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Biomedical subjects

R B Tenser

Publications and source records attributed to R B Tenser.

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

Prostaglandin production in chronic progressive multiple sclerosis.

Peripheral blood monocytes have been implicated in the immune reactions that accompany demyelination in patients with multiple sclerosis (MS). We measured prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) release from peripheral monocytes exposed in vitro to complement. Our studies suggest that there is a significantly higher production of PGE2 in monocytes from patients with chronic progressive MS than in those with exacerbation or remitting MS and healthy controls. No significant differences in TxB2 release were noted between the three groups.

Chromatography, High Pressure Liquid↗
PubMed1989

Latency-associated transcript but not reactivatable virus is present in sensory ganglion neurons after inoculation of thymidine kinase-negative mutants of herpes simplex virus type 1.

The presence of herpes simplex virus (HSV) latency-associated transcript (LAT) was investigated in sensory ganglion neurons of mice after inoculation with thymidine kinase (TK) mutants of HSV. Ganglion serial sections were examined in order to quantitate numbers of LAT-positive neurons. After inoculation with TK-positive HSV, virus was isolated during latency from explants of most ganglia, and LAT was detected by in situ hybridization in 96% of ganglia. After inoculation with HSV TK mutants, virus was isolated from 0% of ganglia, but LAT was detected in 95 to 100% of ganglia. After inoculation of TK mutants of HSV, therefore, although latent infection as indicated by the isolation of virus from ganglion explants was not detected, the presence of LAT was common. These results suggest that the lack of reactivatable virus after inoculation of HSV TK mutants may be related to a role for HSV TK expression in the reactivation process.

Animals↗
PubMed1988

Herpes simplex virus latent infection: reactivation and elimination of latency after neurectomy.

Section of the sciatic nerve during the period of herpes simplex virus (HSV) latent infection was performed to evaluate residual latency in mouse dorsal root ganglion. In control mice without sciatic neurectomy, latency was present in 90-100%, while in those which underwent a neurectomy procedure, latent infection was surprisingly decreased to 28-50%. To investigate the hypothesis that the decrease of latency resulted from HSV reactivation and replication (with subsequent neuron destruction), groups of mice were treated with acyclovir to inhibit HSV reactivation, after having undergone a neurectomy procedure. Acyclovir treatment largely prevented the neurectomy-related elimination of latency and supported the hypothesized mechanism.

Acyclovir↗
PubMed1988

Clinical significance of types of cerebellar amyloid plaques in human spongiform encephalopathies.

We report three patients with both spongiform encephalopathy and cerebellar amyloid plaques; one showed kuru-like plaques and was diagnosed as having Creutzfeldt-Jakob disease (CJD), and two had multicentric plaques and were diagnosed as having Gerstmann-Sträussler-Scheinker disease (GSSD). Evaluation of these cases and review of others previously reported suggests a clinicopathologic correlation between type of cerebellar plaque and neurologic clinical course. CJD patients who showed kuru-like plaques generally had disease with early onset (average age, 49.1 years) and long duration (average, 34 months), as compared with CJD patients without kuru-like plaques. GSSD patients usually had multicentric cerebellar plaques, and cases were usually familial, had early age of onset (average, 42.7 years), and were of long duration (average, 73 months). Myoclonus was infrequent in GSSD patients and pathologically spongiform change was minimal; spinal tract degeneration was common.

Adult↗
PubMed1987

Acyclovir resistance in a patient with chronic mucocutaneous herpes simplex infection.

Chronic cutaneous herpes simplex virus infection is described in a 68-year-old man who was immunocompromised because of chronic lymphocytic leukemia. The herpes infection was not amenable to therapy with acyclovir. Clinical isolates of herpes simplex virus were assessed for viral thymidine kinase activity, which was markedly decreased in two isolates. By the method of viral plaque autoradiography, these isolates were determined to be composed primarily of mutant thymidine kinase-negative herpes simplex virus mixed with occasional standard thymidine kinase-positive herpes simplex virus. Viral plaque autoradiography permitted the quantitation of proportions of thymidine kinase-negative and thymidine kinase-positive herpes simplex virus in the mixed virus populations. The chronic cutaneous infection persisted, unlike other reported infections by thymidine kinase-negative herpes simplex virus.

