Epidemiological evidence for causal relationship between Epstein-Barr virus and Burkitt's lymphoma from Ugandan prospective study

de-Thé, G; Geser, Anton; Day, Nicholas E.; Tukei, P. M.; Williams, Edward H.; Beri, D.; Smith, P. G.; Dean, Andrew G.; Bronkamm, G W; Feorino, Paul M.; Henle, Werner

doi:10.1038/274756a0

Cited by 540 publications

(218 citation statements)

References 33 publications

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“…Because 98% of the high endemic BLs are EBV positive, the probability that a B cell turns into a BL cell is higher if it carries the virus. Prospective epidemiological studies are also consistent with a contribution of a heavy EBV load to the genesis of the lymphoma (3). BLs usually carry multiple viral episomes.…”

supporting

confidence: 52%

T cell leukemia I oncogene expression depends on the presence of Epstein–Barr virus in the virus- carrying Burkitt lymphoma lines

Kiss

Nishikawa

Takada

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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supporting

confidence: 52%

T cell leukemia I oncogene expression depends on the presence of Epstein–Barr virus in the virus- carrying Burkitt lymphoma lines

Kiss

Nishikawa

Takada

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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“…[29][30][31] Although no major loci were significantly associated with any of these pathogen burden measures, there was suggestive evidence for association and/or linkage on chromosomes 8 and 11, including a genetic variant in the oncogene MYEOV for all herpes viruses (various herpes viruses are shown to contribute to the development of cancers, eg, EBV to Burkitt's lymphoma and Hodgkin's lymphoma). 32,33 In summary, this study identified a variant on chromosome 20 that is significantly associated with anti-C. pneumoniae IgG. However, no other antibody level traits obtained genome-wide significance levels of association.…”

Section: Discussionmentioning

confidence: 81%

Genome-wide genetic investigation of serological measures of common infections

et al. 2015

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Populations and individuals differ in susceptibility to infections because of a number of factors, including host genetic variation. We previously demonstrated that differences in antibody titer, which reflect infection history, are significantly heritable. Here we attempt to identify the genetic factors influencing variation in these serological phenotypes. Blood samples from 41300 Mexican Americans were quantified for IgG antibody level against 12 common infections, selected on the basis of their reported role in cardiovascular disease risk: Chlamydia pneumoniae; Helicobacter pylori; Toxoplasma gondii; cytomegalovirus; herpes simplex I virus; herpes simplex II virus; human herpesvirus 6 (HHV6); human herpesvirus 8 (HHV8); varicella zoster virus; hepatitis A virus (HAV); influenza A virus; and influenza B virus. Pathogen-specific quantitative antibody levels were analyzed, as were three measures of pathogen burden. Genome-wide linkage and joint linkage and association analyses were performed using 1 million SNPs. Significant linkage (lod scores 43.0) was obtained for HHV6 (on chromosome 7), HHV8 (on chromosome 6), and HAV (on chromosome 13). SNP rs4812712 on chromosome 20 was significantly associated with C. pneumoniae (P = 5.3 × 10 −8 ). However, no genome-wide significant loci were obtained for the other investigated antibodies. We conclude that it is possible to localize host genetic factors influencing some of these antibody traits, but that further larger-scale investigations will be required to elucidate the genetic mechanisms contributing to variation in antibody levels.

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“…Living in regions of malaria endemicity was a predictor of this early age of primary infection. This aberrant primary EBV infection may set the stage for lymphoma development, as previously hypothesized (4)(5)(6).…”

mentioning

confidence: 68%

Reduced Transplacental Transfer of a Subset of Epstein-Barr Virus-Specific Antibodies to Neonates of Mothers Infected with Plasmodium falciparum Malaria during Pregnancy

Ogolla

Daud

Asito

et al. 2015

Clin Vaccine Immunol

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h Over 35% of children in a region of malaria endemicity are infected with Epstein-Barr virus (EBV) by 6 months of age. This susceptibility may be linked to impaired transplacental transfer of antibodies. In this study, we determined the effect of malaria exposure during pregnancy on the transfer of EBV-specific maternal antibodies in a region of western Kenya that experiences endemic malaria. Pregnant mothers were recruited and followed up until delivery to determine levels of neonatal malaria exposure. Levels of EBV lytic (viral capsid antigen [VCA], Z transcriptional activator [Zta], and early diffuse antigen complex [EAd]) and EBV latent (EBV nuclear antigen-1 (EBNA1]) and tetanus-specific IgG antibodies were measured in 70 paired maternal and cord blood samples using a Luminex-bead-based assay. A high proportion (63%) of the infants were exposed to malaria in utero. Levels of EBV-and tetanus-specific antibodies were similar in malaria-infected mothers and in mothers who had no detectable malaria infection. Malaria-exposed neonates had significantly lower levels of anti-EBNA1, anti-Zta, and anti-EAd antibodies than were seen in their mothers. In utero malaria exposure resulted in significant reductions in transplacental transfer of anti-VCA-p18 and anti-EBNA1 antibodies of 13% and 22%, respectively. Neonates received significantly low levels of anti-Zta and anti-EAd antibodies irrespective of malaria exposure levels. In multivariate analysis, in utero malaria exposure was associated with a significant reduction in the transfer of anti-VCA-p18 and anti-EBNA1 antibodies to the neonates (P ‫؍‬ 0.0234 and P ‫؍‬ 0.0017, respectively). Malaria during pregnancy results in differential levels of transfer of EBV-specific antibodies from the mother to the fetus. The impaired transplacental transfer of some antibodies may lead to the malaria-exposed neonates being susceptible to early EBV infection. E ndemic Burkitt's lymphoma (eBL) is a distinct form of nonHodgkin's lymphoma and is the most common pediatric malignancy in regions of malaria endemicity of sub-Saharan Africa (1). Both infection with Epstein-Barr virus (EBV) and repeated episodes of Plasmodium falciparum malaria are known risk factors for eBL (2), but the mechanism(s) by which these two agents interact to promote the emergence of malignant B cell clones has not been elucidated. Recently, we found that infants from a region of malaria endemicity of western Kenya were infected with EBV by 6 months of age (3). Living in regions of malaria endemicity was a predictor of this early age of primary infection. This aberrant primary EBV infection may set the stage for lymphoma development, as previously hypothesized (4-6).The lytic and latent phases of the EBV life cycle induce distinct antibodies in response to specific lytic and latent antigens. Anti-EBV nuclear antigen-1 (EBNA1) antibodies are produced against EBNA1, the only antigen expressed in latently infected memory B cells and in eBL tumors (7). Anti-viral capsid antigen (anti-VCA), anti-early antigen (ant...

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Epidemiological evidence for causal relationship between Epstein-Barr virus and Burkitt's lymphoma from Ugandan prospective study

Cited by 540 publications

References 33 publications

T cell leukemia I oncogene expression depends on the presence of Epstein–Barr virus in the virus- carrying Burkitt lymphoma lines

T cell leukemia I oncogene expression depends on the presence of Epstein–Barr virus in the virus- carrying Burkitt lymphoma lines

Genome-wide genetic investigation of serological measures of common infections

Reduced Transplacental Transfer of a Subset of Epstein-Barr Virus-Specific Antibodies to Neonates of Mothers Infected with Plasmodium falciparum Malaria during Pregnancy

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