Epidemiological evidence for the role of falciparum malaria in the pathogenesis of Burkitt's lymphoma.

R. H. Morrow

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)177-186
Number of pages10
JournalIARC scientific publications
Issue number60
StatePublished - 1985
Externally publishedYes

Fingerprint

Burkitt Lymphoma
Falciparum Malaria
Malaria
Incidence
B-Lymphocytes
Plasmodium falciparum
Human Herpesvirus 4
Age of Onset
Space-Time Clustering
Sickle Cell Trait
Precipitating Factors
Epstein-Barr Virus Infections
Health Facilities
Antimalarials
Infection
Cytogenetics
Immunoglobulins
Lymphoma
Carcinogenesis

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Epidemiological evidence for the role of falciparum malaria in the pathogenesis of Burkitt's lymphoma. / Morrow, R. H.

In: IARC scientific publications, No. 60, 1985, p. 177-186.

Research output: Contribution to journalArticle

@article{93bee6a3825f4e3ead3dea2322372642,
title = "Epidemiological evidence for the role of falciparum malaria in the pathogenesis of Burkitt's lymphoma.",
abstract = "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.",
author = "Morrow, {R. H.}",
year = "1985",
language = "English (US)",
pages = "177--186",
journal = "IARC (International Agency for Research on Cancer) Scientific Publications",
issn = "0300-5038",
publisher = "IARC",
number = "60",

}

TY - JOUR

T1 - Epidemiological evidence for the role of falciparum malaria in the pathogenesis of Burkitt's lymphoma.

AU - Morrow, R. H.

PY - 1985

Y1 - 1985

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0022309975&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022309975&partnerID=8YFLogxK

M3 - Article

C2 - 3905588

AN - SCOPUS:0022309975

SP - 177

EP - 186

JO - IARC (International Agency for Research on Cancer) Scientific Publications

JF - IARC (International Agency for Research on Cancer) Scientific Publications

SN - 0300-5038

IS - 60

ER -