Biomedical subjects

H K Ng

Publications and source records attributed to H K Ng.

At least 37 records · Page 2Linked to original sources

PubMed2001

Detection of multiple gene amplifications in glioblastoma multiforme using array-based comparative genomic hybridization.

We have used a new method of genomic microarray to investigate amplification of oncogenes throughout the genome of glioblastoma multiforme (GBM). Array-based comparative genomic hybridization (array CGH) allows for simultaneous examination of 58 oncogenes/amplicons that are commonly amplified in various human cancers. Amplification of multiple oncogenes in human cancers can be rapidly determined in a single experiment. Tumor DNA and normal control DNA were labeled by nick translation with green- and red-tagged nucleotides, respectively. Instead of hybridizing to normal metaphase chromosomes in conventional comparative genomic hybridization (CGH), the probes of the mixed fluorescent labeled DNA were applied to genomic array templates comprised of P1, PAC, and BAC clones of 58 target oncogenes. The baseline for measuring deviations was established by performing a series of independent array CGH using test and reference DNA made from normal individuals. In the present study, we examined fourteen GBMs (seven cell lines and seven tumours) with CGH and array CGH to reveal the particular oncogenes associated with this cancer. High-level amplifications were identified on the oncogenes/amplicons CDK4, GLI, MYCN, MYC, MDM2, and PDGFRA. The highest frequencies of gains were detected on PIK3CA (64.3%), EGFR (57.1%), CSE1L (57.1%), NRAS (50%), MYCN (42.9%), FGR (35.7%), ESR (35.7%), PGY1 (35.7%), and D17S167 (35.7%). These genes are suggested to be involved in the GBM tumorigenesis.

Brain Neoplasms↗

PubMed2001

Spinal cord pilocytic astrocytoma with cranial meningeal metastases.

Dissemination of tumour cells along the cerebrospinal fluid (CSF) pathway has been reported mostly in medulloblastomas, germ cell tumours or high grade gliomas. Juvenile pilocytic astrocytoma (JPA) is usually a benign astrocytoma. However, drop metastases of indolent nature from intracranial tumours to the spinal cord are documented. All of the previously reported cases represent metastases of cerebellar or hypothalamic tumours spreading to the spinal cord. We document in this paper the first report of a spinal cord pilocytic astrocytoma spreading via the CSF to the cerebral meninges. A 9 year old girl had a JPA of C5 to C7 subtotally resected. Two and a half years later she presented with hydrocephalus with radiologically meningeal enhancement. The meninges were biopsied which showed metastatic JPA. The girl was relatively well 4 years after initial surgery with residual tumour. Spinal cord JPA can rarely metastasize to the cranial meninges. Similar to intracranial tumours which spread to the spinal cord, such metastatic lesions are indolent.

Astrocytoma↗

PubMed2001

Concurrent hypermethylation of multiple genes is associated with grade of oligodendroglial tumors.

Current evidence suggests that epigenetic changes play an important role in the evolution of human cancers. In this study, we evaluated whether hypermethylation of CpG islands at the gene promotor regions of several tumor-related genes is involved in the carcinogenesis of oligodendroglial tumors. We examined the methylation status of 11 genes in a series of 43 oligodendroglial tumors (19 oligodendrogliomas, 13 anaplastic oligodendrogliomas, 9 oligoastrocytomas, and 2 anaplastic oligoastrocytomas) by methylation-specific polymerase chain reaction. Our results showed that hypermethylation of CpG islands was detectable in 8 of 11 genes studied and 74% of tumors were hypermethylated in at least 1 gene. Promotor hypermethylations were detected in O6-methylguanine-DNA methyltransferase (MGMT), RB1, estrogen receptor, p73, p16INK4a, death-associated protein kinase, p15INK4b, and p14ARF at 60%, 34%, 30%, 16%, 12%, 10%, 7%, and 2%, respectively. No hypermethylation was detected in the promotors of glutathione-S-transferase P1, von Hippel-Lindau or the DNA mismatch repair (hMLH1) genes. Statistical analysis revealed that concordant hypermethylation of at least 2 genes, p16INK4a and p15INK4b were significantly associated with anaplastic oligodendroglial tumors, and hypermethylation of MGMT was significantly associated with loss of chromosome 19q and with combined loss of chromosomes 1p and 19q. More importantly, several candidate tumor suppressor genes such as p16INK4a, p15INK4b, and p73 that were previously reported as unmutated in oligodendroglial tumors were found to be hypermethylated in their CpG islands. Taken together, we conclude that hypermethylation of CpG islands is a common epigenetic event that is associated with the development of oligodendroglial tumors.

