (passive immunization, antiviral drugs, blood product selection); more rapid and sensitive diagnostic methods; and suppressive or early antiviral therapy for common infections, such as genital herpes simplex and varicella.(ABSTRACT TRUNCATED AT 250 WORDS)

Forecasting↗
PubMed1993

The Trypanosoma cruzi ribosomal P protein family: classification and antigenicity.

The multi-copy ribosomal P proteins have been identified on the ribosomes of prokaryotic and eukaryotic cells, and their antigenicity is an important feature of human Trypanosoma cruzi infection. In this review, Mariano Levin, Martin Vazquez, Dan Kaplan and Alejandro Schijman give a rational basis for the classification of these proteins, and discuss their inter-relationship.

Journal Article↗
PubMed1993

Unsuspected varicella-zoster virus encephalitis in a child with acquired immunodeficiency syndrome.

We report a case of progressive encephalitis caused by varicella-zoster virus (VZV) in an adolescent with hemophilia and acquired immunodeficiency syndrome but without cutaneous signs of VZV infection. Magnetic resonance imaging of the brain demonstrated an abnormally increased periventricular signal in T2-weighted images. Infection with VZV was proved by in situ hybridization and immunofluorescence staining of brain tissue, which showed histologic evidence of herpesvirus infection. Encephalitis caused by infection with VZV is a potentially treatable complication of acquired immunodeficiency syndrome and requires a high index of suspicion for diagnosis.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Immune responses to varicella zoster virus infections in healthy children.

The immune responses to varicella zoster virus were studied in 67 otherwise normal children participating in a placebo-controlled trial of acyclovir for the treatment of chickenpox. No differences were observed between acyclovir and placebo groups. Children were studied longitudinally, at onset of chickenpox, and at 1 month, 3 months, 1 year, and 3 years after infection. These data help define the natural history of the immune response to chickenpox in children.

Acyclovir↗
PubMed1993

Profile of enterovirus disease in the first two weeks of life.

We studied 57 infants < or = 14 days of age referred for possible enterovirus (EV) infection to assess the accuracy of that clinical diagnosis and describe the natural history of neonatal EV infection. Twenty-nine neonates proved to have EV infection, 23 had illnesses compatible with (but not proven to be) EV infection, and 5 had alternative diagnoses: bacterial infections (2); herpes simplex virus infection (1); and metabolic disorders (2). Neonates with proved EV infection were generally full term and had uncomplicated immediate postnatal periods but high percentages of ill contacts. Neonatal symptoms and signs included fever, irritability, anorexia, lethargy, hypoperfusion, rash, jaundice and respiratory findings. Laboratory abnormalities included cerebrospinal fluid (CSF) pleocytosis, chest radiograph infiltrates, abnormal urinalyses and elevated transaminases. EVs were most commonly isolated from CSF and rectum/stool but also frequently from serum and urine. Five EV-infected patients had severe multisystem disease (pneumonitis, hepatitis, thrombocytopenia, bleeding and meningitis), requiring supportive care and lengthy hospitalizations. All survived, 2 with residual hepatic dysfunction. Markers of severe disease included: early age of illness onset (especially Day 1 of life); maternal viral symptoms at delivery; absence of fever and irritability; tachypnea; lethargy; abdominal distension; hepatomegaly; and positive serum viral culture. These data support conservative management of ill infants < or = 2 weeks of age and suggest that antiviral therapy for neonatal EV infection would be optimally targeted at infants with early onset illness, multisystem disease and/or viremia.

Cerebrospinal Fluid↗
PubMed1993

Humoral autoimmune response in Chagas' disease: Trypanosoma cruzi ribosomal antigens as immunizing agents.

Molecular expression cloning techniques have revealed that patients with chronic Chagas' heart disease (cChHD) present a strong humoral response against the cloned C-terminal portions of the four Trypanosoma cruzi ribosomal P proteins TcP1, TcP2 alpha (TcP2b), TcP2 beta (TcPJL5), and TcP0. This protein family presents several features that may be important in the immunopathology of Chagas disease. Their exposed location on the ribosome, and the amplification of their parasite-specific, Ser free C-terminal domain, generate a strong anti-parasite P response that may induce anti-P autoimmunity. Evidences indicate that the serological pattern of the anti-P response from chagasic patients may be the consequence of a chronic immunization with T. cruzi ribosomal antigens.

Amino Acid Sequence↗
PubMed1993

The chronic presence of the parasite, and anti-P autoimmunity in Chagas disease: the Trypanosoma cruzi ribosomal P proteins, and their recognition by the host immune system.

Molecular expression cloning techniques revealed that patients with the severest clinical form of Chagas disease, chronic Chagas heart disease, presented a strong humoral response against the cloned C-terminal portion of a Trypanosoma cruzi ribosomal P protein. Parasite P antigens identification led to characterize the ribosomal P protein system in T. cruzi. Their exposed location on the ribosome, and the "amplification" of their parasite specific, serine free C-terminal domain, generate a strong parasite specific anti-P response, that in certain cases may induce anti-P autoimmunity.

Amino Acid Sequence↗
PubMed1992

The 70-kDa heat-shock protein is a major antigenic determinant in human Trypanosoma cruzi/Leishmania braziliensis braziliensis mixed infection.

Five sera from Bolivian individuals chronically infected by Trypanosoma cruzi, and suffering an active Leishmania braziliensis braziliensis metastatic mucocutaneous lesion were characterized. They reacted with the T. cruzi recombinant antigens that are currently used as Chagas diagnostic reagents, and with several L. b. braziliensis proteins as assessed by Western blot. These sera showed an intense reaction with a T. cruzi and an L. b. braziliensis polypeptide of about 70 kDa. Expression cloning techniques demonstrated that the target of this immunologic reaction was a cross-reactive antigen, the 70-kDa heat-shock protein (HSP 70). High levels of anti-HSP 70 reactivity and positive reactions with all or some of the T. cruzi recombinant antigens JL7, JL8, and JL5, defined a serologic pattern that was characteristic of the T. cruzi/L. b. braziliensis mixed infection.

