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Query: UMLS:C1396851 (
Epstein
)
24,119
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Polymerase chain reaction (PCR) was prospectively performed with cerebrospinal fluid (CSF) from 51 patients whose CSF was available for analysis and was submitted for viral culture and/or herpes simplex virus (HSV) serology and 20 patients whose CSF was submitted exclusively to the Clinical Biochemistry Laboratory. Primers were used that flanked a 92 bp segment of the HSV DNA polymerase gene (35 cycles). Amplified products were electrophoresed on agarose gel, blotted onto nylon membrane, and probed with a 32P-labelled sequence internal to the primers. For nested PCR, 1 microliter of PCR product was amplified for an additional 35 cycles before electrophoresis and Southern blot analysis. Review of the clinical records revealed that 15 patients had central nervous system (CNS) infections. Specific HSV DNA sequences were detected in CSF specimens of three of the individuals [PCR(2), nested PCR(1)]. Two of these patients had disseminated HSV infection including encephalitis and one patient had aseptic meningitis. The diagnoses of the 12 patients with CNS infection who did not have HSV DNA detected in CSF included encephalitis [varicella-zoster virus (1), cytomegalovirus (1), Mycoplasma pneumoniae (1)], meningitis [Neisseria meningitidis (1), Coccidioides immitis (1), Enterovirus (1), aseptic meningitis (1)], varicella-zoster radiculitis (2), human
immunodeficiency
virus dementia (2), and transverse myelitis due to
Epstein
-Barr virus (1). Importantly, HSV DNA was also not detected in the CSF of the 36 patients who did not have CNS infection and 20 samples submitted exclusively to the Clinical Biochemistry Laboratory. Our findings demonstrate the utility of PCR as a rapid, non-invasive method for the routine laboratory diagnosis of CNS infection due to HSV.
...
PMID:A prospective study of the polymerase chain reaction for detection of herpes simplex virus in cerebrospinal fluid submitted to the clinical virology laboratory. 133 47
Oral hairy leukoplakia is almost only described in patients infected by the human
immunodeficiency
virus.
Epstein
-Barr virus, sometimes associated with human papillomavirus, is always involved in the occurrence of these lesions. We have investigated two cases of oral hairy leukoplakia with the goal of detecting EBV and HPV by using both in situ hybridization and immunohistochemistry. EBV genome was detected with biotinylated BamHI W cDNA probe in the two cases. Furthermore, EBV was found to be in lytic phase as demonstrated by the strong signal observed with FITC-labelled anti-sense BHLF1 oligonucleotide probes. This finding was further supported by the absence of labelling with EBV-latent-cycle markers such as EBER1/2 oligoprobes and anti-latent membrane protein 1 antibody. In addition, these two cases were positive for HPV genomes: 31-33-51 (n = 1) and 31-33-51 plus 6-11 (n = 1) as detected by in situ hybridization using different sets of biotinylated probes. The signal obtained with in situ hybridization (both HPV and EBV) was localized to the upper layers of epithelial cells. The mechanism of oral hairy leukoplakia remains still unknown, but this work emphasizes the value of in situ hybridization with nonisotopic probes in the detection of viral nucleic acids on routinely processed tissue sections. The fact that these lesions seem to precede the AIDS phase emphasizes the clinical implications of this diagnosis in HIV infected patients.
...
PMID:[Simultaneous detection by non-isotopic in situ hybridization of human papilloma viruses and Epstein-Barr virus during the lytic cycle in oral hairy leukoplakia lesions]. 133 83
The Wiskott-Aldrich syndrome (WAS) is an X-linked disease characterized by eczema, thrombocytopenia, and profound
immunodeficiency
in affected males. While the etiology of the syndrome is currently unknown, abnormalities of CD43 have been described as a biochemical marker of the disease. Several investigators have demonstrated alterations in the expression of the CD43 surface antigen on WAS hematopoietic cells, noting either absence, decreased levels or changes in the characteristic molecular weight of the protein on the lymphocytes of affected patients. Biochemical studies have further indicated that glycosylating activity of specific enzymes which may post-translationally modify CD43 is altered in both T cells and
Epstein
-Barr-virus (EBV)-transformed B cells in WAS patients when compared to unaffected controls. Here we present data on cells derived from two males with a clinical diagnosis of WAS. Analysis of genomic DNA from the mothers of each of these patients (obligate carriers) showed a nonrandom X-chromosome inactivation pattern of nucleated blood cells, confirming the diagnosis of the X-linked syndrome. CD43 was characterized on peripheral blood lymphocytes and long-term EBV-transformed B cell lines, both to further analyze the molecular defects of WAS, as well as to attempt to generate a reproducible method for disease detection. Surprisingly, surface expression, molecular weight and two-dimensional gel analysis failed to demonstrated any reproducible differences in the CD43 expression, whether from disease or normal lymphocytes. Such results suggest possible heterogeneity of this syndrome.
