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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nearly all epidemiological characteristics of Burkitt's lymphoma (BL) can be explained on the basis of relationships of BL to the intensity of the host response to Plasmodium falciparum. The major epidemiological associations are: the high degree of geographic correlation between the incidence rate of BL and the intensity of P. falciparum transmission, both at a global level and within individual countries; the close correlation between the age incidence of BL and the age of acquiring maximum levels of antimalarial immunoglobulin; the relative protection from BL by residence in urban areas, where levels of malaria transmission are lower, compared with rural areas; the decline in BL incidence in areas where death rates due to malaria have declined and, within such areas, a differential decline in BL incidence in people making better use of health facilities; the older age of onset in patients who have migrated from low-intensity to high-intensity malaria areas as compared with patients born in the high-intensity areas - the higher absolute age-specific incidence rate in those above age ten in this immigrant group being consistent with the hypothesis that intense malaria infection and consequent host defence response serve as the major triggering event in the pathogenesis of the lymphoma; the inverse geographic correlation between the average age of onset of BL and the intensity of falciparum malaria infection. An inverse association of BL with sickle-cell trait (AS haemoglobin) would provide strong evidence for the role of intense falciparum malaria, but most studies to date have not achieved statistical significance. Time-space clustering and reports of seasonal variation in BL incidence would indicate that a precipitating factor operates over a relatively short time-span, at least in some areas. Combining the evidence concerning cytogenetics, Epstein-Barr virus (EBV) and falciparum malaria, the following three-phase model for the oncogenesis of BL could account for virtually all the currently known facts and be tested by further laboratory and field studies: Primary infection with EBV, perhaps early and intense, leads to the immortalization of large numbers of B lymphocytes. Severe falciparum malaria then leads to an intense host response with particular proliferation of the EBV-infected B lymphocytes. Finally, the great increase in the B lymphocytes provides a much higher statistical opportunity for the emergence of the cytogenetically abnormal BL cell.
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PMID:Epidemiological evidence for the role of falciparum malaria in the pathogenesis of Burkitt's lymphoma. 390 88

Peripheral blood lymphocytes from 20 individuals living in a malaria endemic area (Burkina Faso) were transformed with Epstein-Barr virus. No antigen specific selection, nor stimulation of B-cells were performed prior to transformation. 20 cell lines were established, 14 secreted polyclonal antibodies directed against erythrocytic stages of Plasmodium falciparum. 4 lines were cloned and the supernatant analysed and characterised against Plasmodium falciparum antigens.
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PMID:[Production of human monoclonal antibodies against various antigens of erythrocyte stages of Plasmodium falciparum]. 393 77

Epstein-Barr virus (EBV), although not an indispensable factor for the development of Burkitt lymphoma, is apparently associated with the 20-fold higher incidence of the disease in Equatorial Africa compared to the incidence in other parts of the world. To determine whether different EBV subtypes are associated with the appearance of the malignant phenotype, we have compared the EBV genomes carried in the Burkitt tumor cells with those carried in the nonmalignant lymphoblastoid cells from the same individuals. From three patients with EBV -associated Burkitt lymphoma, tumor cell lines as well as spontaneously established lymphoblastoid cell lines representing the nonmalignant counterparts were obtained. The viral DNA in these cell lines was analyzed by Southern blot hybridization, using a set of cloned EBV DNA fragments as probes that recognize polymorphic regions in the viral genome. Using a number of different polymorphic markers to distinguish one isolate from another, the virus genome found in the tumor cells could also be identified in the nonmalignant cells of the same patient. In one case, in which two independent lymphoblastoid cell lines were established, evidence was obtained that this patient was infected by at least two distinct EBV subtypes. These results strongly suggest that in Burkitt lymphoma, the risk associated with EBV is related to cofactors such as chronic malaria and the mode of infection rather than to peculiar viral subtypes. The situation seems to be totally different from papillomavirus-associated diseases, in which the risk of progression to malignancy appears to be associated with particular viral strains.
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PMID:No evidence for differences in the Epstein-Barr virus genome carried in Burkitt lymphoma cells and nonmalignant lymphoblastoid cells from the same patients. 608 53

