Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1396851 (Epstein)
 24,119 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Epstein-Barr virus latent membrane protein (LMP) is an integral membrane protein that is expressed in cells latently infected with the virus. LMP is believed to play an important role in Epstein-Barr virus transformation and has been shown to induce expression of several cellular proteins. We performed a series of experiments that demonstrated that LMP is an efficient transactivator of expression from the human immunodeficiency virus type 1 long terminal repeat (HIV-1 LTR). Mutation or deletion of the NF-kappa B elements in the LTR abolished the transactivation, indicating that the LMP effect on HIV expression was due to induction of NF-kappa B activity. Experiments in which the HIV-1 Tat protein was coexpressed in cells together with LMP showed that Tat was able to potentiate the transactivation. Surprisingly, a synergistic effect of the two proteins was observed even in the absence of the recognized target region for Tat (TAR) in the HIV-1 LTR.
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PMID:Epstein-Barr virus latent membrane protein transactivates the human immunodeficiency virus type 1 long terminal repeat through induction of NF-kappa B activity. 140

Infection from human immunodeficiency virus (HIV) is well known for the particular host susceptibility to a variety of opportunistic infections and unusual malignant neoplasms. Although no tumor develops exclusively in concomitance with HIV infection, malignancies in these patients have different clinical behaviour, response to treatment and prognosis than the pattern observed in HIV negative hosts. Kaposi's sarcoma (EKS) and non-Hodgkin's lymphoma (NHL) are tumors per se diagnostic of AIDS in patients with HIV infection. From 1987 to 1991, 210 HIV positive patients underwent ENT examination without symptom-related selection: 128 were intravenous drug users, 50 homosexual males, 22 heterosexuals, 4 intravenous male homosexual drug users, 3 blood recipients and 3 subjects without known risk factors. Sixteen were allocated in group II, 37 in III, 9 in IV A, 2 in IV B, 31 in IV C1, 37 in IV C2, 48 in IV D and 30 in IV E. Fourteen had head and neck EKS localization. All were males, with a median age of 40 of which 11/14 were homosexuals. The concomitant involvement of skin and mucosa was the most common manifestation and the palate was the most frequently affected mucosal site. Twenty-four had NHL localized within the head and neck: 21 males and 4 females with a average age of 38, 10 intravenous drug users, 9 homosexual males, 3 heterosexuals, 1 blood recipient, 1 subject without known risk factors. Extranodal localization was the most frequent characteristic while the gums were the most commonly involved site. The main characteristics of head and neck manifestations of EKS and NHL are reported with references to literature. The majority of HIV infected patients with EKS or NHL have ENT localizations, perhaps because lymphatic tissue, a HIV target, is well represented in this area and contamination by infectious agents (such as Epstein-Barr virus and cytomegalovirus, probably involved in the pathogenesis of EKS and NHL) can easily occur in the head and neck. The otolaryngologist should be aware of the various, and sometimes misleading, characteristics of these diseases.
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PMID:[The cervicofacial manifestations of Kaposi's sarcoma and of non-Hodgkin's lymphomas in HIV-infected patients]. 141 19

Six heterogeneous common variable immunodeficiency (CVID) patients were analysed for germ-line DNA, DNA rearrangements, and RNA expressions of immunoglobulin (Ig) gene by Southern or northern blotting using appropriate probes. We detected no polymorphism in neutrophil DNA hybridized to a C mu and a C gamma probe. In three patients, both serum Ig and Ig-bearing cells were scarcely detected, and by northern hybridization methods, neither mu mRNA, gamma mRNA, alpha mRNA nor kappa mRNA was detected. However, one Epstein-Barr virus-transformed B lymphoblastoid cell line (LCL) of these three patients was different from the germ line in the region of JH, C gamma, and C kappa, and expressed mu mRNA at a higher level. The B cell defects of these three patients lay on the B cell maturation stage similar to X-linked agammaglobulinaemia (XLA). In two others among the six CVID patients, serum IgM and IgM-bearing cells were detected to a certain degree, and by northern hybridization, mu mRNA was detected at a lower level, but neither mu mRNA, alpha mRNA, nor kappa mRNA was detected. One LCL of these two patients could express mu mRNA at the normal level. In the last patient, the serum IgM was normal, serum IgG and IgA were somewhat low, Ig-bearing cells were normal, mu mRNA and kappa mRNA were detected at the normal level, and gamma mRNA and alpha mRNA were detected at a lower level. The defect of this patient affected the class switch stage. These results showed that primary B cell defects in CVID occurred at several B cell differentiation stages which could be classified by expression of the Ig gene, and at the degree of clonal diversity in the B cell repertoire. Furthermore, this study provides support for the idea that the CVID defect is related to a more generalized cellular function, such as regulating the proliferation and/or clonal expansion of cells of the B lymphoid lineage.
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PMID:Diversity in DNA rearrangements and in RNA expressions of immunoglobulin gene on common variable immunodeficiency. 142 Jan 14

