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

Children living in malaria-endemic regions have high incidence of Burkitt's lymphoma (BL), the aetiology of which involves Plasmodium falciparum malaria and Epstein-Barr virus (EBV) infections. Acute malarial infection impairs the EBV-specific immune responses with the consequent increase in the number of EBV-carrying B cells in the circulation. To further understand the potential influence of malarial infection on the EBV persistence in children living in malaria-endemic areas, we studied the occurrence and quantified cell-free EBV-DNA in plasma from 73 Ghanaian children with and without acute malarial infection. Viral DNA was detected in 40% of the samples (47% in the malaria-infected and 34% in the nonmalaria group) but was absent in plasma from Ghanaian adults and healthy Italian children. These findings provide evidence that viral reactivation is common among children living in malaria-endemic areas, and may contribute to the increased risk for endemic BL. The data also suggest that the epidemiology of EBV infection and persistence varies in different areas of the world.
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PMID:Circulating epstein-barr virus in children living in malaria-endemic areas. 1588 38

Epstein-Barr virus (EBV) and Plasmodium falciparum have overlapping distributions and are thought to have causal interactions, particularly with regard to the aetiology of endemic Burkitt's lymphoma. Using real-time PCR, we quantified and compared EBV DNA levels in the blood before and after antimalarial treatment of age- and gender-matched groups of Gabonese children who presented with either mild or severe P. falciparum malaria. Following treatment, the prevalence of EBV DNA declined in the mild malaria group but increased in the severe malaria group, and a significantly higher proportion of the latter had EBV DNA detectable in their blood when they were healthy and parasite free (67% vs. 39%; P=0.013). High EBV DNA loads were associated with more malaria attacks and with elevated plasma concentrations of both TNF-alpha and IL-12p40. Significantly more under 5 year olds had EBV DNA, highlighting the strong age dependence of the interaction between the two pathogens. These findings confirm that EBV is reactivated during acute P. falciparum malaria but, importantly, also reveal that: (i) EBV activity persists at a higher frequency in children with a history of severe malaria; and (ii) higher peripheral blood EBV DNA loads are associated with susceptibility to more frequent P. falciparum episodes and with altered cytokine activity.
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PMID:Persistent Epstein-Barr viral reactivation in young African children with a history of severe Plasmodium falciparum malaria. 1631 33

Children living in malaria-endemic regions have a high incidence of Burkitt lymphoma (BL), the etiology of which involves Plasmodium falciparum malaria and Epstein-Barr virus (EBV) infections. In the present study, we compared EBV DNA loads in plasma and saliva samples from Ugandan children with acute malaria (M+) at the time of diagnosis and 14 days after antimalaria treatment, children without malaria (M-), and children with BL. EBV DNA was detected, by real-time polymerase chain reaction, in 31% of the plasma and in 79% of the saliva samples from children in the M+ group. Antimalaria treatment led to clearance of plasma viral load in 85% of the cases but did not affect the levels in saliva. There was a significant difference in plasma EBV loads across the groups. The lowest levels were detected in samples from the M- group, increased levels were detected in samples from the M+ group, and levels reached the highest values in samples from children with BL. The same trend was evident in the frequency and levels of anti-BZLF1 antibodies, which is indicative of viral reactivation. In the M+ group, the positive plasma samples clustered around 7-9 years of age, the peak incidence of BL. The clearance of circulating EBV after antimalaria treatment suggests a direct relationship between active malaria infection and viral reactivation.
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PMID:Clearance of circulating Epstein-Barr virus DNA in children with acute malaria after antimalaria treatment. 1651 59

This review considers recent studies regarding the role of environmental factors in the etiology of childhood leukemia and lymphoma. Potential environmental risk factors identified for childhood leukemia include exposure to magnetic fields of more than 0.4 micro Tessla, exposure to pesticides, solvents, benzene and other hydrocarbons, maternal alcohol consumption (but only for certain genotypes), contaminated drinking water, infections, and high birth weight. The finding of space-time clustering and seasonal variation also supports a role for infections. There is little evidence linking childhood leukemia with lifetime exposure to ionizing radiation although fetal exposures to X-rays are associated with increased risk. Breast-feeding, consumption of fresh fruit and vegetables and having allergies all appear to be protective. Burkitt lymphoma (BL) is confined to areas of the world where malaria is endemic, with the additional involvement of the Epstein-Barr virus (EBV) as a co-factor. Environmental risk factors suggested for other types of non-Hodgkin lymphoma (NHL) include exposure to ionizing radiation (both lifetime and antenatal), pesticides, and, in utero exposure to cigarette smoke, benzene and nitrogen dioxide (via the mother). Hodgkin lymphoma (HL) is especially associated with higher levels of socioeconomic deprivation, but breast-feeding seems to confer lower risk. This is consistent with an infection or immune-response mediated etiology for HL.
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PMID:Environmental factors and childhood acute leukemias and lymphomas. 1669 May 16

