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W G Stroop

Publications and source records attributed to W G Stroop.

At least 37 records · Page 2Linked to original sources
PubMed1990

Spread of herpes simplex virus type 1 in the central nervous system during experimentally reactivated encephalitis.

Because many of the features of reactivated herpes simplex virus type 1 (HSV-1) central nervous systems (CNS) infections in vivo are incompletely understood, we used an animal model to study the development of the morphological, ultrastructural, radiological and immunological changes which occurred during acute and experimentally reactivated diseases. Rabbits were intranasally inoculated with HSV-1, and their latent trigeminal ganglionic and CNS infections were reactivated by intravenous injection of cyclophosphamide and dexamethasone. Technetium brain scans were performed to localize areas of blood-brain barrier breakdown, and cerebrospinal fluid (CSF) was analysed for IgG content by radial immunodiffusion assays. Nervous system tissues were studied by in situ hybridization and by immunofluorescent, light and electron microscopic techniques. Diffuse uptake of technetium was observed as HSV-1 spread transsynaptically into the brain during the acute phase of infection, and viral antigens and nucleic acids were detected in both the CNS olfactory and trigeminal systems. During latency, viral RNA was detected in the nuclei of neurons within the CNS olfactory cerebral and entorhinal cortices, indicating that HSV-1 became latent within the same CNS structures that were involved during the acute phase of infection. Following drug-induced reactivation, the brain scans revealed a more focal breakdown of the blood-brain barrier, and both neurons and neuronal processes in the entorhinal and olfactory cortices contained viral nucleic acids which correlated with the ultrastructural presence of HSV-1 virions. During the reactivated phase of infection a marked increase in the CSF IgG index occurred without an increase in the CSF: serum albumen ratio indicating a prompt intrathecal response in infected rabbits as compared to controls. To some extent, the CSF IgG index reflected the degree of histopathological damage.

Animals↗
PubMed1989

Comparative effect of microwaves and boiling on the denaturation of DNA.

The effect of heat and microwave denaturation of small volumes of double-stranded plasmid DNA has been compared. Samples of intact plasmid DNA had plasmid DNA linearized by digestion with EcoRI were conventionally denatured in a boiling water bath or denatured by 2450 MHz of microwave energy for 0-300 s. Heat denaturation for periods longer than 120 s caused breakdown of linearized plasmid DNA; however, microwave denaturation for 10-300 s caused no apparent degradation of linearized DNA. Breakdown of DNA forms II and III was noted in plasmid DNA subjected to 300 s of either heat or microwave denaturation but breakdown of forms II and III occurred more quickly with heat than with microwave treatment. Microwave treatment was also found to be better than heat to denature 32P-labeled DNA probes subsequently used to detect homologous DNA samples immobilized on nitrocellulose filters. A microwave-treated 32P-labeled DNA probe was able to hybridize to DNA samples 20 times more dilute than a heat-treated 32P-labeled DNA probe. Depending on the form of DNA to be analyzed, these results indicate that small volumes of DNA solutions and radiolabeled DNA probes can be effectively denatured in a conventional microwave oven.

DNA↗
PubMed1989

Neurovirulence of two clonally related herpes simplex virus type 1 strains in a rabbit seizure model.

Herpes simplex virus type 1 (HSV-1) strains vary widely with regard to neurovirulence, but their tropism for specific central nervous system structures and their ability to induce seizures are poorly defined. We have used the clonally related +GC and -GC strains of HSV-1 to define the pathophysiological basis of neurovirulence in a rabbit model. Following intranasal inoculation, +GC infection was nearly uniformly fatal while -GC infection was asymptomatic. The +GC infected animals developed electroencephalographic (EEG) abnormalities which preceded severe motor seizures. Tropism of the +GC strain for specific CNS nerve centers and the expression of viral antigens within them correlated with its virulence. Although both viruses invaded and replicated within the brain, +GC replicated to slightly higher titers and expressed more abundant viral antigen than -GC. The relatively less efficient replication of -GC appeared to correlate with its temperature-sensitive phenotype in vitro. Both +GC and -GC antigens were found in cerebral cortical layers IV-VI, and in several central nervous system trigeminal and olfactory system structures. However, +GC spread more completely throughout the brain to involve the amygdala, nucleus accumbens, several brainstem nuclei and the locus ceruleus. The +GC antigens were also found in cerebral cortical layer I of animals that developed seizures. These results indicate that the ability of HSV-1 to induce electrophysiologic brain abnormalities is associated with its ability to replicate within specific brain nerve centers.