Thirty-six sexually active couples serologically discordant for human immunodeficiency virus, type 1 (HIV-1), within the Baltimore Multicenter AIDS Cohort Study (MACS) were assessed to determine whether evidence of HIV-1 infection could be detected in the HIV-1-antibody-negative partners and whether factors associated with lack of transmission of HIV from the seropositive to the seronegative partner could be ascertained. Six HIV-1 seropositive couples and 18 seronegative couples were followed concurrently for comparison. None of the seropositive subjects had an AIDS-defining illness at entry into the study, and all subjects were followed for 1 year. A separate evaluation of unprotected anal receptive and insertive intercourse between discordant couples indicated high-risk activities for a median of 40 months, as reported by the HIV seropositive partner. Despite this finding, none of the HIV-1 seronegative men in discordant couples had evidence of HIV-1 infection by viral culture, p24 antigen testing, or polymerase chain reaction for HIV-1 DNA. Discordant seronegatives and seropositives did not differ from concordant seronegatives and seropositives in numbers of circulating CD4, CD8, and natural killer lymphocytes or in prevalence of antibodies to herpes simplex virus, type 1, Epstein-Barr virus, or cytomegalovirus, except that discordant seronegative men were less likely than their seropositive partners to have antibodies to herpes simplex virus, type 2. The reason for the apparent lack of HIV-1 infection in seronegative discordant individuals remains unexplained and did not appear to be associated with type of sexual activity, T-lymphocyte subsets or natural killer cells, or early stage of HIV-1 disease.
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PMID:Longitudinal study of homosexual couples discordant for HIV-1 antibodies in the Baltimore MACS Study. 145 31

Although the subject is now seldom formally addressed, much of the pathologic research into malignant lymphoma is still tacitly directed at developing a rational and reproducible classification. Pure morphology, while remaining of critical importance in the diagnosis of malignant lymphomas, has been exhausted as a means of understanding the biology of these tumors, which must be the eventual basis of a firm, enduring and clinically relevant classification. Thus, histopathologists have turned first to immunohistochemistry and now to molecular genetics to make sense of their morphologic observations. Correlation of various genetic (including oncogenetic) rearrangements with morphology has preoccupied pathologists this past year and has led to important advances in the understanding of B- and T-cell lymphomas. Lymphomas occurring in a setting of immunodeficiency, whether therapeutically induced or acquired, have received special attention, and the possible role of the Epstein-Barr virus in their pathogenesis has induced pathologists to develop exciting in situ molecular hybridization techniques for its identification in tissues. The certainties underlying the diagnosis and classification of Hodgkin's disease (in which Epstein-Barr virus also appears to play a role), formally the only truly secure area for pathologists, have been disturbed, and the borderline between Hodgkin's disease and non-Hodgkin's lymphoma is now seriously blurred. The lymphoma pot has been well and truly stirred; we must now wait to see what the new sediment offers.
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PMID:Pathology of malignant lymphomas. 145 95

