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

In a controlled study in Ghana, the hemoglobin electrophoretic pattern in 112 patients with Burkitt's lymphoma was compared to that of their nearest neighbor controls of the same age, sex, and tribe, as well as their sibling controls. Analysis of the data obtained did not show any statistically significant protective advantage for sickle cell trait against Burkitt's lymphoma. Hemoglobin C trait appeared to offer a slight protective advantage (p less than 0.1), but this did not reach statistical significance. These results do not disprove the malaria co-factor hypothesis in the etiology of 0urkitt's lymphoma, but deprive it of an additional indirect evidence in its favor.
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PMID:Sickle cell trait, hemoglobin C trait, and Burkitt's lymphoma. 96 85

A hypothesis which explains disease prevalence among different socio-economic groups following early infantile modulation of cell-mediated immunity by infection and nutrition related stress is presented. Wealthy populations living under highly hygienic circumstances can develop their cell-mediated immunity to genetic expectation while their humoral systems remains unstimulated. Primitive populations protect the infant's immune development by breast feeding and suffer from temporary cell-mediated immune deficiencies due to intercurrent infectious disease and famine later on. Intermediary populations harbour a small percentage of people, whose cell-mediated immune system has been permanently damaged by infection in early childhood, leading to a high incidence of diseases linked to cell-mediated immune deficiency. The possible cocarcinogenesis of the cell-mediated immune deficiency following repeated gastroenteritis and persistent stimulation of B cells, leading to alpha heavy chain disease and primary intestinal lymphoma, or due to falciparum malaria in newborns and its impact on the EB virus genome in development of Burkitt's lymphoma, are discussed.
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PMID:Immune modulation and disease patterns in population groups. 122 70

The epidemiology of Epstein-Barr virus (EBV) infection in populations at different risk for EBV-associated diseases indicates significant differences between the populations. EBV infection takes place much earlier in Uganda, where all children are infected before the age of 2 to 3 years, than in Southeast Asia, where nasopharyngeal carcinoma is prevalent. It is proposed that such early infection in Equatorial Africa is related to the risk for Burkitt's lymphoma. Four possible interventions to control EBV-associated diseases are presented: (a) simple hygienic measures to delay natural primary infection by EBV; (b) EBV vaccine; (c) intervention against cofactors such as malaria in Burkitt's lymphoma; and (d) characterization of high-risk groups to allow early detection and successful treatment.
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PMID:Epstein-Barr virus behavior in different populations and implications for control of Epstein-Barr virus-associated tumors. 125 56

An epidemiologic study of 123 patients residing in the Mengo Districts of Uganda, with onset of symptoms of diagnosed Burkitt's lymphoma (BL) in the period 1959-68, revealed a substantial decline in incidence of BL during that decade. Other significant findings included differences by ethnic group in age of patient at onset of BL, a change in the proportions of patients by ethnic group over the decade, a lower incidence rate of BL in the countries of higher altitude, and a seasonal pattern of onset. There was no evidence of the time space clustering previously reported for BL in Uganda. The changing pattern of BL in the Mengo Districts was consistent with the hypothesis that severe malaria infection not only is important in the development of BL but also precipitates onset.
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PMID:Burkitt's lymphoma in the Mengo Districts of Uganda: epidemiologic features and their relationship to malaria. 125 80

PCR was used to screen EBV-positive lymphomas from endemic and sporadic Burkitt's lymphoma patients, including EBV-positive lymphomas derived from patients with HIV infection. Only 10% of sporadic lymphomas from either North America (1/15) or South America (2/14) were associated with the type 2 EBV strain, whereas 50% (8/16) of lymphomas from equatorial Africa and 46% (10/22) of HIV-associated lymphomas were positive for the type 2 strain. These data, in conjunction with previous reports, suggest that the proportions of strain types in Burkitt's lymphoma reflect the proportions of strain types in peripheral lymphocytes, and not simply the prevailing regional strain. The increased association of the type 2 strain in lymphocytes and lymphomas from HIV-infected individuals and from Africa may be a result of intermittent (malaria) or continuous (HIU) compromise of immune function in these populations.
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PMID:Epstein-Barr virus genotypes in AIDS-associated lymphomas are similar to those in endemic Burkitt's lymphomas. 132 81

Recent investigations indicate that Burkitt's lymphoma consists of several subtypes, defined by their clinical and molecular features. Each geographical region so far studied appears to consist of a different mixture of subtypes. Interestingly, there appear to be geographic 'gradients' with respect to the fraction of tumors associated with EBV and the type of 8;14 chromosomal translocation. The rate of EBV association is highest in Equatorial Africa, lowest in North America and intermediate in South America. The fraction of tumors with breakpoints far upstream of the c-myc gene follows a similar pattern. These findings strongly suggest that the subtypes of Burkitt's lymphoma are environmentally determined, and we propose that the pattern of infection (e.g. malaria) to which the young child is exposed influences the tumor subtype distribution by altering the relative and absolute numbers of various B cell precursors at sites of B cell ontogeny (the bone marrow, and possibly mesentery). These B cell precursors are the cells which are susceptible to the specific chromosomal translocations associated with Burkitt's lymphoma. We further propose that immunoglobulin enhancers (recognized and unrecognized) both influence the likelihood of the translocation occurring, and in at least a fraction of cases, contribute to the deregulation of a c-myc. EBV, via EBNA-1, the only invariably expressed latent-gene in Burkitt's lymphoma, probably influences c-myc expression in Burkitt's lymphoma by increasing immunoglobulin enhancer function. Thus, in effect, EBV collaborates with the translocations associated with Burkitt's lymphoma in causing c-myc deregulation. This collaboration is independent of the breakpoint location. While other molecular abnormalities must be able to contribute to myc deregulation in the same way, EBV association in Burkitt's lymphoma is probably determined by the age at which EBV infection occurs (being more likely when infection occurs in very young children) and perhaps also by other infectious diseases that numerically influence the fraction, and predominant stage of differentiation (and hence translocation breakpoint sites) of immature B cells infected by EBV. The presence of EBV in many such cells greatly increases the incidence rate of Burkitt's lymphoma, since one of the genetic lesions needed to deregulate c-myc is already present.
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PMID:Epstein-Barr virus and Burkitt's lymphoma. 133 92