Astrocytoma↗

PubMed2001

Iliofemoral deep vein thrombosis: conventional therapy versus lysis and percutaneous transluminal angioplasty and stenting.

OBJECTIVE: To compare conventional treatment (heparin and warfarin) of iliofemoral venous thrombosis with multimodality treatment (lysis and stenting). SUMMARY BACKGROUND DATA: Several studies have reported on conventional therapy for iliofemoral venous thrombosis with disappointing results. However, more recent studies have reported better results with multimodality treatment. METHODS: Fifty-one consecutive patients with extensive iliofemoral venous thrombosis were treated during a 10-year period. If there were no contraindications, patients were given the option to choose between conventional therapy (group 1) and multimodality therapy (group 2). The multimodality treatment strategy included catheter-directed lysis followed by percutaneous transluminal balloon angioplasty (PTA) and stenting for residual iliac stenoses. All patients underwent routine venous duplex imaging at 30 days, 3 months, 6 months, and every 6 months thereafter. RESULTS: There were 33 patients in group 1 and 18 patients in group 2. Demographic and clinical characteristics were comparable for both groups. Initial lysis was achieved in 16 of 18 patients (89%) in group 2. Ten of 18 patients in group 2 had residual stenosis after lysis (8 primary and 2 secondary to malignancy), and they were treated with PTA/stenting with an initial success rate of 90%. Two patients in group 1 (6%) had a symptomatic pulmonary embolism (none in group 2). At 30 days, venous patency and symptom resolution were achieved in 1 of 33 patients (3%) in group 1 versus 15 of 18 (83%) in group 2. Kaplan-Meier analysis showed primary iliofemoral venous patency rates at 1, 3, and 5 years of 24%, 18%, and 18% and 83%, 69%, and 69% for groups 1 and 2, respectively. Long-term symptom resolution was achieved in 10 of 33 patients (30%) in group 1 versus 14 of 18 (78%) in group 2. Kaplan-Meier life table analysis showed similar survival rates at 1, 3, and 5 years of 100%, 93%, and 85% for group 1 and 100%, 93%, and 81% for group 2. CONCLUSIONS: Lysis/stenting treatment was more effective than conventional treatment in patients with iliofemoral vein thrombosis.

Angioplasty, Balloon↗

PubMed2001

Analysis of loss of heterozygosity on chromosomes 10q, 11, and 16 in medulloblastomas.

OBJECT: The loss of genetic material from specific chromosome loci is a common feature in the oncogenesis of tumors and is often indicative of the presence of important tumor suppressor genes at these loci. Recent molecular genetic analyses have demonstrated frequent loss of chromosomes 10q, 11, and 16 in medulloblastomas. The aim of this study was to localize the targeted deletion regions on the three aforementioned chromosomes in medulloblastomas. METHODS: Loss of heterozygosity (LOH) was examined on chromosomes 10q, 11, and 16 in a series of 22 primary and two recurrent medulloblastomas by using polymerase chain reaction-based microsatellite analysis. The DNA extracted from the tumors and corresponding normal blood samples were amplified independently in the presence of radioactively labeled microsatellite primers, resolved by denaturing gel electrophoresis and processed for autoradiography. The DNA obtained from control blood samples that displayed allelic heterozygosity at a given microsatellite locus were considered informative. Loss of heterozygosity was inferred when the allelic signal intensity of the tumor sample was reduced by at least 40%, relative to that of the constitutional control. The LOH analysis demonstrated that deletions of chromosomes 10q, 11p, and 16q are recurrent genetic events in the development of medulloblastomas. Three subchromosomal regions of loss have been identified and are localized to the deleted in malignant brain tumors 1 [DMBT1] gene site on chromosomes 10q25, 11p13-11p15.1, and 16q24.1-24.3. CONCLUSIONS: These results indicate that DMBT1 is closely associated with the oncogenesis of medulloblastomas and highlight regions of loss on chromosomes 11p and 16q for further fine mapping and cloning of candidate tumor suppressor genes that are important for the genesis of medulloblastoma.

Adolescent↗

PubMed2001

Identification of novel regions of allelic loss in ependymomas by high-resolution allelotyping with 384 microsatellite markers.

