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At least 91 records · Page 5Linked to original sources
PubMed1999

Transcriptional activation signals found in the Epstein-Barr virus (EBV) latency C promoter are conserved in the latency C promoter sequences from baboon and Rhesus monkey EBV-like lymphocryptoviruses (cercopithicine herpesviruses 12 and 15).

The Epstein-Barr virus (EBV) EBNA2 protein is a transcriptional activator that controls viral latent gene expression and is essential for EBV-driven B-cell immortalization. EBNA2 is expressed from the viral C promoter (Cp) and regulates its own expression by activating Cp through interaction with the cellular DNA binding protein CBF1. Through regulation of Cp and EBNA2 expression, EBV controls the pattern of latent protein expression and the type of latency established. To gain further insight into the important regulatory elements that modulate Cp usage, we isolated and sequenced the Cp regions corresponding to nucleotides 10251 to 11479 of the EBV genome (-1079 to +144 relative to the transcription initiation site) from the EBV-like lymphocryptoviruses found in baboons (herpesvirus papio; HVP) and Rhesus macaques (RhEBV). Sequence comparison of the approximately 1,230-bp Cp regions from these primate viruses revealed that EBV and HVP Cp sequences are 64% conserved, EBV and RhEBV Cp sequences are 66% conserved, and HVP and RhEBV Cp sequences are 65% conserved relative to each other. Approximately 50% of the residues are conserved among all three sequences, yet all three viruses have retained response elements for glucocorticoids, two positionally conserved CCAAT boxes, and positionally conserved TATA boxes. The putative EBNA2 100-bp enhancers within these promoters contain 54 conserved residues, and the binding sites for CBF1 and CBF2 are well conserved. Cp usage in the HVP- and RhEBV-transformed cell lines was detected by S1 nuclease protection analysis. Transient-transfection analysis showed that promoters of both HVP and RhEBV are responsive to EBNA2 and that they bind CBF1 and CBF2 in gel mobility shift assays. These results suggest that similar mechanisms for regulation of latent gene expression are conserved among the EBV-related lymphocryptoviruses found in nonhuman primates.

Animals↗
PubMed2004

Host cell gene expression during human immunodeficiency virus type 1 latency and reactivation and effects of targeting genes that are differentially expressed in viral latency.

The existence of reservoirs of cells latently infected with human immunodeficiency virus (HIV) is a major obstacle to the elimination of HIV infection. We studied the changes in cellular gene expression that accompany the reactivation and completion of the lytic viral cycle in cell lines chronically infected with HIV-1. We found that several genes exhibited altered expression in the chronically infected cells compared to the uninfected parental cells prior to induction into lytic replication. A number of gene classes showed increased expression in the chronically infected cells, notably including genes encoding proteasomes, histone deacetylases, and many transcription factors. Following induction of the lytic replication cycle, we observed ordered, time-dependent changes in the cellular gene expression pattern. Approximately 1,740 genes, many of which fall into 385 known pathways, were differentially expressed (P < 0.001), indicating that completion of the HIV replication cycle is associated with distinct, temporally ordered changes in host cell gene expression. Maximum changes were observed in the early and intermediate phases of the lytic replication cycle. Since the changes in gene expression in chronically infected cells suggested that cells latently infected with HIV have a different gene expression profile than corresponding uninfected cells, we studied the expression profiles of three different chronically infected cell lines to determine whether they showed similar changes in common cellular genes and pathways. Thirty-two genes showed significant differential expression in all cell lines studied compared to their uninfected parental cell lines. Notable among them were cdc42 and lyn, which were downregulated and are required for HIV Nef binding and viral replication. Other genes previously unrelated to HIV latency or pathogenesis were also differentially expressed. To determine the effects of targeting products of the genes that were differentially expressed in latently infected cells, we treated the latently infected cells with a proteasome inhibitor, clastolactacystin-beta-lactone (CLBL), and an Egr1 activator, resveratrol. We found that treatment with CLBL and resveratrol stimulated lytic viral replication, suggesting that treatment of cells with agents that target cellular genes differentially expressed in latently infected cells can stimulate lytic replication. These findings may offer new insights into the interaction of the latently infected host cell and HIV and suggest therapeutic approaches for inhibiting HIV infection and for manipulating cells latently infected with HIV so as to trigger lytic replication.

Cell Line↗
PubMed1984

Latency of visually evoked saccadic eye movements. I. Saccadic latency and the facilitation model.

