Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021345 (infectious mononucleosis)
3,358 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epstein-Barr virus (EBV) has long been implicated in nasopharyngeal carcinoma (NPC). Recent studies in our and other laboratories have shown a correlation between the disease and high antibody titers to EBV-specific DNase. These data led us to also examine serial sera from healthy adults and patients with infectious mononucleosis or NPC, for their capacity to neutralize the EBV-specific thymidine kinase (TK) activity from chemically induced EBV-carrying human lymphoblastoid cells. Our results were the following: (i) sera were found that efficiently blocked the EBV-specific TK activity of induced-Raji TK- cell extracts, but not the host-cell TK activity from EBV-negative BJAB cells; (ii) a relationship appeared between high levels of EBV-specific TK-neutralizing activity in sera and NPC pathology, even though in this preliminary study the degrees of EBV-induced TK-blocking activity detected in sera were not significantly correlated with EBV-specific antibody titers; (iii) the EBV-induced TK-neutralizing activity was found in the main IgG fraction derived from NPC sera. These data must be compared with other known antibody responses to EBV for their clinical interest in NPC control.
Int J Cancer 1989 Jan 15
PMID:Relationship between nasopharyngeal carcinoma and high antibody titers to Epstein-Barr virus-specific thymidine kinase. 253 7

This report describes the first of 2 investigations studying mechanisms of Epstein-Barr virus (EBV) persistence in the infected host; specifically, we wish to determine the extent to which virus carriage within the B-cell system is dependent upon continued replication of the virus in permissive oropharyngeal epithelium. Levels of EBV infection at these 2 sites have been monitored in 21 acute infectious mononucleosis (IM) patients before, during and after treatment with high doses of acyclovir (ACV). Twelve patients received oral ACV for 10 days and 9 patients received i.v. ACV for 5 days before the 10-day oral course; all were followed prospectively for 28 days. Infectious EBV, detectable at high initial levels in the patients' throat washings, disappeared almost completely during ACV treatment, then returned again to high levels post treatment. In contrast, levels of virus-infected B cells in the blood showed no reduction linked to the period of ACV treatment nor any increase with resumption of EBV shedding. During IM, therefore, maintenance of high levels of virus carriage within the B-cell pool is not dependent upon the continual recruitment of newly infected B cells. This might reflect an inability of the immune T-cell response in acute IM patients to prevent continued expansion of the existing EBV-infected B-cell pool. Alternatively, it raises the possibility that EBV carriage in B cells in vivo is maintained through a virus:cell interaction which is not sensitive to virus-specific T-cell surveillance.
Int J Cancer 1989 Jan 15
PMID:The Epstein-Barr virus:host balance in acute infectious mononucleosis patients receiving acyclovir anti-viral therapy. 253 8

Varicella-zoster virus (VZV) and Epstein-Barr virus (EBV) are two of the human herpesviruses. The others include herpes simplex virus (HSV) type 1, HSV type 2, and cytomegalovirus (CMV). In a series of two articles, we review the clinical diseases caused by VZV and EBV infections; we pay particular attention to the manifestations of these two viral infections in immunosuppressed and immunocompromised patients. In addition to the clinical reviews, each of the two articles begins with a brief discussion of the molecular aspects of VZV and EBV, respectively; this introduction describes features of the genome and immunogenic viral proteins which have clinical relevance. A model for pathogenesis is included. The first review concerns VZV infections. Recent data about the DNA sequence of the entire VZV genome are included, as well as a review of the VZV glycoproteins. Primary VZV infection (chickenpox) and VZV reactivation (zoster) are described in detail in both healthy individuals and people with cancer. The decade-long VZV vaccine trials in children with leukemia receive special emphasis because they have engendered considerable interest and debate. The second review (published here) covers EBV infections. This virus has been implicated in the causation of a wide variety of human hematological and oncological disorders, besides classical infectious mononucleosis. In particular, Burkitt's lymphoma, nasopharyngeal carcinoma, and lymphoproliferative disorders are strongly associated with EBV infection of the transformed cells. In addition, immunologically mediated cytopenias occasionally follow EBV infection. Finally, treatment regimens with antiviral chemotherapy and other agents are discussed for both VZV and EBV infections.
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PMID:Epstein-Barr virus: the hematologic and oncologic consequences of virus-host interaction. 254 65