OBJECT: Ependymomas are rare glial neoplasms; little is known about the molecular pathogenesis of this tumor entity. In a previous study the authors found multiple genomic imbalances in ependymomas resected in 20 adults and eight children, including loss of chromosomes 1p, 6, 16, 17, 19q, 20q, and 22q, as well as gain of chromosomes 4q, 5q, 7q, 9q, and 12q on comparative genomic hybridization. The aim of this study was to map in more detail the commonly affected regions in ependymomas. METHODS: A comprehensive allelotype analysis of 16 ependymomas was conducted using 384 microsatellite markers that span the 22 autosomes. Based on this high-resolution loss of heterozygosity analysis, multiple overlapping deletion regions were identified as follows: 6q25.2-27, 16p12-13.1, 16q22.3-24.1, 17q22-24, 19q12-13.2, 20q13.2-13.3, and 22q13.1-13.3. CONCLUSIONS: These data confirmed previous reports that loss of chromosomes 17 and 22 were common in ependymomas. Moreover, the authors were able to identify loss of chromosomes 13, 16, 19, and 20 as novel findings in ependymomas. It is believed that potential tumor suppressor genes that reside in these commonly deleted regions may contribute to the molecular tumorigenesis of ependymomas.

Adolescent↗

PubMed2001

Frequent death-associated protein kinase promoter hypermethylation in multiple myeloma.

UNLABELLED: Death-associated protein (DAP) kinase is a novel gene regulating apoptosis induced by IFN-gamma. In B-cell malignancies, loss of DAP kinase expression is commonly associated with promoter hypermethylation. These characteristics of DAP kinase may be of particular relevance in multiple myeloma (MM), a B-lineage malignancy in which prolonged survival capacity of the malignant plasma cells may be critical in the induction and maintenance of tumor cells. PURPOSE: The involvement and potential role of DAP kinase in MM pathogenesis was examined. EXPERIMENTAL DESIGN: In this investigation, methylation-specific PCR was conducted on primary MM and MM cell lines. Methylation status findings were correlated with clinical parameters. RESULTS: We first demonstrated frequent DAP kinase hypermethylation in 24 of 36 primary MMs (20 of 26 at diagnosis and 4 of 10 with relapse/residual MM after treatment), 1 of 2 patients with monoclonal gammopathy of undetermined significance, and 1 of 3 MM cell lines studied. The high frequency of DAP kinase hypermethylation was similarly observed in MM of different stages, immunoglobulin isotypes, and histological grades, with or without plasmacytomas. Although not statistically significant, the overall survival of patients with DAP kinase methylation was notably shortened among 23 MM patients followed prospectively (P = 0.38 by Kaplan-Meier method and log-rank test). This preliminary finding suggests prognostic implications of DAP kinase in MM that may deserve further investigation. CONCLUSIONS: Our data suggest an important role for DAP kinase in MM tumorigenesis.

Adult↗

PubMed2001

Variant Creutzfeldt-Jakob disease in Hong Kong.

A 34-year-old Chinese woman who had lived in the United Kingdom in the 1980s was admitted to hospital in Hong Kong because of a 7-month history of progressive neurological deterioration. Initially, she complained of heartburn and paraesthesia of the hands and feet. She then developed slowness of speech and gait, and was noted to be forgetful and irritable. In January 2001, she was brought back to Hong Kong for treatment. On admission in May she was dysarthric, ataxic, and dystonic. Magnetic resonance imaging showed high signals in both thalami suggestive of variant Creutzfeldt-Jakob disease. Other investigations, including electroencephalogram and lumbar puncture, were unremarkable. A tonsil biopsy showed the presence of prions. This patient's presentation is typical of the variant Creutzfeldt-Jakob disease cases that have been reported since 1996. Because of her residential history, we conclude that this is an imported case from the United Kingdom.

Adult↗

PubMed2001

[A preliminary study of loss of heterozygosity on chromosome 14 in glioblastoma].