Animals↗
PubMed1989

Porphyrin-laser photodynamic induction of focal brain necrosis.

A noninvasive photodynamic method has been developed to produce focal brain necrosis using porphyrin activated in vivo with laser light. After peripheral injection of the photosensitive porphyrin derivative, Photofrin I, mice were irradiated on the posterior lateral aspect of the head through the intact depilated scalp with 632 nm argon-dye laser light. Animals were studied at one, two and seven days after irradiation. Blood-brain barrier damage was detected by the intravenous injection of Evans blue, horseradish peroxidase and heterologous immunoglobulins. At one and two days after irradiation, the lesions were characterized by extravasation of immunoglobulin and Evans blue, and by edema, ischemia and infiltration by monocytes. On the seventh day after irradiation, the lesion was smaller than it had been two days after irradiation, and had reactive changes at its edges and coagulative necrosis at its center. Extravasation of Evans blue and immunoglobulin was markedly reduced by the seventh day after irradiation, but uptake of horseradish peroxidase by macrophages located at the periphery of the lesion was evident.

Animals↗
PubMed1988

Simultaneous electroelution and concentration of DNA fragments from agarose gels.

A rapid and inexpensive method for the electroelution of DNA fragments from agarose gels is described. DNA fragments were separated by agarose gel electrophoresis and visualized by staining with ethidium bromide. Selected DNA fragments were placed into electroeluter tubes capped with dialysis membrane and electroeluted into a small volume of buffer using a conventional horizontal gel electrophoresis apparatus. The method successfully eluted and concentrated DNA fragments with molecular weights ranging from 2.7 to 13.9 MDa in 3 h.

DNA↗
PubMed1988

Neurovirulence in an experimental focal herpes encephalitis: relationship to observed seizures.

An animal model of focal herpes simplex encephalitis was used to study several strains of type-1 herpes simplex virus. Rabbits were inoculated in the olfactory bulb by a standardized technique. Virus strains resulting in mortality of greater than 70% produced seizures of 3 types, and all animals that seized became moribund or died. In contrast, a virus strain resulting in a 20% mortality produced no seizures. Administration of 60 mg phenobarbital intramuscularly daily reduced mortality significantly in animals given the epileptogenic viruses. Cultures from temporal and frontal lobes showed viral growth more frequently than did cultures of other brain areas. Microscopic examination of routine and immunoperoxidase-stained brain sections confirmed the focal nature of the infection. Clinical syndromes such as seizures arising from viral brain disease may influence mortality in animal model systems.

Animals↗
PubMed1987

Herpes simplex virus, type 1 invasion of the rabbit and mouse nervous systems revealed by in situ hybridization.

Using a 3H-labelled virion DNA probe applied to tissue sections, we have previously identified the precise microscopic anatomical location of herpes simplex virus (HSV) during the acute and latent stages of infection of the mouse trigeminal ganglia and central nervous system (CNS). In the present investigation, we compared the mouse and the rabbit with respect to their ability to support acute and latent infections of trigeminal ganglionic and central nervous system neurons. We found that HSV-1, strain F, produced acute and latent infection of trigeminal ganglion cells in both mice and rabbits; however, lower levels of HSV-1 RNA were expressed in rabbit neurons as compared to mouse neurons, and many fewer neurons of the rabbit supported an acute infection than in the mouse. Studies of the trigeminal system within the CNS revealed that HSV-1 established latency more readily in the mouse than in the rabbit. The histopathology observed in acutely infected rabbit brain was less intense and less widespread than in mouse brain.