A high frequency of lymphoma in human immunodeficiency virus-infected individuals has been reported since the outbreak of the acquired immunodeficiency syndrome (AIDS) epidemic in 1982. In the vast majority of cases, these lymphomas are highly aggressive B-cell, non-Hodgkin's lymphoma of intermediate or high grade of malignancy. AIDS-associated non-Hodgkin's lymphoma are histologically classified as small noncleaved cell lymphoma, large cell immunoblastic plasmacytoid lymphoma, or large noncleaved cell lymphoma. Host factors predisposing to lymphoma development in AIDS patients include decreased immunosurveillance as well as human immunodeficiency virus-induced chronic perturbation of the immune system leading to cytokine overproduction and increased B-cell stimulation. These alterations are associated with the development of multiple oligoclonal B-cell expansions, which are characterized by persistent generalized lymphadenopathy. The presence of Epstein-Barr virus within a persistent generalized lymphadenopathy clone further increases the risk of its neoplastic transformation. The appearance of non-Hodgkin's lymphoma is characterized by the presence of a monoclonal B-cell population displaying several genetic lesions, including monoclonal Epstein-Barr virus infection, c-myc rearrangements, Ras mutations, and p53 inactivation. The number and type of lesions varies among the different types of AIDS-non-Hodgkin's lymphoma, defining multiple alternative molecular pathways in AIDS-associated lymphomagenesis.
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PMID:Biologic aspects of human immunodeficiency virus-related lymphoma. 145 5

The association of malignancies, such as non-Hodgkin's lymphoma and Kaposi's sarcoma, with human immunodeficiency virus infection has been recognized since the beginning of the epidemic. However, an increasing number of tumors not diagnostic of acquired immunodeficiency syndrome has been described in this setting. Taking into consideration that survival of patients with human immunodeficiency virus infection is increasing because of improvement of supportive care and better control of human immunodeficiency virus and related opportunistic infections, oncogenic viruses such as human papillomavirus, hepatitis B virus, Epstein-Barr virus, in a setting of prolonged immunosuppression could increase the risk of a variety of malignant tumors.
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PMID:Human immunodeficiency virus as a risk factor in miscellaneous cancers. 145 6

Low levels of anti-viral antibodies may facilitate virus infection of Fc-receptor bearing cells. For human immunodeficiency virus (HIV) it has been reported that antibodies can enhance infection of phagocytic cells. We show that HIV-1 can infect an Epstein-Barr virus transformed B cell line and that low levels of anti-HIV antibodies enhance infection. The enhanced infection was characterized by an increase in viral DNA and increased HIV p24 protein production. Detection of cell surface antigen expression of CD4, the receptor for HIV, Fc-receptor type II for IgG, but not of type I and III could be demonstrated by immunofluorescence cytometry. The enhancement was abrogated when infection was performed in presence of a monoclonal antibody directed against CD4. Based on these results we conclude that antibody mediated enhancement of HIV-1 infection can also occur in non-phagocytic cells in a CD4 dependent manner and that IgG Fc-receptors other than types I or III are involved in this process.
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PMID:Antibody mediated enhancement of HIV-1 infection of an EBV transformed B cell line is CD4 dependent. 145 71

Oral hairy leukoplakia occurs mainly on the tongue of human immunodeficiency virus (HIV)-infected persons. An HIV-infected patient with hairy leukoplakia involving the tongue and buccal mucosa was studied by light and electron microscopic methods, in situ hybridization, and polymerase chain reaction. Our findings indicate that hairy leukoplakia may involve the buccal mucosa and should be considered in the differential diagnosis of white oral lesions in HIV-positive patients. Epstein-Barr virus particles were found in the epithelial cells of both buccal and tongue mucosa.
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PMID:Hairy leukoplakia with involvement of the buccal mucosa. 146 45

In 4.4% of human immunodeficiency virus-associated non-Hodgkin's lymphoma the presenting lesion is seen in the mouth. Often the lesion may clinically resemble a less sinister process, and a definitive diagnosis of lymphoma may be delayed. We describe three unusual cases of non-Hodgkin's lymphoma, appearing intraorally in association with other oral lesions, in HIV-positive homosexual men. The three patients reported here were all diagnosed as having diffuse, large-cell malignant non-Hodgkin's lymphoma. We performed Epstein-Barr virus DNA in-situ hybridization on our cases and Epstein-Barr virus DNA sequences were not seen. We review the pertinent literature and stress the importance of including non-Hodgkin's lymphoma in the differential diagnosis of oral lesions in patients at risk of HIV infection.
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PMID:Unusual oral presentation of non-Hodgkin's lymphoma in association with HIV infection. 151 49


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