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Primary epstein‐barr virus infections in african infants. I. Decline of maternal antibodies and time of infection
Author(s) -
Biggar Robert J.,
Henle Werner,
Fleisher Gary,
Böcker Jörg,
Lennette Evelyne T.,
Henle Gertrude
Publication year - 1978
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910220304
Subject(s) - antibody , antigen , immunology , titer , incidence (geometry) , virus , medicine , virology , biology , physics , optics
Thirty‐one infants living in Accra, Ghana, an area endemic for Burkitt's lymphoma, were visited at monthly intervals for the first 15 months of life and once again at 21 months. Sera obtained at each visit were tested for antibodies to Epstein‐Barr virus (EBV) capsid antigen (VCA), EBV‐induced early antigens (EA) and EBV‐associated nuclear antigen (EBNA) by immunofluorescence techniques as well as for EBV‐neutralizing antibodies and antibody‐dependent cell‐mediated cytolysis. All infants had maternal antibodies to VCA at 1 month of age and the majority also antibodies detected by the other tests, except anti‐EA. The maternal anti‐VCA titers declined in subsequent months according to a half‐life of nearly 5 weeks. Depending on the initial titers, all infants became seronegative for all antibodies by 2–8 months of age, with anti‐VCA persisting longest. The earliest primary EBV infection occurred in the third month after maternal antibodies to VCA had become non‐detectable. By 12 months of age, 44% of the infants had seroconverted, by 15 months, 62% and by 21 months, 81%. There was no seasonal variation in the incidence of infections. Infants from families of the lowest socio‐economic level tended to become infected somewhat earlier than those from better situated families (p = 0.22) but no other factors, such as household size or crowding, seemed to be associated with enhanced risk of early infection.