The function of c-myc in physiology is only partially known. Its product has DNA binding properties and plays a role in the control of proliferation and differentiation. In general, increased c-myc expression leads to proliferation and abolishment of differentiation. The involvement of c-myc in mouse plasmacytomas and human Burkitt's lymphoma is well known: due to chromosomal translocation c-myc comes under the influence of regulatory elements of immunoglobulin genes, leading to increased expression of the gene and proliferation of the cells. In man, the chromosomal translocations may occur within the increased pool of (pre) B-cells due to Epstein Barr virus (EBV) and malaria infection with subsequent immunosuppression. Apart from these early (primary?) events in lymphomagenesis, c-myc is also often involved in tumour progression, probably by a similar mechanism. Different types of c-myc involvement are associated with specific types of lymphoma: there are differences between endemic, sporadic and ileocecal Burkitt's lymphoma as well as between those and primary extranodal large cell lymphoma and large cell lymphoma which has progressed. These differences are associated with the differentiation of the involved lymphoid cells and may point to the stage of differentiation in which the oncogenic event occurred.
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PMID:The association of c-myc rearrangements with specific types of human non-Hodgkin's lymphomas. 149 39

Burkitt's lymphoma (BL) is a highly malignant B cell tumor characterized by three types of chromosomal translocation which constitutively activate the c-myc oncogene by juxtaposing it to Ig coding sequences. Epstein-Barr virus (EBV) infection, hyperendemic malaria and HIV-caused immunosuppression are thought to contribute to the pathogenesis of the tumor. Cell lines derived from EBV carrying and EBV negative BLs often show altered MHC class I antigen expression. The defects include a lower expression of all HLA class I antigens compared to EBV transformed normal B-blasts, and selective down-regulation of certain HLA-A and HLA-C alleles. As a consequence BL cells are often resistant to cytotoxic T lymphocyte (CTL) mediated destruction. Alleles selective down-regulations are found only in cell lines that maintain the tumor cell phenotype while shift towards a more activated 'B-blast like' phenotype is accompanied by HLA class I up-regulation. A similar pattern of HLA class I expression can be found in a subpopulation of germinal center B cells which express a 'BL like' phenotype. Our findings suggest that the HLA class I expression of BL cells reflects the characteristics of the normal B cell precursor and is probably not the result of immune selection.
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PMID:Cell phenotype dependent expression of MHC class I antigens in Burkitt's lymphoma cell lines. 165 15

Epstein-Barr virus (EBV) infection and Plasmodium falciparum malaria are two known cofactors in the aetiology of endemic Burkitt's lymphoma. To assess the relation between these factors, limiting dilution analysis was used to assess the number of EBV-carrying B cells in the circulation of Gambian children during and after acute malaria. Numbers of virus-carrying cells were five times higher in acute malaria patients and in UK patients with infectious mononucleosis than in convalescent malaria patients and in healthy control adults from the UK. Spontaneous outgrowth in limiting dilution cultures from acute malaria samples was inhibited by acyclovir, a viral DNA polymerase inhibitor. The mechanism of outgrowth, therefore, was virus release from the in-vivo infected cell, which led to infection and immortalisation of co-cultured normal B cells. The findings provide evidence that acute malaria is associated with an increase in the number of EBV-carrying B cells in the circulation. Because of this increase, there is a greater chance of a cytogenetic abnormality occurring in such a cell, with consequent evolution of Burkitt's lymphoma.
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PMID:Circulating Epstein-Barr virus-carrying B cells in acute malaria. 167 68

Eighteen tissue samples from lymphoproliferative lesions and lymphomas in immunodeficiency states were investigated for their content of Epstein-Barr virus (EBV) genome by dot blotting and for the distribution of EBV in tissue sections by in situ hybridization. Fourteen lymphomas from AIDS patients and four children with disorders of the immune system were available. For control reasons, six cases of infectious mononucleosis (IM) and eight Burkitt's lymphomas (BL) from malaria-free regions of Africa were included in the study. Two different patterns of EBV distribution are described: 1) heterogeneous scattered EBV-positive cells, as originally seen in IM and therefore called the IM-type pattern, 2) and a BL-type pattern seen in endemic Burkitt's lymphoma with homogeneous EBV-positive cells all over the tumor. In lymphomas in patients with inborn immunodeficiencies, an IM-type pattern was found. In lymphomas from AIDS patients, the two different patterns were found. There were lymphomas with the IM-type pattern as well as some with the BL-type pattern. In some AIDS-associated lymphomas, both patterns occurred in one tumor. The findings suggest that it is not the disease process that is the distinguishing feature between the two patterns of EBV infection but rather the patient's underlying disease and the extent of this disease.
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PMID:Different Epstein-Barr virus expression in lymphomas from immunocompromised and immunocompetent patients. 169 92


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