Serum thymidine kinase (TK), measured using Prolifigen TK-REA, from AB Sangtec Medical, was investigated in 24 HIV seropositive patients without immunological alterations, 26 seropositives with immunological alterations, 125 LAS, 25 ARC, and 20 AIDS. Subjects with serological markers of prior EBV, HBV, and CMV infection were included but none with acute infectious mononucleosis or acute viral hepatitis. Serum TK was elevated from the beginning of the HIV infection, the seropositive stage, and more markedly afterwards during the course of the infection, with a close correlation with the stage. TK also increased during AZT treatment, due to bone-marrow toxicity. On lowering the dosage or discontinuing the drug TK returned to basal levels. Although the rise in serum may well not be correlated only with the HIV infection, it does add to the picture given by other clinical and/or laboratory methods. Serum TK can be a helpful laboratory test in the follow-up of patients with HIV infection, especially when serum levels are disproportionate to the stage, opportunistic infections, lymphoproliferative malignancies. In such cases bone-marrow toxicity due to treatment can be suspected.
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PMID:Serum thymidine kinase (TK) evaluation in HIV infection. 274 46

Epstein-Barr virus (EBV) is a ubiquitous transforming virus of the herpes group showing tropism for B lymphocytes. Primary infection in normal hosts results in a transient lymphoproliferative disorder, acute infectious mononucleosis (IM), that is restricted by cytotoxic and suppressive lymphocytes. However, in the immunodeficient host, EBV-induced lymphoproliferation may behave in a biologically malignant fashion. Patients with primary immunodeficiencies and those with immune incompetence resulting from suppressive therapy in allograft transplantation or infection with human immunodeficiency virus (HIV) have EBV-related illness ranging from fulminant mononucleosis and invasive polyclonal B cell hyperplasia to monoclonal B cell malignancies. While the direct link between EBV and malignant B cell proliferation in these patients has not been elucidated, the association has been increasingly recognized with improved techniques of viral detection. Clinical management can be guided by the location and extent of tumor, histologic features, and clonality. Regional and node-based polyclonal proliferations may respond to prompt reduction of immunosuppressive therapy and efforts to interrupt the replicative cycle with antiviral agents. Systemic cytotoxic therapy often leads to further immunosuppression and should be reserved for patients with progressive disease, advanced visceral involvement, and monoclonal lymphoid malignancies.
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PMID:Lymphoproliferative diseases in immunocompromised hosts: the role of Epstein-Barr virus. 282 Nov 99

Epstein-Barr virus (EBV) persists for life in a person who has been infected. Investigators are uncertain what this means to the host, particularly an immunocompromised one. EBV is the most common cause of infectious mononucleosis, but the diagnosis must be based on clinical, hematologic, and serologic criteria because other agents are the cause in about 10% of cases. EBV is the first virus to be associated with a neoplasm--Burkitt's lymphoma. This childhood malignancy is relatively common in central Africa, and EBV is a cofactor in its development, although direct evidence for a causal relationship has not been found. In southern China, nasopharyngeal carcinoma is an important health problem in adults in areas where the infection rate of EBV in childhood is high. Rare cases of primary EBV infection that evolved into uncontrolled lymphoproliferative disease have also been reported. EBV's relationship to these diverse diseases, its varying effects on certain individuals and in certain geographic locations, and the testing of a vaccine against the virus are areas of ongoing study.
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PMID:The many faces of Epstein-Barr virus. 282 48

Infection with the Epstein-Barr virus (EBV), a ubiquitous herpesvirus, may be asymptomatic or may result in any one of a number of mild to severe hematopoietic disorders. Besides causing infectious mononucleosis, EBV has been associated with 95% of endemic African Burkitt's lymphoma and 10%-20% of the sporadic form of Burkitt's lymphoma outside Africa. EBV has also now been associated with all histological forms of nasopharyngeal carcinoma. During the acute phase of infectious mononucleosis, a surprisingly large number of EBV-infected cells can be detected in the peripheral circulation (up to 0.05%). EBV also replicates in epithelial cells in the oropharyngeal region. It is known that physicochemical carcinogens can act synergistically with tumor viruses to enhance both viral replication and cellular transformation. Several laboratories have shown that chemical carcinogens and, in particular, DNA-alkylating agents can enhance EBV replication, EBV-induced lymphocyte transformation, and EBV-associated malignant conversion. Since there are approximately 10(12) lymphocytes in an adult, the large number of EBV-infected cells present in the circulation and oropharynx during infection would present an extraordinarily large target for carcinogen interaction. Moreover, after infection, EBV remains latent in lymphoid cells for life. When these findings are considered in light of analytical and descriptive epidemiological evidence suggesting that, in addition to EBV infection, other environmental cofactors are important in EBV-associated tumor formation, the question could be asked whether these cofactors are physicochemical carcinogens. In an attempt to answer this question, I will review the ways in which physicochemical carcinogens can influence viral replication and virally induced transformation; aspects of the biology of the EBV-lymphocyte-epithelial cell interaction that make this system perhaps unique in terms of possible physicochemical interactions; the epidemiological and experimental evidence supporting EBV-physicochemical carcinogen synergisms; and finally, possible mechanisms whereby chemicals could influence the outcome of EBV infection and the probability of these events occurring during naturally acquired EBV infection.
J Natl Cancer Inst 1988 Jun 01
PMID:Physicochemical-viral synergism during Epstein-Barr virus infection: a review. 283 90