Acyclovir↗
PubMed1987

Trigeminal ganglion infection by thymidine kinase-negative mutants of herpes simplex virus after in vivo complementation.

Infection of trigeminal ganglion by herpes simplex virus (HSV) thymidine kinase-negative (TK-) mutants was investigated in mixed infection studies in mice. Mice were corneally inoculated with TK- HSV alone or with mixtures of TK- HSV-TK+ HSV. When inoculated alone, an arabinosylthymine-selected HSV type 1 TK- mutant and a HSV type 2 TK- deletion mutant infected mouse ocular tissues but rarely infected ganglion tissues. However, both TK- mutants readily infected ganglion tissues when they were inoculated in mixtures with TK+ HSV. By means of mixed infection studies, it was demonstrated that TK- HSV could readily establish acute and latent ganglion infections. It was thought that the frequent infection of trigeminal ganglion tissue by both TK- mutants after mixed TK(-)-TK+ HSV infection was the result of in vivo complementation. After mixed TK(-)-TK+ HSV infection and subsequent cultivation of ganglion explants in arabinosylthymine, results supported the conclusion that when TK- was present in ganglia it was in the same neurons that contained TK+ HSV.

Animals↗
PubMed1986

Isolation of JC virus capsomer-like structures from progressive multifocal leukoencephalopathy brain.

Brain tissue from a patient with progressive multifocal leukoencephalopathy (PML) was analyzed by molecular biological and electron-microscopic techniques. Viral DNA was isolated directly from brain tissue, cloned into a plasmid vector, and subjected to restriction endonuclease analysis. The pattern of restriction fragments identified by gel electrophoresis was almost indistinguishable from that of prototype JC virus. By this procedure the etiologic agent of PML in this patient was identified without the isolation of infectious virus. After centrifugal clarification of brain homogenates, high speed centrifugal pellets were studied by electron microscopy. Large numbers of 9-nm polygonal particles, sometimes in paracrystalline arrays, were observed. It was thought likely that these particles were capsomer subunits of 41-43 nm JC virus virions. That the particles were capsomers was supported by negative stain electron microscopy, including reconstruction studies with simian virus 40.

Aged↗
PubMed1986

Thymidine kinase (TK) activity in herpes simplex virus type 1 recombinants that carry insertions affecting regulation of the TK gene.

Determinations of the possible importance of herpes simplex virus type 1 (HSV) thymidine kinase (TK) expression in the pathogenesis of viral latency depend in part on the use of defined mutants. In a recent study by A. E. Sears, B. Meignier, and B. Roizman (J. Virol. 55, 410-416 (1985], in which they utilized genetically engineered viral recombinants considered to be TK-, the role of HSV TK expression in latency was reported to be minimal. To further investigate this conclusion we intensively studied the TK phenotypes of their M316-2 and M316-10 HSV-1 mutants. TK activity was investigated by phosphorylation of thymidine, by arabinosylthymine (ara-T) inhibition and by virus plaque autoradiography. TK activity of the M316-2 and M316-10 HSV mutants was not detected in 5-min assays (as performed by Sears et al.), but in longer assays substantial activity was apparent. In contrast, in assays of control TK- viruses, activity was minimal or absent at all time points. In ara-T inhibition assays the M316-2 and M316-10 viruses were inhibited more than 10-fold, consistent with viruses of intermediate TK activity. By plaque autoradiography both of these viruses produced plaques which incorporated significant amounts of thymidine. Based on these results we conclude that the M316-2 and M316-10 viruses should likely be considered to express intermediate levels of TK activity. HSV latency results using these mutants may need to be interpreted with this in mind.