Endemic Burkitt's lymphoma, a tumour of children in which B lymphocytes are infected with Epstein-Barr virus (EBV), is common in areas of Africa where malaria is holoendemic. The tumour is characterized by chromosome translocations; usually the terminal portion of chromosome 8 containing the c-myc gene is translocated to chromosome 14, near the enhancer of the immunoglobulin heavy-chain locus. Less frequent are translocations of chromosome 8 to the kappa light-chain locus of chromosome 2 or to the lambda light-chain locus of chromosome 22. In vitro, EBV induces B cells to proliferate and secrete immunoglobulin and antibody. However, in vivo the infected B lymphocytes are under immunological control, so that abnormal proliferation is found only in immunosuppressed patients. Such patients are subsequently liable to develop lymphomas. Burkitt believed that the tumour he had described resulted from interaction between a virus(es) and a "reticuloendothelial system altered by chronic and heavy infection by malarial or other parasites". We report here that during an attack of Plasmodium falciparum malaria, T-cell subpopulations are radically altered so that, in vitro, B lymphocytes infected with EBV proliferate abnormally to secrete large amounts of immunoglobulin and antibody. This phenomenon offers some explanation for the increased incidence of Burkitt's tumour and the high levels of immunoglobulin found in people living in areas where P. falciparum malaria is common.
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PMID:T-cell control of Epstein-Barr virus-infected B cells is lost during P. falciparum malaria. 609 4

There is a considerable volume of evidence linking Epstein-Barr virus (EBV) etiologically with Burkitt's lymphoma (BL). BL has satisfied the Henle-Koch criteria. Thus BL patients have significantly higher EBV antibody titres than normal or tumour controls. EBV DNA and EBV-determined nuclear antigen (EBNA) have been demonstrated in a high proportion (greater than 90%) of endemic BL tissues. EBV can transform and immortalize human B-lymphocytes and is known to cause lymphoreticular tumours in New World monkeys. The fact that endemic BL is almost invariably associated with EBV while this is rarely true of the non-endemic form suggests disease heterogeneity in spite of morphological uniformity. The role of malaria as a co-factor in causing immunosuppression and promoting proliferation of EBV-transformed cell is discussed. The identification of specific chromosomal abnormalities in both endemic and non-endemic BL underscores the importance of a suitable genetic background.
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PMID:Etiology of endemic Burkitt's lymphoma. 610 Feb 85

The relationship between viruses and naturally occurring cancers, such as hepatocellular carcinoma and genital cancers, is of great importance to Africa. On the other hand, lymphomas, leukaemias and immunodeficiencies, although of less immediate public health importance, constitute an area of outstanding interest for research and their association with the Epstein-Barr virus (EBV) and the newly discovered human retroviruses merits world-wide attention. EBV-related malignancies in Africa include both Burkitt's lymphoma (BL) and nasopharyngeal carcinoma (NPC). Whether X-linked polyclonal lymphoproliferations exist in Africa remains an open question. The interrelationship between EBV, holoendemic malaria and genetic factors (oncogenes) has been deciphered in recent years, to make BL a kind of Rosetta stone for the understanding of multistage carcinogenesis. Although the role of EBV in the causation of NPC is not well understood, the viral capsid antigen (VCA) IgA test already allows both early detection of NPC in high-incidence areas and differential diagnosis in low-incidence areas. The question whether an EBV vaccine would be of value in African countries, in relation to EBV-associated malignancies, remains an open one. The diseases associated with the recently discovered human retroviruses (human T-lymphocyte leukaemia viruses: HTLVs) represent a new area for both research and public health assessment. Limited information is available today on the geographical distribution, age prevalence and association with disease in Africa of the different members of the retrovirus family (HTLV-1, HTLV-2, LAV/HTLV-3). The proportion of HTLV-related T-cell malignancies in different parts of Africa as well as the importance of immunodeficiencies caused by the different members of the retrovirus family remain to be determined. Typical acquired immunodeficiency syndrome (AIDS) appears to exist in Central Africa, especially Zaire, and HTLVs could be of public health importance if they cause severe forms of viral, bacterial or parasitic diseases through impairment of cell-mediated immunity. Africa, is and will long remain a continent of crucial importance with regard to the role of viruses in human malignancies and especially in haematopoietic proliferative disorders.
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PMID:Virus-associated lymphomas, leukaemias and immunodeficiencies in Africa. 610 Feb 86