OBJECTIVE: In order to locate the deletion areas probably harboring tumor suppressor genes on chromosome 14 and provide clues for discovering novel tumor suppressor genes. METHODS: Fourteen loci on chromosome 14 were examined to detect loss of heterozygosity(LOH) in 20 cases of glioblastoma(GBM) by PCR based microsatellite polymorphism analyses, in which fluorescence-labeled primers and Perkin Elmer 377 DNA Sequencer were applied. RESULTS: 50% informative cases of GBM displayed LOH on chromosome 14; 38.2% of informative loci showed LOH in our series, in which the most frequent LOH was observed at locus D14S65(57.1%) on 14q31-32.3 and in the chromosomal region from locus D14S63 (46.7%) to D14S74(47.1%) on 14q21-24.1. 32% of informative cases displayed LOH on 14p and 50% on 14q. No microsatellite instability was observed. CONCLUSION: Loss of genetic material on chromosome 14q may play an important role in molecular genetic pathogenesis of GBM. The chromosomal regions at D14S65 on 14q31-32.3 and from D14S63 to D14S74 on 14q21-24.1 may harbor novel tumor suppressor genes associated with GBM.

Brain Neoplasms↗

PubMed2000

Comparative genomic hybridization detects losses of chromosomes 22 and 16 as the most common recurrent genetic alterations in primary ependymomas.

In this study, we used comparative genomic hybridization to provide an overview of chromosomal imbalances in a series of 20 adult and 8 childhood ependymomas. All tumors displayed multiple genomic imbalances. Loss of genetic material was observed in chromosomes 22q (71%), 16 (57%), 17 (46%), 6 (39%), 19q (32%), 20q (32%), and 1p (29%), with the overlapped deletion regions determined at 16p13.1-13.3, 16q22-q24, 19q13.1-13.4, 20q13.1-13.2 and 1p36.1-36.3. Gain of DNA was commonly detected on chromosomes 5q (46%), 12q (39%), 7q (36%), 9q (36%), and 4q (32%), with overlapped regions of gain mapped to 5q21-22, 12q15-24.1, 7q11.2-31.2, 9q12-32, and 4q23-28, respectively. These findings suggest a greater degree of genomic imbalance in ependymomas than has been recognized previously and highlight chromosomal loci likely to contain oncogenes or tumor suppressor genes that may contribute to the molecular pathogenesis of this tumor. Our study also confirmed previous findings on frequent losses of 17 and 22q in ependymomas and further identified chromosome 16 loss as a common recurrent genetic aberration in ependymomas.

Adult↗

PubMed2000

Apolipoprotein E isoforms in Alzheimer's disease pathology and etiology.

The apolipoprotein E (apoE) epsilon4 allele increases risk of Alzheimer's disease (AD), perhaps by accelerating plaque formation, or by impairing neuron repair. Considerable evidence supports both mechanisms. AD patients with epsilon4 have more and earlier amyloid deposits than do patients without epsilon4. The same is true of non-demented control subjects. In vitro, all apoE isoforms inhibit amyloid beta protein (Abeta) aggregation, but apoE4 less effectively than apoE3. Transgenic amyloid-producing mice expressing apoE3 or apoE4 develop less Abeta deposition than apoE knockout mice. These observations are consistent with an effect of apoE isoforms on Abeta aggregation in AD. ApoE is important for neurite maintenance since apoE knockout mice lose neurites and suffer behavioral deficits with aging or treatment with excitotoxins. ApoE4 mice show similar defects, but apoE3 mice are normal. AD patients with epsilon4 show more neuritic deficits than epsilon3 carriers. ApoE epsilon4 also worsens neurological impairment in head injury, stroke, and multiple sclerosis. Thus, apoE4 is less effective at neurite maintenance. Perhaps epsilon4 increases AD risk by both mechanisms: allowing amyloid deposition and failing to repair neurites. In either case, introducing apoE3 or apoE2 into the brain, for example by gene therapy or cell grafts, might delay AD progression.

Alzheimer Disease↗

PubMed2000

Prevalence and distribution of human herpesvirus 7 in normal brain.

Although it has been recognised that human herpesvirus 7 (HHV-7) establishes latent infection in CD4+ T lymphocytes and productive infection in salivary glands, recent data suggest that its in vivo tropism may be more widespread. In this study, the prevalence and distribution of HHV-7 in brain tissues of 30 consecutive post-mortems were examined by nested polymerase chain reaction. For each post-mortem, 10 fresh autopsy tissue samples were collected respectively from the cerebellum, frontal, temporal, parietal, and occipital lobes of both cerebral hemispheres. These patients were aged from 20-95 years (mean = 61.4, SD = 20.2) with a male:female ratio of 2:1. Three patients died of intracranial haemorrhage, the others died of causes unrelated to the central nervous system. Overall, 5% (15/300) of the brain tissue samples were positive for HHV-7 DNA. The positive rates with respect to anatomical positions were similar (0-3/30). When analysed by patient, 36.7% (11/30) were HHV-7 DNA positive. The viral DNA-positive and -negative groups did not show a significant difference in gender or age distribution. The majority (81.8%) of viral DNA-positive patients had HHV-7 DNA detected at only one anatomical position; only two patients had viral DNA detected simultaneously at three anatomical sites. These results suggest that HHV-7 persists in brain tissues of a substantial proportion of the adult population, and in most individuals, its distribution is probably confined to one site rather than pervasive. Further studies to elucidate the role of this ubiquitous virus in neuropathology are warranted.