Animals↗
PubMed1985

Sequential changes of sensory neuron (fluoride-resistant) acid phosphatase in dorsal root ganglion neurons following neurectomy and rhizotomy.

Five to seven days after sciatic nerve section in rats, fluoride-resistant acid phosphatase (FRAP) expression in dorsal root ganglion (drg) neurons was markedly decreased. The decrease was in contrast to increased acid phosphatase which has been reported to occur in other neurons after nerve section. FRAP expression in ganglion neurons subsequently increased 14-21 days after nerve section; this preceded the restitution of enzyme expression in the spinal cord substantia gelatinosa. FRAP expression in drg neurons was not decreased after dorsal root section.

Acid Phosphatase↗
PubMed1984

Herpes simplex and herpes zoster. Nervous system involvement.

Mainly discussed are neurologic complications of two neurotropic herpesviruses: herpes simplex viruses types 1 and 2 and varicella-zoster virus. Briefly discussed are cytomegalovirus and Epstein-Barr virus. Treatment of immunosuppressed and nonimmunosuppressed patients is reviewed.

Antiviral Agents↗
PubMed1983

Varicella-zoster virus RNA in human trigeminal ganglia.

The technique of in situ hybridisation was used to examine human trigeminal ganglia for the presence of varicella-zoster virus (VZV) RNA. The ganglia were removed from fresh cadavers of individuals without a history of current or recent herpes zoster. Of the various types of cell in the ganglia, only the neurons appeared positive for VZV RNA. 0 to 0.3% of neurons were positive for VZV RNA.

Aged↗
PubMed1983

The role of pseudorabies virus thymidine kinase expression in trigeminal ganglion infection.

The role of pseudorabies virus (PRV) thymidine kinase (TK) expression in the pathogenesis of PRV infection of mice was studied with TK-negative (TK-) mutants. Thymidine phosphorylation and arabinosylthymine inhibition of PRV replication and efficiency of plating were used to characterize TK+ and TK- PRV. In addition, a plaque autoradiography procedure was utilized to determine the TK phenotype of individual plaques. TK+ and TK- PRV replicated well in ocular tissues, while TK+ but not TK- did so in ganglion tissue. Mortality was absent after TK- PRV inoculation and widespread after inoculation of similar amounts of TK+ PRV. Latent infection in mice was not detected with either TK+ or TK- PRV. This study indicated the probable importance of PRV TK expression in acute trigeminal ganglion infection.

Animals↗
PubMed1983

Hepatic infection by thymidine kinase-positive and thymidine kinase-negative herpes simplex virus after partial hepatectomy.

Herpes simplex virus (HSV) infection of mouse liver after partial hepatectomy was studied. Partial hepatectomy resulted in the rapid onset of cellular DNA synthesis and the appearance of many mitotic figures (peak, 3 days after surgery). Similar changes were not seen in control animals. After partial hepatectomy, the mice were infected with thymidine kinase-positive (TK+) and -negative (TK-) HSV to investigate virus titers in liver tissue during liver cell replication. In control unoperated mice, liver titers of TK+ HSV (2 X 10(3) PFU/g) were greater than those of mice inoculated with TK HSV (4 X 10(1) to 5 X 10(2) PFU/g). After partial hepatectomy, TK+ and TK- HSV titers increased, and peak TK+ and TK- HSV titers were similar (6 X 10(5) to 8 X 10(5) PFU/g). Hepatic infection was further investigated by infectious center (IC) assays. The numbers of ICs for TK+ HSV increased 50-fold after partial hepatectomy, whereas the increase was less for TK- HSV. From the results of these studies, we hypothesize that the increase in hepatic TK+ HSV after hepatectomy may have been largely due to the increase in ICs, whereas the increase in hepatic TK- HSV was due, in part, to the increase in ICs, but may also have been due to the enhanced synthesis of TK- HSV in replicating liver cells.

Animals↗