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53 - The epidemiology of EBV and its association with malignant disease

from Part III - Pathogenesis, clinical disease, host response, and epidemiology: gammaherpesviruses

Published online by Cambridge University Press:  24 December 2009

Henrik Hjalgrim
Affiliation:
Department of Epidemiology Research, Statens Serum Institut, Artillerivej 5, 2300 Copenhagen S. Denmark
Jeppe Friborg
Affiliation:
Department of Epidemiology Research, Statens Serum Institut, Artillerivej 5, 2300 Copenhagen S. Denmark
Mads Melbye
Affiliation:
Department of Epidemiology Research, Statens Serum Institut, Artillerivej 5, 2300 Copenhagen S. Denmark
Ann Arvin
Affiliation:
Stanford University, California
Gabriella Campadelli-Fiume
Affiliation:
Università degli Studi, Bologna, Italy
Edward Mocarski
Affiliation:
Emory University, Atlanta
Patrick S. Moore
Affiliation:
University of Pittsburgh
Bernard Roizman
Affiliation:
University of Chicago
Richard Whitley
Affiliation:
University of Alabama, Birmingham
Koichi Yamanishi
Affiliation:
University of Osaka, Japan
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Summary

EPSTEIN-BARR VIRUS EPIDEMIOLOGY

Epidemiology of primary Epstein-Barr virus infection

Epstein-Barr virus (EBV) is an ancient virus, and has probably coevolved with its different hosts over the last 90–100 million years (McGeoch et al., 1995). With the ability to establish lifelong latency and intermittent reactivation after primary infection and with limited clinical symptoms in the majority of infected individuals, EBV has become ubiquitous in all human populations

Age at primary infection

Children in developing countries acquire the infection in the first few years of life, and universal seroconversion is often seen by ages 3–4 years, whereas infection in developed countries often is delayed until adolescence (de The et al., 1975; Haahr et al., 2004; Henle and Henle, 1967; Melbye et al., 1984a,b) (Figure 53.1). In some developed countries a bimodal infection rate, with peaks in children below 5 years and again after 10 years of age, has been described (Edwards and Woodroof, 1979; Henle and Henle, 1967; Lai et al., 1975). Oral EBV excretion between parents and infants, and from intimate partners in adolescence and early adulthood is the likely explanation for the observed bimodality (Crawford et al., 2002; Fleisher et al., 1979).

EBV antibody titers in seropositive individuals vary according to age following a U-shaped pattern, with high titers among infants and in the elderly (above 50 years) (Glaser et al., 1985; Venkitaraman et al., 1985).

Type
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Information
Human Herpesviruses
Biology, Therapy, and Immunoprophylaxis
, pp. 929 - 959
Publisher: Cambridge University Press
Print publication year: 2007

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