...
PMID:CD43 is expressed normally on Wiskott-Aldrich-derived lymphocytes. 133 89
A highly sensitive in situ hybridization methodology for
Epstein
-Barr virus (EBV) RNA was used to determine the topography of EBV infection in 16 cases of human
immunodeficiency
virus-associated lymphoid tissues. Four lymphomas, 11 persistent generalized lymphadenopathy (PGL) lymph nodes, and one lymphoepithelial cyst were studied. The pattern of EBV infection was diffuse in all lymphoma cases and predominantly interfollicular in PGL nodes. No discernable pattern of infection was present in the lymphoepithelial cyst. Germinal center cells were also infected in seven of the PGL cases, and this pattern predominated in one case. Double labeling immunohistochemistry/in situ hybridization studies on four cases of PGL indicated that the EBV infection was primarily involving B-lymphocytes, but rare infected T-lymphocytes were also identified. These studies further clarify the pattern and cellular site of EBV infection in human
immunodeficiency
virus-related lymphoid disease.
...
PMID:Characterization of the topography of Epstein-Barr virus infection in human immunodeficiency virus-associated lymphoid tissues. 134 20
Interaction between herpesviruses and human
immunodeficiency
virus (HIV)1 is postulated in the progression of HIV disease. In order to evaluate the specific antibody responses directed to
Epstein
-Barr virus (EBV) and cytomegalovirus (CMV) and to provide serological evidence suggesting reactivation of these viruses able to accelerate the
immunodeficiency
, we studied IgA and IgG titres to EBV and CMV in the serum of HIV positive patients in relation to the CD4 cell number. The titres of IgG antibodies to EBV and the prevalence of IgG to CMV were significantly higher in HIV positive patients compared to control high risk HIV negative subjects. In HIV infected patients, anti-VCA IgG antibodies increased and anti-EBNA IgG antibodies decreased progressively in relation to the decline of CD4 cell number whereas anti-CMV IgG antibodies did not varied significantly at the same time. Anti-VCA IgA and anti-EA IgG antibodies were found uncommonly and with low titres. IgA antibodies to EA and CMV were not detected in any patient. The variations in EBV antibody response that we describe in HIV infection were previously reported in other
immunodeficiency
states and could be distinctive of these diseases.
...
PMID:Antibodies to Epstein-Barr virus and cytomegalovirus in relation to CD4 cell number in human immunodeficiency virus 1 infection. 134 40
We found that naive (CD45RA+) CD4 T cells have a lower capacity of adhesion to
Epstein
-Barr virus (EBV) immortalized B cells than memory (CD45RO+) CD4 T cells, as judged by conjugate formation. This would appear to be due to differences in the expression of adhesion molecules [lymphocyte function-associated antigen (LFA)-1, CD2]. However, kinetic studies showed that the degree of adhesion of naive T cells to B cells was stable over 60 min while that of memory T cells, like that of unseparated CD4 T cells, was characterized by a rapid formation and rapid dissociation of conjugates. This could be explained by a difference in the sensitivity of naive and memory CD4 T cells to down-regulation of antigen-independent adhesion by CD4-MHC class II interaction. Indeed, memory T cells also adhered stably to MHC class II(-) B cells. The adhesion of memory T cells, but not naive T cells, to MHC class II(+) B cells was sensitive to inhibition by OKT4a an anti-CD4 antibody, human
immunodeficiency
(HIV) gp160 (env) protein and a 12-mer peptide encompassing the 35-46 sequence of the HLA, DR beta 1 domain and previously shown to inhibit activation of HLA class II-restricted CD4 T cell responses. Since MHC class II expression did not influence the degree of conjugate formation by naive or memory CD4 T cells with B cells, CD4-MHC class II interaction does not appear to be involved in binding itself, but may down-regulate the adhesion of memory but not naive CD4 T cells.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Antigen-independent adhesion of CD45RA (naive) and CD45RO (memory) CD4 T cells to B cells. 135 61
Antibody-dependent cellular cytotoxicity (ADCC) against human T lymphotropic virus (HTLV) types I and II was investigated using sera obtained from infected individuals or from rabbits immunized with HTLV-I or -II envelope peptides. Target cells included an HTLV-I-transformed cell line (C91/PL), an HTLV-II-transformed cell line (729pH6neo), and
Epstein
Barr virus (EBV)-transformed B lymphocytes expressing HTLV-I or -II env or gag gene products after infection with vaccinia/HTLV recombinants. ADCC activity was directed at HTLV-I and -II envelope glycoproteins but not against core (gag) components. In contrast to the human
immunodeficiency
virus system, significant cross-reactivity between HTLV-I- and -II-directed ADCC activity was observed. Epitope mapping studies using sera from rabbits that had been immunized with HTLV-I or -II envelope peptides suggested that the critical epitopes for ADCC activity are located primarily in hydrophilic regions of the exterior (gp46) part of the envelope glycoprotein.
