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Biomedical subjects

E Lavi

Publications and source records attributed to E Lavi.

At least 91 records · Page 5Linked to original sources
PubMed1994

Pathogenesis of cerebral infarction and hemorrhage induced by a murine leukemia virus.

BACKGROUND: Inoculation of neonatal BALB/c mice with the Friend murine leukemia virus TR1.3 uniformly induces cerebral infarctions and hemorrhages within 18 days. The primary target of TR1.3 infection are endothelial cells of capillaries and small vessels. Preliminary post-mortem histologic analysis revealed multifocal endothelial cell pathology associated with the presence of thrombi and extravasation of red blood cells into the brain parenchyma. The consequences of viral infection on endothelial cell integrity and its relevance to hemorrhagic and ischemic lesions are unclear. EXPERIMENTAL DESIGN: Neonatal BALB/c mice were infected with TR1.3 murine leukemia virus and were monitored daily for symptoms of tremor, seizure and paralysis. Diseased mice were killed and the brains prepared for histopathologic analysis and electron microscopy studies. RESULTS: Hematoxylin and eosin-stained sections revealed widespread areas of infarction throughout white and grey matter with numerous scattered thrombi. Endothelial cell pathology was widespread and pronounced. This included enlarged cytoplasm, intracytoplasmic clefts, separation of tight junctions, swollen mitochondria, changes to the basal lamina and in many instances the formation of syncytia. Ultrastructural studies identified numerous viral particles within the endothelial cell cytoplasm and budding from the abluminal and luminal cell surfaces. CONCLUSIONS: These data confirm that TR1.3 virus replicates within endothelial cells and provides the first direct evidence of retrovirus-induced endothelial cell pathology. These results suggest that hemorrhage may be a direct consequence of this endothelial cell pathology, and that endothelial cell damage initiates the formation of thrombi and vessel occlusion that results in multiple cerebral infarctions.

Animals↗
PubMed1993

Intracerebral hemorrhages and syncytium formation induced by endothelial cell infection with a murine leukemia virus.

The mechanisms of endothelial cell damage that lead to cerebral hemorrhage are not completely understood. In this study, a cloned murine retrovirus, TR1.3, that uniformly induced stroke in neonatal BALB/c mice is described. Restriction digest mapping suggests that TR1.3 is part of the Friend murine leukemia virus (FMuLV) family. However, unlike mice exposed to other FMuLVs, mice infected with TR1.3 virus developed tremors and seizures within 8 to 18 days postinoculation. This was uniformly followed by paralysis and death within 1 to 2 days. Postmortem examination of TR1.3-inoculated mice revealed edematous brain tissue with large areas of intracerebral hemorrhage. Histologic analysis revealed prominent small vessel pathology including syncytium formation of endothelial cells. Immunohistochemical analysis of frozen brain sections using double fluorescence staining demonstrated that TR1.3 virus specifically infected small vessel endothelial cells. Although infection of vessel endothelial cells was detected in several organs, only brain endothelial cells displayed viral infection associated with hemorrhage. The primary determinant of TR1.3-induced neuropathogenicity was found to reside within a 3.0-kb fragment containing the 3' end of the pol gene, the env gene, and the U3 region of the long terminal repeat. The restricted tropism and acute pathogenicity of this cloned murine retrovirus provide a model for studying virus-induced stroke and for elucidating the mechanisms involved in syncytium formation by retroviruses in vivo.

Animals↗
PubMed1992

Experimental allergic encephalomyelitis and multiple sclerosis: lesion characterization with magnetization transfer imaging.

Magnetization transfer imaging (MTI) was initially performed in normal guinea pigs and human volunteers. A magnetization transfer ratio (MTR) was calculated in the normal white matter and was found to be 42%-44%, with less than 2.5% variation, which indicates the high reproducibility of the measurement. MTI was then applied to an animal model of white matter disease, acute experimental allergic encephalomyelitis (EAE). In this model of EAE, pathologically proved lesions were edematous with essentially no demyelination. MTRs decreased slightly but significantly (5%-8%) compared with the MTRs of the same tissue region measured before the onset of the lesion [corrected]. Fifteen patients with multiple sclerosis (MS) also underwent MTI. In the 15 patients with MS, all lesions (209 plaques) had a significantly decreased MTR (average, 26%). The authors believe that demyelination produced the lower MTR, and, thus, lesions varied in transfer ratio on the basis of the extent of myelin loss. In patients with MS, particularly those with chronic and/or progressive MS, the MTR of the normal-appearing white matter was significantly decreased. The data suggest that calculated MTR obtained with in vivo MTI may enable differentiation of edema from demyelination, and that MTI can demonstrate white matter abnormalities that cannot be seen with standard spin-echo or gradient-echo magnetic resonance imaging.

Adult↗
PubMed1991

Magnetic resonance imaging of Creutzfeldt-Jacob disease.