Simultaneous infection with multiple pathogens of the same species occurs with HIV, hepatitis C, Epstein-Barr virus, dengue, tuberculosis, and malaria. However, available methods do not distinguish among or quantify pathogen genotypes in individual patients; they also cannot test for novel insertions and deletions in genetically modified organisms. The strategy reported here accomplishes these goals with real-time polymerase chain reaction (PCR) and capillary electrophoresis. Real-time PCR with allotype-specific primers defines the allotypes (strains) present and the intensity of infection (copy number). Capillary electrophoresis defines the number of genotypes within each allotype and the intensity of infection by genotype. This strategy can be used to study the epidemiology of emerging infectious diseases with simultaneous infection by multiple genotypes, as demonstrated here with malaria. It also permits testing for insertions or deletions in genetically modified organisms that may be used for bioterrorism.
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PMID:Identifying and quantifying genotypes in polyclonal infections due to single species. 1670 87

The newly obtained data supplemented our knowledge about risk for travellers, tourists and natives of Europe connected with malaria, leishmaniasis and other tropical diseases. It was discovered that healthy carriers of Epstein-Barr virus (nearly 90% of human population) have a great risk to get chronic Burkitt lymphoma disease as a result of Plasmodium falciparum (tropical malaria agent) infection. HIV carriers being occasionally in contact with visceral leishmaniasis vectors (sand-flies infected on dogs in the Mediterranean area) not only got a heavy form of disease but became a source of infection for healthy people. Airport malaria and outbreaks of dengue fever sometimes were (and are) connected with an import of infective Anopheles or Aedes mosquitoes. The high risk of borreliosis and ehrlichiosis infection exists in the forested European areas along the highways, where picnics and other types of recreation of travellers and tourists are typical and where the anthropogenically changed Ixodes ticks subpopulations are distributed. Such physiologically changed part of tick population is more aggressive and "changed ticks" more often are vectors of one, two or even more agent species simultaneously.
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PMID:Bloodsucking arthropods: the danger for travellers and hazard of vector travelling. 1688 48

Hepatosplenic gammadelta T-cell lymphoma (HSTL) is a clinicopathological entity associated with an immunocompromised status in approximately 25% of patients. Herein is described a case of HSTL in a 53-year-old Brazilian man with seven previous malaria infections, initially misdiagnosed as a hyperreactive splenomegaly due to chronic malaria. A characteristic lymphoid infiltrate was observed in spleen, liver and bone marrow sinusoids/sinuses. Neoplastic cells had a CD45RO+, CD2+, CD7+, CD3+, CD5-, CD8+, CD56+, perforin+, FasL-negative, T-cell receptor (TCR)alphabeta-negative, TCRgammadelta+ profile. Analyses of gamma and delta TCR rearrangements confirmed diagnosis of gammadelta T-cell lymphoma by detecting VgammaI/Vdelta1-Jdelta1 clonal rearrangements. Sensitive polymerase chain reaction (PCR) for Plasmodium falciparum, Epstein-Barr virus and herpesvirus-8 failed to demonstrate infection. The disease progressed to a fatal outcome following cutaneous infiltration and leukemic proliferation. The authors also comment on the association of lymphoma and infection, focusing on PCR diagnosis of TCRgamma and delta clonal rearrangements and the presumed pathogenic events leading to HSTL in the context of chronic malaria infection. Initial lymphomagenic stages might not be direct consequences of antigenic stimulation of Vdelta1 T-cells, but might depend on interactions between gammadelta T and B cells during cooperative or regulatory responses to Plasmodium sp.
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PMID:Hepatosplenic gammadelta T-cell lymphoma following seven malaria infections. 1704 Feb 89