Adult↗

PubMed2000

The impact of acute hyponatraemia on severe traumatic brain injury in rats.

The effect of experimental acute hyponatraemia on severe traumatic brain injury (TBI) was studied in a modified impact-acceleration model. The cortical contusional volume was quantified by image analysis on serial sections, injured axons were visualized and quantified by beta-Amyloid Precursor Protein (beta-APP) immunohistochemical staining. Regional brain water content was estimated by the wet-dry weight method. The experiment was conducted in Group I (injury only) and Group II (injury followed by acute hyponatraemia). Comparison between the two groups showed that acute hyponatraemia significantly increased contusional volume (3.24 +/- 0.70 mm3 vs. 1.80 +/- 0.65 mm3, P = 0.009) and the number of injured axons (128.7 +/- 44.3 vs. 41.7 +/- 50.1, P = 0.04) in the right thalamus & basal ganglia region. Water content of the brain stem region was also significantly increased by acute hyponatraemia (73.71 +/- 0.14% vs. 72.28 +/- 0.93%, P = 0.004). These results suggest that acute hyponatraemia potentiates secondary brain damage in severe TBI by augmentation of both focal contusion and diffuse axonal injury. The injured brain stem region is more susceptible to edema formation induced by experimental acute hyponatraemia.

Amyloid beta-Protein Precursor↗

PubMed2000

Telomere length and telomerase catalytic subunit expression in non-astrocytic gliomas.

Telomerase activation has been implicated as a major factor in the development of cancer. In our previous study we reported on the telomerase activity of a variety of gliomas. To further investigate the role of telomere and telomerase regulation in the pathogenesis of non-astrocytic gliomas, we examined the telomere length and the mRNA expression of telomerase reverse transcriptase gene (hTERT) and telomerase-associated protein (hTEP) in a series of 27 oligodendroglial and 18 ependymal tumors in this study. No statistical difference was found between the mean telomere length in telomerase-positive and telomerase-negative tumors (11.5 kb vs 13.1 kb; p = 0.424), although a slightly shorter length was observed in telomerase-positive oligodendroglial tumors. mRNA expression of hTERT was highly correlated with the telomerase activity status. hTERT was expressed in 8/8 (100%) and 2/2 (100%) telomerase-positive oligodendroglial and ependymal tumors, respectively, whereas 3/6 (50%) telomerase-negative oligodendroglial tumors and no telomerase-negative ependymal tumors showed expression. In contrast, hTEP1 mRNA was widely expressed in both telomerase-positive and telomerase-negative oligodendroglial and ependymal tumors. Our data support the notion that hTERT plays a critical role in determining the enzymatic activity of human telomerase. It has recently been proposed that both p16(INK4)/Rb pathway inactivation and telomerase activity were required for immortalization of epithelial cells. Although lack of p(16INK4a) expression was detected in a substantial proportion of tumors, no correlation between the p16(INK4a) or pRb protein expression and telomerase activity was observed in our series of non-astrocytic tumors.

Adolescent↗

PubMed2000

Central neurocytomas are genetically distinct from oligodendrogliomas and neuroblastomas.