Both Epstein-Barr virus and malaria have been implicated as possible factors in Burkitt's lymphoma. To examine this implication a cross-sectional serological survey of an urban and a rural population in Ghana was conducted. Malaria was more prevalent in the rural areas, but there was no difference in antiviral capsid antigen (VCA) antibody titres between urban and rural dwellers. There was also no correlation between anti-malaria antibody titres and anti-VCA antibody titres. Thus malaria does not seem to influence immunological response to Epstein-Barr virus infection, as measured by anti-VCA antibodies. These results suggest that if Epstein-Barr virus infection and malaria are important in the aetiology of Burkitt's lymphoma, they produce their effects independently. The survey also showed that those in rural areas seroconverted earlier than those in urban areas, and that antibody levels were consistently higher in females than in males in every age-group. Case-control studies and screening programmes involving anti-VCA levels will therefore have to take these two findings into account.
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PMID:Malaria, sex, and place of residence as factors in antibody response to Epstein-Barr virus in Ghana, West Africa. 611 82

Clinical and epidemiologic features of Burkitt's lymphoma are reviewed. Epidemiologic studies suggest that simultaneous infection with Epstein-Barr (E-B) virus and malaria may be involved as etiologic agents. On the other hand we have found that in the Amazon region of Brazil and Peru both malaria and E-B virus infection is common among children, yet Burkitt's lymphoma is rare. The possibility exists that other concomitant etiologic agents and genetic factors are also involved. Several investigators suggested the possible involvement of Reo 3 virus. We have found antibodies against Yaba virus. A laboratory worker who accidentally inoculated himself with Yaba virus developed a histiocytoma which when inoculated into Asiatic monkeys produced typical Yaba tumors. This was the first case that Koch's postulates were fulfilled in a virus induced neoplasm in man. Therapeutically, the best clinical results were obtained in those patients who were treated with small doses of cyclophosphamide. On the basis of somewhat inadequate follow-up studies, it is estimated that "five year cures" were obtained in about 10% of the patients.
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PMID:Burkitt's lymphoma. 627 88

Epstein-Barr virus genome-positive Burkitt's lymphoma is endemic in Africa and Papua New Guinea and in both countries the tumour is restricted to regions with holoendemic malaria. The present work has compared groups of healthy indigenous individuals living in malarious and non-malarious regions of Papua New Guinea for Epstein-Barr virus-specific T-cell-mediated immunity using the in vitro regression assay. Residents of the malarious region (55 tested), when compared with either residents of the non-malarious area (35 tested) or Caucasian controls (27 tested) showed a significant (p less than 0.0001) impairment of virus-specific T-cell immunity but no obvious disturbance (p greater than 0.05) of anti-viral antibody titres. These results may be important in explaining the postulated role of malarial infection as a co-factor in the pathogenesis of Burkitt's lymphoma.
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PMID:A comparison of Epstein-Barr virus-specific T-cell immunity in malaria-endemic and -nonendemic regions of Papua New Guinea. 630 50

Different aetiological factors of Burkitt's disease, or Burkitt's lymphoma (BL) are considered in an analytical, then synthetical point of view, according to present admitted facts. Epidemiologic data are recalled in order to assign a place to the disease. Relations with Epstein-Barr virus (E.B.V.) are well-known by comparative pathology (connections between animal tumors and herpetic virus), virologic and serologic studies; the role of E.B.V. is based on the presence of viral genomas and nuclear antigens in tumoral cells of B.L.; there are B.L. without E.B.V., but constantly improved study of anti-E.B.V. antibodies, and viral markers, will may be decrease their number. Connections with malaria caused by Plasmodium falciparum are recognized. Discovery of chromosomal aberrations is a new important stage. At the present time, it is generally guessed that: a) the initiation of malignant process might be induced by E.B.V. b) an external agent might cause the promotion of cellular division. c) chromosomal abnormality might be responsible for the malignant transformation.
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PMID:[Etiological factors in Burkitt's disease]. 631 Mar 11


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