A strong association exists between Epstein-Barr (EB) virus and two human cancers, endemic Burkitt's lymphoma and nasopharyngeal carcinoma. In addition, the virus causes infectious mononucleosis [reviewed in Epstein and Achong, 1979, 1986] and more recently has been implicated in lymphomas arising in immunosuppressed individuals [Cleary et al., 1986]. The possibility of preventing or influencing the course of these diseases by vaccination has been advocated for a number of years [Epstein, 1976], especially in the case of undifferentiated nasopharyngeal carcinoma, which is the most common tumour of men in southern China and is prevalent in other specific regions; it therefore represents a major world cancer problem [Shanmugaratnam, 1971]. Two vaccinia virus strains were employed to make recombinants expressing the gene coding for the EB virus envelope glycoprotein, gp340, and were used to vaccinate cottontop tamarins. Protection against EB-virus-induced lymphoma was obtained in animals immunized with the laboratory (WR) strain recombinant but not with those recombinants derived from the vaccine (Wyeth) strain. Circulating antibodies to EB virus gp340 were not detected in any of the immunized animals.
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PMID:Recombinant vaccinia virus expressing Epstein-Barr virus glycoprotein gp340 protects cottontop tamarins against EB virus-induced malignant lymphomas. 283 12

We have previously shown that antigen-specific T-suppressor (Ts) cells can be generated in vitro by antigens of Epstein-Barr virus (EBV). However, patients with EBV-associated disorders and particularly those with EBV-induced infectious mononucleosis characteristically have nonspecific Ts cells in their peripheral circulation. To explore this apparent paradox, we have now examined the interaction of EBV antigens with either an unrelated antigen (tuberculo-protein-PPD) or a T-cell mitogen (phytohemagglutinin-PHA) in the in vitro generation of Ts cells. Our findings are: (1) the presence of unrelated antigens results in the generation of nonspecific Ts cells in a system wherein an EBV antigen (in excess) alone otherwise induces only antigen-specific Ts cells; (2) the unrelated antigen may be present in a wide range of concentrations and (3) can contribute to nonspecific Ts cell generation when added as long as 2 days after initiation of induction by EBV antigen; (4) the unrelated antigen must be recognized by the sensitized lymphocytes in order for nonspecific Ts cells to be induced; and most interestingly (5) when a second, immunologically different, EBV antigen is substituted for the unrelated antigen (PPD), again nonspecific Ts cells are induced in this system. We propose that the presence of unrelated (or multiple) antigens, in addition to the antigen-specific Ts cell-inducing antigen, contributes to the generation of nonspecific Ts cells in vivo, and that this phenomenon may be important in infections, malignancies, and immunodeficiency states.
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PMID:Epstein-Barr virus immunosuppression: II. Generation of nonspecific suppressor T lymphocytes in vitro. 285 75

An elderly woman is described with infectious mononucleosis in whom cervical node biopsy was interpreted as showing immunoblastic lymphoma. Concomitant reactive lymphocytosis, Epstein-Barr virus serologic results consistent with an acute infection, and demonstration of polyclonal B cell infiltration of other tissues argued against intervention. Defective in vitro T cell responses were demonstrated during the acute phase of Epstein-Barr virus infection. Infectious mononucleosis has rarely been reported as mimicking a non-Hodgkin's lymphoma. At 18 months, our patient's course has been typical for infectious mononucleosis with no evidence of disseminated malignancy.
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PMID:Infectious mononucleosis mimicking a B cell immunoblastic lymphoma associated with an abnormality in regulatory T cells. 285 6


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