Animals↗
PubMed1987

Severity of experimentally reactivated herpetic eye disease is related to the neurovirulence of the latent virus.

The authors examined the eye diseases produced during acute and experimentally reactivated infections of rabbits intranasally inoculated with high and low neurovirulent strains of herpes simplex virus, type-1 (HSV-1). Experimental reactivation of latent trigeminal ganglionic infection was accomplished by an injection of cyclophosphamide followed by one injection of dexamethasone the next day. Neither drug, when given as a single injection, reactivated latent HSV-1 infection. During acute and reactivated phases of high neurovirulent HSV-1 strain infection, many rabbits developed very severe conjunctivitis and keratitis. Some rabbits developed hemorrhagic corneal lesions, and a few became blind. Only a few rabbits with acute and reactivated low neurovirulent virus strain infections developed mild conjunctivitis. The high neurovirulent strain was recovered from tear film more frequently than the low neurovirulent strain during reactivated infections. By use of 3H-labelled DNA prepared from purified virus to probe trigeminal ganglionic tissues in situ, both strains of virus were found to establish ganglionic latency to about the same degree. Reactivation correlated with an increase in the amount of HSV-1 RNA per ganglionic neuron and a change in subcellular location. These studies indicate that the relative neurovirulence of the infecting strain determines the ease with which it can be reactivated from latency and the severity of the reactivated ocular disease produced.

Animals↗
PubMed1986

Production of encephalitis restricted to the temporal lobes by experimental reactivation of herpes simplex virus.

A model was developed in which reactivation of latent infections with herpes simplex virus type 1 was induced in trigeminal ganglia and central nervous system olfactory centers of rabbits by administration of cyclophosphamide and dexamethasone. Latent infections were reactivated at a significantly higher frequency in rabbits infected with a highly virulent strain of virus than in those infected with a strain of lower neurovirulence. Electroencephalographic abnormalities that were largely confined to the posterior lateral cerebral hemispheres and corresponding inflammatory lesions were seen in rabbits acutely infected with the highly virulent strain, whereas no brain electrical abnormalities and only mild inflammatory lesions were seen in rabbits acutely infected with the strain of low neurovirulence. Reactivation of the highly neurovirulent strain produced focal brain necrosis restricted to the temporal lobes, which was similar to the disease produced in humans and which correlated with progressive worsening of brain electrical abnormalities.

Animals↗
PubMed1985

Enhancement of encephalomyeloradiculitis in mice sensitized with spinal cord tissue and infected with lactate dehydrogenase-elevating virus.

C57BR/cdJ mice develop encephalomyeloradiculitis following peripheral inoculation of the C strain of lactate dehydrogenase-elevating virus (LDV-C). We investigated the effect of subcutaneous administration of syngeneic spinal cord homogenate mixed with phosphate buffered saline or emulsified in complete or incomplete Freund's adjuvant 1 week before or after inoculation of LDV-C on the incidence and severity of central nervous system lesions. C57BR/cdJ mice developed an acute histological allergic encephalomyelitis when given 2 weekly sensitizing injections of homogenate in complete Freund's adjuvant. When peripheral inoculation of LDV-C was substituted for one of the two sensitizing injections, a higher percentage of mice developed lesions, and the lesions were more severe and persisted for much longer periods of time. This same lesion-enhancing effect was not observed if the mice were sensitized with homogenate suspended in buffer or emulsified in incomplete Freund's adjuvant. Interestingly, mice sensitized with complete Freund's adjuvant alone before or after infection with LDV-C also developed intense central nervous system lesions, suggesting that the mycobacterial component of the adjuvant was the critical element in enhancing the lesions.

Animals↗
PubMed1985

Ultrastructural and immunofluorescent studies of acute and chronic lactate dehydrogenase elevating virus-induced nonparalytic poliomyelitis in mice.