The paper deals with the initiation of visually guided saccades, in order to break down the saccadic reaction time into functionally different periods of time. It takes into account that spatial processing of information is so basic that modelling of saccadic control properties should include spatio-temporal arrangements. The output signal of the saccadic system was measured in response to visual stimuli in which the time between the appearance of a visual stimulus in the peripheral field and the disappearance of the central fixation point was varied. The variation of the mean saccadic latency time, measured with respect to the onset of the peripheral stimulus, as a function of stimulus asynchrony was highly significant. This variation may be represented by a so-called gap-overlap curve, which is characterized here by means of five parameters. A facilitation model is introduced to fit the results of the gap-overlap experiments. The facilitation model for the initiation of visually evoked saccades incorporates a mechanism which governs the efficiency of processing of signals that arise from a stimulus presented at a particular position in space. It explains how visual information may be affected by other sensory information before it is used to command further saccades. It allows determination of saccadic system parameters, such as the peripheral and the foveal afferent processing time, the central processing time for a saccade and the degree of facilitation. These quantities were found to be characteristic for the given test subjects, and where these data could be compared with neurophysiological data, the agreement was within the experimental error.

Electronystagmography↗
PubMed1990

A herpes simplex virus type 1 variant, deleted in the promoter region of the latency-associated transcripts, does not produce any detectable minor RNA species during latency in the mouse trigeminal ganglion.

In peripheral sensory ganglia latently infected with herpes simplex virus type 1 (HSV-1) transcription is restricted. A set of viral latency-associated transcripts, the LATs, have been characterized by Northern blotting and in situ hybridization. These transcripts have previously been mapped to a 3 kb region of the viral genome within the repeat long region. However, transcription from adjacent regions of the genome can be detected by in situ hybridization, which cannot be detected by Northern blotting. These RNAs are termed minor LATs or m-LAT. In this study we show that in ganglia latently infected with the HSV-1 variant 1704, which is deleted in one complete copy of the LAT gene and in the promoter and 5' portion of the other copy, m-LATs are not detected by in situ hybridization. Furthermore, the levels of DNA in nervous system tissue latently infected with the parental and the 1704 variant virus are similar. Thus we propose that the sequence elements necessary for initiating transcription or stabilizing m-LATs are within the region deleted in variant 1704 that codes for the promoter and the 5' end of the LATs.

Animals↗
PubMed2005

Effects of lorazepam on short latency afferent inhibition and short latency intracortical inhibition in humans.

Experimental studies have demonstrated that the GABAergic system modulates acetylcholine release and, through GABA(A) receptors, tonically inhibits cholinergic activity. Little is known about the effects of GABA on the cholinergic activity in the human central nervous system. In vivo evaluation of some cholinergic circuits of the human brain has recently been introduced using a transcranial magnetic stimulation (TMS) protocol based on coupling peripheral nerve stimulation with TMS of the motor cortex. Peripheral nerve inputs have an inhibitory effect on motor cortex excitability at short intervals (short latency afferent inhibition, SAI). We investigated whether GABA(A) activity enhancement by lorazepam modifies SAI. We also evaluated the effects produced by lorazepam on a different TMS protocol of cortical inhibition, the short interval intracortical inhibition (SICI), which is believed to be directly related to GABA(A) activity. In 10 healthy volunteers, the effects of lorazepam were compared with those produced by quetiapine, a psychotropic drug with sedative effects with no appreciable affinity at cholinergic muscarinic and benzodiazepine receptors, and with those of a placebo using a randomized double-blind study design. Administration of lorazepam produced a significant increase in SICI (F(3,9) = 3.19, P = 0.039). In contrast to SICI, SAI was significantly reduced by lorazepam (F(3,9) = 9.39, P = 0.0002). Our findings demonstrate that GABA(A) activity enhancement determines a suppression of SAI and an increase of SICI.

Adult↗
PubMed1991

[Measurement and clinical using of motor conduction latency time and motor conduction latency rate of facial nerve in health subjects and facial paralysis patients].

The motor conduction latency time (MCLT) and rate (MCLR) of facial nerve in 70 cases of health subjects and 60 cases of facial paralysis patients were measured using evoke EMG. The results showed that MCLT is below 4 ms and MCLR is above 25 m/sec in 70 cases of health subjects, while the MCLT is above 4 ms and MCLR is below 25 m/sec in 60 cases of facial paralysis patients. We have observed the difference of MCLR and MCLR on different age groups in health subjects. The results showed that MCLT is prolonged gradually and MCLR is gradual reduced after 50 years old groups. But the MCLT does not exceed 4 ms and MCLR is not slower than 25 m/sec. The results of this studies suggested that if MCLT is above 4 ms, and MCLR is below 25 m/sec, it is a index of facial nerve paralysis.

