Maintenance of serum immunoglobulin G antibodies to Epstein-Barr virus (EBV) nuclear antigen 2 in healthy individuals from different age groups in a Japanese population with a high childhood incidence of asymptomatic primary EBV infection.
Immunoglobulin G (IgG) antibodies to Epstein-Barr virus (EBV) nuclear antigens 2 and 1 (EBNA-2 and EBNA-1, respectively) were studied using sera from healthy individuals of a population with a high incidence of asymptomatic primary EBV infections during infancy or childhood in Japan. Two CHO-K1 cell lines expressing EBNA-2 and EBNA-1 were used for anticomplement and indirect immunofluorescence assays. The positivity rate for EBNA-2 IgG rose in the 1- to 2-year age group, increased and remained at a plateau ( approximately 45%) between 3 and 29 years of age (3- to 4-, 5- to 9-, 10- to 14-, and 15- to 29-year age groups), and then reached 98% by age 40 (>/== 40-year age group). Both seropositivity for EBNA-1 and seropositivity for EBNAs in Raji cells (EBNA/Raji) were detected in the 1- to 2-year age group, remained high, and finally reached 100% by age 40. The geometric mean titer (GMT) of EBNA-2 IgG reached a plateau in the 5- to 9- and 10- to 14-year-old groups and remained elevated in the older age groups (15 to 29 and >/== 40 years). The GMT of EBNA-1 IgGs increased to a plateau in the 1- to 2-year-old group and remained unchanged in the older age groups. The GMT of EBNA/Raji IgGs also reached a plateau in the 1- to 2-year-old group, remained level throughout the 3- to 14-year age groups, and decreased in the 15- to 29-year-olds. EBNA-2 IgGs emerged earlier than EBNA-1 IgGs in 8 of 10 patients with infectious mononucleosis, who were between 1 and 27 years old, and declined with time in three of eight cases. These results suggest that EBNA-2 IgG antibodies evoked in young children by asymptomatic primary EBV infections remain elevated throughout life, probably because of reactivation of latent and/or exogenous EBV superinfection.
Harada
Shizuko
S
Herpesvirus Laboratory, Department of Virology I, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan.
Kamata
Yoshio
Y
Ishii
Yasuyuki
Y
Eda
Hiroyuki
H
Kitamura
Ryo
R
Obayashi
Maya
M
Ito
Sayuri
S
Ban
Fumihiko
F
Kuranari
Jun
J
Nakajima
Haruhiko
H
Kuze
Tomoko
T
Hayashi
Masao
M
Okabe
Nobuhiko
N
Senpuku
Hidenobu
H
Miyasaka
Nobuyuki
N
Nakamura
Yoshiko
Y
Kanegane
Hirokazu
H
Yanagi
Kazuo
K
D000293:Adolescent; D000328:Adult; D000818:Animals; D000914:Antibodies, Viral / Q000097:blood*; D016466:CHO Cells; D002648:Child; D002675:Child, Preschool; D003169:Complement Inactivator Proteins / Q000032:analysis; D006224:Cricetinae; D020031:Epstein-Barr Virus Infections / Q000453:epidemiology / Q000276:immunology*; D019309:Epstein-Barr Virus Nuclear Antigens / Q000276:immunology*; D019084:Fluorescent Antibody Technique, Indirect; D004854:Herpesvirus 4, Human / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D007223:Infant; D007564:Japan / Q000453:epidemiology; D014764:Viral Proteins
D000914:Antibodies, Viral; D003169:Complement Inactivator Proteins; C402641:EBNA-2 protein, Human herpesvirus 4; D019309:Epstein-Barr Virus Nuclear Antigens; D007074:Immunoglobulin G; D014764:Viral Proteins; C012749:anticomplement; C417029:EBV-encoded nuclear antigen 1