Light microscopic, electron microscopic, and immunofluorescent studies have been performed on young C58/J mice following administration of cyclophosphamide and peripheral inoculation of the C strain of lactate dehydrogenase-elevating virus (LDV-C). Using special fixation techniques, all three types of studies were performed on the spinal cord tissues obtained from the same mice. LDV-C infection-specific immunofluorescence was detected in anterior horn neurons. Ultrastructurally, anterior horn neurons during the acute inflammatory phase of the disease were characterized by various degrees of chromatolysis, an increase in the number of lamellar inclusion bodies, and extensive membrane proliferation of perinuclear endocytoplasmic reticulum. A chronic vacuolar appearance of the anterior horn was due to intraneuronal vacuolation as well as vacuolation of the neuropil; these changes may have been due to expansion of proliferated intracytoplasmic membranes and/or focal ischemia secondary to the acute inflammatory response. Direct evidence was obtained that indicated the cytopathology was not immune mediated in that highly poliomyelitis-susceptible 18-month-old C58/J mice developed severe paralysis without inflammation of the spinal cord when treated with cyclophosphamide before infection.

Animals↗
PubMed1984

Spinal leptomeningeal epidermoid cysts in inbred mouse strains.

The anatomic location and histological appearance of spinal cord epidermoid cysts in a variety of inbred mouse strains was examined. A variable incidence of cysts was found in mice of the C57BR/cdJ, C57BL/6J, B10.BR/SgSnJ, C58/J, AKR/J, C57L/J, and RF/J strains. Cysts were largely found in the leptomeninges, adjacent to the posterior horn and the lateral or anterior columns. The cysts consisted of a central whorled mass of keratinized cells surrounded by polygonal epithelial cells; some of these cells contained keratohyaline granules. Basal cells were absent. The presence of cysts did not correlate with the H-2k or H-2b haplotypes of the mouse.

Animals↗
PubMed1984

Localization of herpes simplex virus in the trigeminal and olfactory systems of the mouse central nervous system during acute and latent infections by in situ hybridization.

The precise anatomical location of latent herpes simplex virus (HSV) infection of the mouse central nervous system (CNS) has been identified by application of a 3H-labeled HSV-specific probe to deparaffinized sections of mouse brain tissue in situ. At times after corneal inoculation with HSV type 1 (HSV-1), strain F, representing the acute and latent phases of infection, BALB/c mice were perfused with a fixative containing sodium m-periodate, lysine, and paraformaldehyde and their CNS tissues and trigeminal ganglia embedded in paraffin, sectioned, and and subjected to hybridization. During the acute phase, HSV-1 was localized to neurons and some small supporting cells in the sensory portion of the 5th cranial nerve including the trigeminal ganglia and nerve root, principal sensory nucleus, mesencephalic nucleus, descending tract and nuclei, and cerebral cortex. During the latent phase, HSV-1 was found only in neurons located primarily in the descending nuclei and mesencephalic nucleus. Evidence was also obtained that implicated the olfactory tract as an additional route of entry into the CNS, in that positive hybridization was found in the olfactory bulb, the entorhinal cortex, and adjacent cerebral cortex. Additionally, HSV-1 established latent infections in neurons of the olfactory system. HSV-1-specific RNA was detected in ganglionic and CNS neurons throughout the acute and latent phases of infection, whereas HSV-1-specific DNA was detected only during the acute phase, indicating that the relationship between HSV and latently infected CNS and ganglionic neurons involves limited transcription of the viral genome.

Acute Disease↗
PubMed1983

The cultivation of human rotavirus, strain 'Wa', to high titer in cell culture and characterization of the viral structural polypeptides.

The structural proteins of the 'Wa' (serotype 2) strain of human rotavirus have not been described previously. Single-cycle virus growth in MA-104 cells using 5 micrograms/ml of trypsin in the growth medium was rapid with maximal viral yields (approximately 10(6) PFU/ml) obtained 10-12 h post-infection. There was a continuous progression of cytopathic effect (CPE) from 6- to 5-h post-infection. Under conditions of multiple-cycle growth, a greater concentration of trypsin (40 micrograms/ml) in the growth medium was required to obtain rapid progression of CPE and production of a high titer (approximately 10(7) PFU/ml) of infectious (double-shelled) virus. Single- and double-shelled virions were separated by isopycnic centrifugation in CsCl and analyzed by SDS-PAGE. Five proteins with molecular weights of 116,000, 92,000, 88,000, 84,000 and 41,000 were identified as components of the inner shell and four proteins with molecular weights of 60,000, 38,000, 32,000 and 27,000 were located in the outer shell.