...
PMID:Human T lymphotropic virus types I- and II-specific antibody-dependent cellular cytotoxicity: strain specificity and epitope mapping. 137 51
Down-regulation of
Epstein
-Barr virus (EBV) induced transformation of human lymphocytes in vitro by dehydroepiandrosterone (DHEA), a naturally occurring human steroid secreted by the adrenal gland has been demonstrated. This article reports on the effects of DHEA and its novel synthetic analogs 16 alpha-fluoro-5-androsten-17-one (8354) and 3 beta-hydroxy-16 alpha-fluoro-5 alpha-androstan-17-one (OH8356) on human
immunodeficiency
virus (HIV-1) replication. Treatment with DHEA, 8354, or OH8356 resulted in a modest down-regulation of HIV-1 replication in phytohemagglutinin-stimulated peripheral blood lymphocytes as measured by syncytia formation, release of p24 antigen, and accumulation of reverse transcriptase activity. DHEA and 8354 also reduced syncytia formation in HIV-1-infected SupT1 lymphoblasts. DHEA and synthetic analogs of DHEA, which have been shown previously to have antiproliferative effects, now are shown to reduce HIV-1 replication. DHEA or synthetic analogs of DHEA could provide an alternative and/or adjuvant for HIV-1 infection.
...
PMID:Dehydroepiandrosterone (DHEA) and synthetic DHEA analogs are modest inhibitors of HIV-1 IIIB replication. 138 Dec 6
In situ hybridization or hybridohistochemistry has evolved in recent years in a new histologic modality. In situ hybridization (ISH) can be used for the detection of DNA (DISH) or RNA (RISH). The potential diagnostic value within a pathologic setting are well recognized. In this review paper, we summarize the use of DISH in a pathologic setting for the detection of chromosomal aberrations and localization of DNA-viruses like cytomegalovirus and
Epstein
Barr virus. RISH which is still in a more experimental stage can be applied for the localization of RNA-virus, like human
immunodeficiency
virus. However, the most important application of RISH will be the detection of gene-expression at the level of mRNA. Potentially this has many applications especially in early diagnostics of neoplastic tissues. Finally, we have summarized some pitfalls which may hamper the introduction of in situ hybridization for diagnostic purposes and some future developments in ISH.
...
PMID:In situ hybridization: a valuable tool in diagnostic pathology. 138 93
In the Lewis rat immunisation with the myelin P0 glycoprotein can induce an inflammatory demyelinating disease of the peripheral nervous system, experimental allergic neuritis (EAN), which has many clinical and histopathological parallels with the human disease the Guillain-Barre syndrome. In view of the reported association of GBS with a number of infectious agents we have investigated whether "molecular mimicry" may occur between microbial antigens and the P0 protein that could possibly trigger a similar pathogenic autoimmune response in man. A computer search of the available protein sequence data bases identified several absolute sequence homologies between P0 and viral proteins that involve five or more consecutive amino acid residues. Four of these sequence homologies involved viral pathogens previously associated with the Guillain-Barre syndrome, namely
Epstein
-Barr virus (EBV), cytomegalovirus (CMV), Varicella zoster virus (VZV) and human
immunodeficiency
virus I (HIV I). Although, sequence homologies were also found between viral peptides and the neuritogenic determinants of P0, residues 56-71 and 180-199, these homologies proved incapable of eliciting EAN in the Lewis rat. These observations are discussed with reference to the role that molecular mimicry between T cell epitopes on pathogen derived antigens and the P0 protein may play in the pathogenesis of the Guillain-Barre syndrome.
...
PMID:Molecular mimicry and the autoimmune response to the peripheral nerve myelin P0 glycoprotein. 138 42
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