Adolescent↗
PubMed1997

[Experimental study of response latency of visual search processes and premotor decision latency in dyslexic and non-dyslexic children. Model of linear regression: derived parametric estimates].

BACKGROUND: For some time the question of a visual impairment in dyslexic children has been a source of controversy in the literature. Depending on the method used, the findings point either to receptor or neural impairment or to a visual deficit in information processing. The question remains of whether these findings mask retardation in the motor planning and execution of a response. METHOD: In this investigation 61 children (15 dyslexic boys and 15 dyslexic girls aged 8 years 0 months to 10 years 8 months and 16 non-dyslexic boys and 15 non-dyslexic girls aged 8 years 0 months to 10 years 10 months) were tested using a computer-assisted visual display method (visual scan procedure). The results were included into a linear regression model. RESULTS: Compared to the non-dyslexic children the dyslexic children had a significant retardation in the speed of motor response (MANCOVA, Mann-Whitney U-test). For the "pure" visual process no differences in time course were found. Another important findings is the surprisingly wide range of results obtained for individual dyslexic children. In some instances there were deviations as great as 3.6 sigma (SEM). These findings indicate that we may be dealing with an individual partial impairment. It should be noted that the calculation of the linear regression model cannot be detailed for the group of dyslexic children. The prerequisites for a linear regression model are not satisfied. The comparability of the results is therefore limited. CONCLUSIONS: We cannot assume there will be a manifest visuomotor impairment in all dyslexic children when the stimulus is presented at the center and periphery of the field of vision. However, if such an impairment is present it is highly likely that the findings contain a mixture of retardation of pre-motor and visual decision latency. This would have substantial consequences for therapy, as visuomotor perception training would not be indicated in all instances. Some dyslexic children, both boys and girls, achieve completely "normal" results.

Attention↗
PubMed1991

Identification of a novel latency-specific splice donor signal within the herpes simplex virus type 1 2.0-kilobase latency-associated transcript (LAT): translation inhibition of LAT open reading frames by the intron within the 2.0-kilobase LAT.

Herpes simplex virus type 1 establishes latent infection in trigeminal ganglia of mice infected via the eye. A family of three colinear viral transcripts (LATs), 2.0, 1.5, and 1.45 kb, is present in latently infected ganglia. To characterize these LATs, lambda gt10 cDNA libraries were constructed with RNAs isolated from the trigeminal ganglia of latently infected mice. A series of recombinant bacteriophage were isolated containing cDNA inserts covering 1.7 kb of the 2.0-kb LAT. Splice junctions of the smaller LATs and the 3' end of the 2.0-kb LAT were identified by sequence analysis of RNA polymerase chain reaction products. No splice acceptor site, which does not support the hypotheses that the 2.0-kb LAT is an intron. However, the data are consistent with the possibility of a short leader sequence or multiple LAT transcription start sites. To generate the smaller 1.5- and 1.45-kb LATs, there is a 559-nucleotide intron spliced from the 2.0-kb LAT in strain F and a 556-nucleotide intron in strain 17+. The nucleotide sequences at the 5' and 3' ends of these introns are characteristic of spliced transcripts from eukaryotic protein-encoding genes, with one significant difference; i.e., the 5' end of the LAT intron is GC instead of the consensus sequence GT. This splice donor sequence is conserved in herpes simplex virus type 1 strains F, 17+, and KOS. Processing of the 2.0-kb LAT to form the spliced LATs preserves two open reading frames (ORFs) at the 3' end of the LATs; no new ORFs are created. Splicing of the LATs positions a 276-nucleotide leader sequence close to these ORFs and removes an intron that inhibits their translation in vitro. The novel 5' structure of the intron within the 2.0-kb LAT may be part of a control mechanism for transcription processing that results in splicing of the LATs only in sensory neurons during latent infection and reactivation but not during the viral replication cycle.

Animals↗
PubMed1995

Early genital stimulation of rats lowers limbic seizure latencies for females but increases latencies for males.

The genitals of male and female rats were tactilely stimulated (glass rod) for 10 successive days beginning on postnatal Days 5, 15, 35; handled but nonstimulated litter mates served as the reference groups. Limbic seizures were induced by a single systemic injection of lithium and pilocarpine when the rats were adults. The genitally stimulated female rats displayed a lower seizure threshold (as inferred from shorter seizure-onset times) relative to their cage mates. The single largest effect occurred for those females which had been stimulated after the vagina had opened (postnatal 35-45 days).

Animals↗