We report a biopsy-diagnosed patient with Creutzfeldt-Jacob disease showing on magnetic resonance images bilateral increased signal intensity in the basal ganglia on long repetition time images. Creutzfeldt-Jacob disease (CJD) is a degenerative process of the brain, induced by a novel infectious agent, and is usually characterized by a rapidly progressive dementia. We report a biopsy-diagnosed patient with CJD with a distinctive magnetic resonance (MR) appearance.

Biopsy↗
PubMed1991

Thrombotic microangiopathy isolated to the central nervous system.

A man with plasma cell dyscrasia and bone marrow infiltration presented with rapidly progressive encephalopathy. Magnetic resonance imaging revealed multiple small areas of abnormal signal that correlated with the autopsy findings of thrombotic microangiopathy isolated to the central nervous system.

Caudate Nucleus↗
PubMed1991

Monoclonal antibody 2H1 detects a 60-65 KD membrane polypeptide of the rough endoplasmic reticulum of neurons and selectively stains cells of several rat tissues.

Monoclonal antibody (MAb) 2H1, raised in mice immunized with membrane fractions from cultured rat pheochromocytoma cells (clonal line PC-12), detects a polypeptide from rat brain and PC-12 cell membranes of 60-65 KD apparent molecular mass. The polypeptide has been localized by immunoelectron microscopy in the rough endoplasmic reticulum (RER) of neurons. By light microscopic immunocytochemistry, several rat tissues and two rat-derived cultured cell types show selective patterns of staining with 2H1. In the central nervous system, the antibody stains neuronal cytoplasm; in the spleen, staining is seen only in certain cells of the marginal zone of the white pulp, and in lymph nodes, in plasma cells, and in areas populated by monocytes and macrophages. Whereas astrocytes and adrenal medullary cells in situ are virtually unstained with 2H1, primary cultures of astrocytes and PC-12 cells, which are derived from adrenal medullary cells, stain intensely with 2H1. The strong staining of cultured astrocytes and PC-12 cells with 2H1 suggests that the levels of the 60-65 KD polypeptide are up-regulated during cell proliferation and growth. Only a few hepatocytes stain with 2H1; intestinal epithelial and pancreatic cells are not stained with 2H1. The organelle-specific antibody 2H1 may prove a useful probe in structural and functional studies of membranes of the rough endoplasmic reticulum in neurons, and in certain cells of the immune system.

Adrenal Gland Neoplasms↗
PubMed1991

Fetal akinesia deformation sequence (Pena-Shokeir phenotype) associated with acquired intrauterine brain damage.

An infant with Pena-Shokeir phenotype was born to a cocaine-using mother. The pathologic findings included polyhydramnios, facial anomalies, arthrogryposis, camptodactyly, pulmonary hypoplasia, and tetralogy of Fallot. The neuropathologic findings were diffuse brainstem and spinal cord neuronal degeneration and focal cerebral infarction, consistent with acquired intrauterine ischemic damage.

Abnormalities, Multiple↗
PubMed1990

Passive immunity to fatal reovirus serotype 3-induced meningoencephalitis mediated by both secretory and transplacental factors in neonatal mice.

The role of passively acquired immunity to reovirus-induced meningoencephalitis in neonatal mice was examined. It was determined that female mice were capable of conferring protection against viral infection and meningoencephalitis in neonates depending on the route by which the dams were immunized and the serotype of the immunizing virus. Female mice immunized with homotypic virus via the oral route developed the most potent response. Infected neonates born and nursed by these females developed no signs of disease, and no virus was recoverable from their small intestines, livers, or brains following infection. Neonates born to females immunized with homotypic virus by the subcutaneous route manifested no evidence of meningoencephalitis or virus dissemination, yet virus was recovered from neonatal intestines. Mice immunized with heterotypic virus by either the subcutaneous or the oral route also conferred protection against disease; however, virus was recovered in small intestines and livers of infected neonates. Based on results from foster-nursing experiments, it appears that factors obtained both during suckling and by transplacental transfer contribute to protection. Passive transfer of reovirus-immune mouse serum also protected neonates from disease. These results demonstrate that passive immune mechanisms can mediate the protection of neonates against reovirus infection and provide further evidence of the importance of the mucosal immune response in protection against pathogens that invade the host via mucosal tissues.

Animals↗
PubMed1990

Determinants of coronavirus MHV pathogenesis are localized to 3' portions of the genome as determined by ribonucleic acid-ribonucleic acid recombination.

Recombinant viruses derived from coronaviruses mouse hepatitis virus strains JHM and A59, were used to map biologic properties of the virus to viral genes. The 3' portion (about 25%) of the viral genome, including the genes coding for all of the structural proteins, controls biologic properties such as organ tropism of the virus, pattern of the virus-induced central nervous system pathology in mice, plaque morphology, and virus yield in tissue culture.

Animals↗
PubMed1989

Induction of MHC class I antigens on glial cells is dependent on persistent mouse hepatitis virus infection.