Although malaria and Epstein-Barr (EBV) infection are recognized cofactors in the genesis of endemic Burkitt lymphoma (BL), their relative contribution is not understood. BL, the most common paediatric cancer in equatorial Africa, is a high-grade B cell lymphoma characterized by c-myc translocation. EBV is a ubiquitous B lymphotropic virus that persists in a latent state after primary infection, and in Africa, most children have sero-converted by 3 y of age. Malaria infection profoundly affects the B cell compartment, inducing polyclonal activation and hyper-gammaglobulinemia. We recently identified the cystein-rich inter-domain region 1alpha (CIDR1alpha) of the Plasmodium falciparum membrane protein 1 as a polyclonal B cell activator that preferentially activates the memory compartment, where EBV is known to persist. Here, we have addressed the mechanisms of interaction between CIDR1alpha and EBV in the context of B cells. We show that CIDR1alpha binds to the EBV-positive B cell line Akata and increases the number of cells switching to the viral lytic cycle as measured by green fluorescent protein (GFP) expression driven by a lytic promoter. The virus production in CIDR1alpha-exposed cultures was directly proportional to the number of GFP-positive Akata cells (lytic EBV) and to the increased expression of the EBV lytic promoter BZLF1. Furthermore, CIDR1alpha stimulated the production of EBV in peripheral blood mononuclear cells derived from healthy donors and children with BL. Our results suggest that P. falciparum antigens such as CIDR1alpha can directly induce EBV reactivation during malaria infection that may increase the risk of BL development for children living in malaria-endemic areas. To our knowledge, this is the first report to show that a microbial protein can drive a latently infected B cell into EBV replication.
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PMID:A molecular link between malaria and Epstein-Barr virus reactivation. 1755 3

Burkitt lymphoma, a childhood tumor common in parts of sub-Saharan Africa, has been directly associated with Epstein-Barr virus (EBV) and indirectly with prevalence of malaria. We studied antibodies to both EBV and malaria in children diagnosed with this cancer in Uganda. We performed a case-control study of HIV-seronegative children (<or=15 years) admitted to hospital. Cases were diagnosed with Burkitt lymphoma and controls with non-malignant conditions or non-lymphatic cancers. Interviews were conducted and serological samples collected and, when possible, tested for both EBV and malaria. Adjusted odds ratios (ORs) for Burkitt lymphoma were estimated using unconditional logistic regression adjusting for sex, age, residential district, household income and tribe. The mean age of cases was 7 years and 61% were male. Compared to controls, cases were more likely to be reported having received more frequent treatment for malaria in the past year (OR = 2.0; p = 0.001) and less likely to be living in a home where insecticides were used (OR = 0.2; p < 0.0001). Odds ratios for Burkitt lymphoma in children increased with increasing antibody levels against EBV (p < 0.0001) and malaria (p = 0.05). Findings were similar for children residing in districts close to the capital city and in remote areas. Cases were 5 times more likely than controls to have raised levels of both EBV and malaria antibodies (OR = 5.0; p = 0.003). Our findings suggest that EBV and malaria may act synergistically in the pathogenesis of childhood Burkitt lymphoma. Malaria prevention measures may also prevent this childhood cancer.
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PMID:Antibodies against malaria and Epstein-Barr virus in childhood Burkitt lymphoma: a case-control study in Uganda. 1800 Aug 23

Burkitt lymphoma (BL), a tumor occurring in endemic, sporadic and AIDS-associated forms, is the classic example of a human malignancy whose pathogenesis involves a specific cellular genetic change, namely, a chromosomal translocation deregulating expression of the c-myc oncogene, complemented in many cases by the action of an oncogenic virus, the Epstein-Barr virus (EBV). Here we review recent work in two complementary areas of research: (1) on cellular genetic changes that occur in addition to the c-myc translocation in BL, in particular the capacity of p53/ ARF pathway breakage or of c-myc mutation to decouple the pro-proliferative effects of c-myc deregulation from its pro-apoptotic effects; and (2) on a postulated role for EBV in BL pathogenesis, through adopting restricted forms of virus latent gene expression that remain compatible with the c-myc-driven growth program but offer the tumor additional protection from apoptosis. We stress the many fundamental questions that remain to be resolved and, in that regard, highlight the general lessons that might be learned through understanding how two other infectious agents, malaria and HIV, dramatically enhance BL incidence.
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PMID:Burkitt lymphoma: revisiting the pathogenesis of a virus-associated malignancy. 1802 41


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