Animals↗
PubMed1983

Mouse strain-specific central nervous system lesions associated with lactate dehydrogenase-elevating virus infection.

The histopathologic and virologic features of several mouse strains inoculated with the C strain of lactate dehydrogenase-elevating virus are described. Young C58 and AKR mice were found to develop histologic poliomyelitis when injected with cyclophosphamide prior to peripheral inoculation of lactate dehydrogenase-elevating virus. None of the C58 mice developed serious hindlimb paralysis, but some of the AKR mice did. Chronic poliomyelitis persisted for many weeks after infection in some C58 mice, but a spongioform poliomyopathy of the anterior horn was found in others. In contrast, inoculation of young C57BR/cd mice with lactate dehydrogenase-elevating virus produced inflammatory lesions restricted to central nervous system white matter that could be detected many weeks after infection. The most frequent findings were moderate leptomeningitis and myelitis localized to the white matter, however, radiculitis was also occasionally observed. Severe necrosis of spinal cord white matter was seen rarely. Development of lesions in C57BR/cd mice did not require immunosuppression prior to peripheral inoculation with virus and was not age related, sex linked, or exclusively controlled by the H-2 histocompatibility locus. Lactate dehydrogenase-elevating virus-infected C57L, C57BL/6, and RF mice did not develop poliomyelitis; however, C57L and C57BL/6 mice displayed a low incidence of mild encephalomyelitis. Poliomyelitis-susceptible C58 mice had the highest levels of viral infectivity in plasma and central nervous system tissues. White matter disease-susceptible C57BR/cd mice had viral titers in plasma and central nervous system tissues comparable to poliomyelitis-resistant C57L, C57BL/6, and RF mice. These studies demonstrate that different strains of mice have differing susceptibilities to the development of central nervous system inflammatory diseases.

Animals↗
PubMed1982

Detection of tissue culture-adapted Theiler's virus RNA in spinal cord white matter cells throughout infection.

The appearance of histological lesions and the localization of viral RNA in the central nervous system of mice infected with tissue culture-adapted Theiler's murine encephalomyelitis virus (WW strain) (TMEV-WW) was studied. Viral RNA was detected by autoradiography after in situ hybridization, using a (3)H-labeled DNA probe complementary to virion RNA, which was applied to deparaffinized sections of central nervous system tissues from infected mice. Subjacent histological sections of tissues were used to assess the location and extent of lesions. Lesions were first observed at 20 days post-inoculation and appeared to enlarge throughout infection. They consisted of infiltrates of mononuclear cells and lymphocytes in spinal cord white matter and leptomeninges; at 78 days post-inoculation severe necrotizing and demyelinative myelitis and gliosis were observed. In contrast to the pathogenesis of brain-derived TMEV-WW-infected mice, no lesions were found in the central nervous system gray matter of mice infected with tissue culture-adapted TMEV-WW at any time post-infection. Tissue culture-adapted viral RNA was found in the cells of spinal cord white matter throughout infection; only one neuron in close proximity to the injection site was found to contain viral RNA shortly after infection. At early times after infection, spinal cord white matter cells containing viral RNA were found before development of inflammatory lesions; at later days post-inoculation, positive cells were found within, at the periphery of, or at a distance from lesions. The number of infected cells and the amount of viral RNA per cell appeared to remain constant from 20 to 78 days post-inoculation despite the increasing intensity of the inflammatory response. The nearly exclusive spinal cord white matter tropism of tissue culture-adapted TMEV-WW appeared to directly correlate with the disease-inducing potential of this virus.

Animals↗