H-2 class I antigens, but not class II antigens, were detected on the surface of glial cells persistently infected with mouse hepatitis virus strain A59 (MHV-A59) as late as 90 days post-infection. Uninfected glial cells remained negative for H-2 class I and class II surface antigens. We have previously shown that conditioned media from infected glial cell cultures (supernatants) contain a factor unrelated to infectious virus and capable of inducing H-2 class I antigens on uninfected glial cells. The synthesis of this factor appears to be dependent on production of infectious virus since the H-2 inducing activity could not be detected 3 days following the addition of neutralizing antibodies to the cultures. This suggests that H-2 inducing activity contains an unstable component, the synthesis of which is dependent on continual virus production. Persistent MHV infection and H-2 class I antigen expression may play a role in MHV-induced demyelination.

Animals↗
PubMed1988

Induction of glial cell MHC antigen expression in neurotropic coronavirus infections. Characterization of the H-2-inducing soluble factor elaborated by infected brain cells.

Neurotropic coronavirus (mouse hepatitis virus strain A59) infection induces major histocompatibility complex class I (H-2) surface antigens on oligodendrocytes and astrocytes, cells that do not normally express detectable MHC antigens on their surface. The induction on MHC antigen expression potentially allows immunocytes to interact with infected glial cells and may play a critical role in the development of virus-induced, immune-mediated demyelination in the central nervous system, a possible model of human multiple sclerosis. In this study, we characterized the soluble factor involved in MHC antigen induction, quantitated induction of MHC antigens, and analyzed the central nervous system cell type involved in the production of the factor. The H-2-inducing factor, most likely produced by astrocytes, was found to be nondialyzable, heat- and trypsin-sensitive, but resistant to treatment at pH 2.0. The m.w. of the factor was estimated as 50 to 100 kDa. Studies on fractionation by ultrafiltration and sucrose density gradient along with antibody-blocking experiments indicate that the factor is not interferon or virus particles.

Animals↗
PubMed1988

Tumor necrosis factor induces expression of MHC class I antigens on mouse astrocytes.

The effect of tumor necrosis factor (TNF) on expression of major histocompatibility complex (MHC) antigens was examined in mouse glial cells in vitro. TNF induced MHC class I, but not class II, antigen expression on the surface of astrocytes but not on oligodendrocytes. Glial cells do not normally express detectable amounts of MHC antigens. Thus TNF may play a role in the immunopathogenesis of neurologic diseases that involve MHC class I-restricted reactions.

Animals↗
PubMed1988

Latent herpes simplex virus type 1 transcripts in peripheral and central nervous system tissues of mice map to similar regions of the viral genome.

Herpes simplex virus type 1 (HSV-1) DNA and RNA have been detected in peripheral nervous system (PNS) and central nervous system (CNS) tissues of latently infected mice. However, explant methods are successful in reactivating HSV-1 only from latently infected PNS tissues. In this report, latent herpesvirus infections in mouse PNS and CNS tissues were compared by in situ hybridization to determine whether the difference in reactivation was at the level of the virus or the host tissue. It was demonstrated that the HSV-1 transcripts present during latency in the mouse PNS and CNS originated from the same region of the genome, the repeats which bracket the long unique sequence. Therefore, the difference in reactivation with PNS and CNS tissues cannot be accounted for by differences in the extent of the HSV-1 genome transcribed during herpesvirus latency. Latent HSV-1 RNA was detected in the trigeminal ganglia (PNS) and the trigeminal system in the CNS from the mesencephalon to the spinal cord as well as other regions of the CNS not noted previously. Latent HSV-1 RNA was found predominantly in neurons but also in a small number of cells which could not be identified as neuronal cells. It is suggested that host differences in CNS and PNS tissues, rather than differences in latent virus transcription, may be important determinants in the HSV-1 reactivation process in explanted tissues.

Animals↗
PubMed1988

Latent herpes simplex virus type 1 transcription in human trigeminal ganglia.

We studied latent herpes simplex virus type 1 gene expression in human trigeminal ganglia. Two transcripts were mapped to a 3.0-kilobase region within the long repeat region and appeared to be located in neuronal nuclei. These viral RNAs were not abundant during lytic replication and may represent an alternative pattern of herpes simplex virus type 1 gene expression involved in the pathogenesis of latent infection.

Adult↗
PubMed1988

Limbic encephalitis after inhalation of a murine coronavirus.

The spread of a neurotropic coronavirus, mouse hepatitis virus strain A59, in the mouse central nervous system was studied after intranasal inoculation. Mouse hepatitis virus strain A59 spread during the 3- to 5-day postinoculation period, through the olfactory pathway into the limbic system. Coronavirus particles were detected in the limbic system by electron microscopy. The combination of temporal propagation through an anatomical-physiological central nervous system pathway and anatomical restriction of viral infection suggests that specific interneuronal transport is important in spread of the virus. This experimental system may represent a model for diseases associated with human coronaviruses (common cold viruses) and/or the human limbic system.

Administration, Intranasal↗