AIMS: Central neurocytoma is a rare central nervous system tumour typically found in the lateral ventricles and at the septum pellucidum. Histologically, it resembles oligodendrogliomas and yet ultrastructurally, it shows neuronal differentiation. Its molecular oncogenesis is not known. The aim of this study was to examine whether major genetic events found in oligodendrogliomas and neuronal tumours, namely allelic deletions of chromosomes 1p and 19q and N-myc amplification, can be found in central neurocytomas. As there was one report describing gain of chromosome 7 in central neurocytomas, we also examined epidermal growth factor receptor (EGFR) amplification, as the EGFR gene is located at chromosome 7p. METHODS AND RESULTS: Nine central neurocytomas and matched blood samples were examined for loss of heterozygosity (LOH) of 1p and 19q13.2-13.4 with 23 finely mapped microsatellite markers. N-myc amplification was studied by fluorescence in-situ hybridization using paraffin-embedded sections. EGFR amplification was tested for by differential PCR. Six of nine (67%) tumours showed LOH at one or more loci at 1p and 5/9 (56%) of cases showed LOH at 19q. However, common regions of deletion cannot be identified. The majority of informative markers are retained at 1p (84%) and 19q (86%). Only one tumour showed amplification of N-myc and none of the cases showed amplification of EGFR. CONCLUSION: Central neurocytomas are genetically distinct from oligodendrogliomas, and chromosomes 1p and 19q probably do not play an important role in their pathogenesis. N-myc and EGFR amplification are rare.

Adolescent↗

PubMed2000

Pilocytic astrocytomas do not show most of the genetic changes commonly seen in diffuse astrocytomas.

AIMS: While it is well known that pilocytic astrocytomas are clinically distinct from diffuse astrocytomas, few comprehensive studies have focused on their genetic differences. The aim of this study was to examine pilocytic astrocytomas for genetic alterations that are commonly seen in diffuse astrocytomas. METHODS AND RESULTS: By using molecular genetic and immunohistochemical techniques, we evaluated p16, p53, CDK4 and PTEN genes in 29 pilocytic astrocytomas. Mutation screening of p53 and PTEN was performed by single strand conformation polymorphism analysis followed by direct sequencing. Loss of heterozygosity (LOH) of p53, p16 and 10q23-25 loci was performed with microsatellite markers and genomic microsatellite instability (MSI) was also screened. Protein expression of p16, p53, CDK4 and PTEN was examined by immunohistochemistry. Five tumours were found to have single genetic alterations, which included a p53 mutation, a PTEN mutation, MSI at a single microsatellite marker of the p16 locus, and one single LOH at each p16 and 10q23 loci. Protein expressions of p16, CDK4 and PTEN were detected in 73%, 61% and 38% of tumours, respectively. Significantly and in sharp contrast to diffuse astrocytomas, no pilocytic astrocytoma in our series stained for p53 protein. CONCLUSION: Pilocytic astrocytomas have neither MSI phenotype nor recurrent alterations of the p53 and p116 genes. However, altered expression of PTEN may be important in the genesis of pilocytic astrocytomas. We conclude that pilocytic astrocytomas are genetically distinct from diffuse astrocytomas. Lack of p53 mutation/immunostaining may serve as a diagnostic adjunct for differentiating pilocytic astrocytomas from diffuse astrocytomas in small neurosurgical biopsies.

Adolescent↗

PubMed2000

Expression of p19INK4d, CDK4, CDK6 in glioblastoma multiforme.

Deregulation of the G1/S checkpoint is a frequent event in the development of glioblastoma multiforme (GBM). Previous studies have shown more than 50% of primary GBM tumours contain either complete loss of the p16INK4a locus or amplification of the CDK4 gene. Moreover, many heterozygosity studies have shown deletion on human chromosome 19p13.2, where the p19INK4d gene has been localized. We examined the expression of p19INK4d and its two CDK substrates in a series of glioma-derived cell lines and tumours. No gene rearrangement or deletion was observed in the p19INK4d gene in these cell lines; however, expression of CDK4 and CDK6 was elevated relative to matched normal brain tissue in eight of 18 GBM tumours (44%). Furthermore, CDK6 expression level was increased in 12/14 glioblastomas, but undetectable in tumour samples of a previous lower grade tumour from the same patient. These data attest to the functional importance of both CDK4 and CDK6 in astrocytic tumourigenesis, particularly during the later stages of tumour progression.

Blotting, Western↗

PubMed2000

Survey for the presence and distribution of human herpesvirus 8 in healthy brain.

Brain tissues from both sides of the cerebellum and frontal, temporal, parietal, and occipital lobes were collected postmortem from 30 patients for human herpesvirus 8 (HHV-8) detection by PCR. Overall, 42 of 300 (14.0%) samples were positive, with similar rates for each position. Nineteen patients (63.3%) were positive and showed a significant increase in positivity with age (P = 0.007). The results indicate a neuroinvasive and neuropersistent potential of HHV-8.

Adult↗