Amino Acid Sequence↗
PubMed1992

Characterization of the C-terminal region of a Trypanosoma cruzi 38-kDa ribosomal P0 protein that does not react with lupus anti-P autoantibodies.

A Trypanosoma cruzi cDNA lambda gt11 recombinant, C-P0, encoding the carboxyterminus of a highly antigenic ribosomal P protein, was isolated. Sequence comparisons and immunological evidence allowed its identification as the C-terminal region of the T. cruzi 38-kDa ribosomal P0 protein. This recombinant failed to react with systemic lupus erythematosus (SLE) anti-P antibodies. The T. cruzi ribosomal P0 protein is the first reported eukaryotic ribosomal P protein presenting this immunological property, probably due to its peculiar C-terminal-amino-acid sequence, FGMGALF, which differs from the conserved eukaryotic ribosomal P protein C-terminal consensus, MGFGLFD.

Amino Acid Sequence↗
PubMed1992

Immune response to split-product influenza vaccine in preterm and full-term young children.

Humoral and cellular immune responses to two doses of influenza antigens were measured in children 6-48 months of age. These vaccinees comprised a previously unimmunized cohort of 18 healthy full-term children and 15 sick preterm children with bronchopulmonary dysplasia and an additional 30 ex-preterm children who were reimmunized. Half of the reimmunized cohort were recovered from bronchopulmonary dysplasia and half had active bronchopulmonary dysplasia. Antibody response was measured by haemagglutination inhibition (HI) and ELISA, and cellular immunity was measured by enumerating memory T cells. Six weeks after immunization, ELISA antibody levels were significantly higher in previously unimmunized full-term vaccinees than in previously unimmunized sick preterm infants (p less than 0.002). No difference was found between sick and recovered reimmunized children. By HI testing greater than 90% of children in both cohorts developed titres greater than or equal to 1:32, and these were generally maintained for at least 20 weeks. T-cell proliferative responses to influenza antigen were greater in the full-term children than in the preterm children (p less than 0.02), irrespective of state of health or prior immunization status. Split-product vaccine was immunogenic in all the cohorts studied; however, factors such as prematurity, health status and previous influenza immunization played important roles in the magnitude of some responses.

Antibodies, Viral↗
PubMed1992

Immune response of elderly individuals to a live attenuated varicella vaccine.

The Oka strain live attenuated varicella-zoster virus (VZV) vaccine was administered subcutaneously to 202 VZV-immune individuals who were 55 to greater than 87 years old. The dose administered varied from 1100 to 12,000 pfu. One cohort received 3000 pfu with a 3000 pfu booster 3 months later. The vaccine was well tolerated. VZV-specific immunologic responses were evaluated over a 24-month period. The mean anti-VZV antibody level was significantly increased for 12 months after vaccination. Interferon-gamma production in vitro by peripheral blood mononuclear cells (PBMC) of vaccinees was also increased for 6 months after vaccination. Most significantly, VZV-specific proliferating T cells in PBMC of vaccinees were increased in frequency from 1 in 68,000 to 1 in 40,000. This vaccine-enhanced frequency of VZV-responding T cells is similar to the frequency observed in 35- to 40-year-old adults. Dose and age of the vaccinees did not significantly influence the magnitude of the mean cell-mediated immune response. The data indicate that VZV immunity in the elderly can be boosted by active immunization. If the increased incidence of herpes zoster that accompanies aging results from the natural waning of immunity, active immunization may prevent or attenuate zoster in the elderly.

Aged↗
PubMed1992

In vitro activities of penciclovir and acyclovir against herpes simplex virus types 1 and 2.

Penciclovir (PCV) and acyclovir are acyclic guanine analogs which inhibit herpes simplex virus (HSV) DNA polymerase. Their 50% infective doses were 0.5 to 0.8 microgram/ml for clinical isolates of HSV-1 and 1.3 to 2.2 micrograms/ml for HSV-2. Furthermore, HSV-infected cultures receiving 2-h pulses of PCV had 2- to 50-fold less HSV than acyclovir-treated cultures, consistent with the prolonged intracellular half-life of PCV triphosphate.

Acyclovir↗
PubMed1992

Latency in vitro of varicella-zoster virus in cells derived from human fetal dorsal root ganglia.

A potential in vitro model of varicella-zoster virus (VZV) latency was developed. Dissociated human dorsal root ganglion cultures were infected with VZV and maintained for 1 wk in the presence of bromovinyl arabinosyl uracil, a potent inhibitor of VZV. Seven to 21 d after removing the inhibitor (> or = 14 d after infection), the cells were trypsinized, passed to monolayers of human embryonic lung fibroblasts, and observed for VZV reactivation as indicated by typical cytopathic effects and the appearance of VZV antigens. VZV reactivated from 56% of the cultures containing both neurons and satellite cells but not from cultures specifically enriched for either neurons, satellite cells, or ganglion-derived fibroblasts. The failure to isolate VZV from cell suspensions that were sonicated before cocultivation with fibroblasts indicated that infectious VZV was not present before reactivation. Moreover, immunohistochemical and immunoprecipitation studies revealed no VZV-specific antigens in any cultures before the reactivation stimulus. VZV antigens were detected after trypsinization and cocultivation. These findings suggest that cultures containing both neurons and satellite cells provide a model system for VZV persistence that possesses many properties of a latent infection.

Cells, Cultured↗