The pathogenesis of posttransfusion hepatitis was determined in 14 chi
ldren with beta-thalassemia. All had blood samples obtained in 1980 or
1981, were vaccinated against hepatitis B virus in 1983 and had anoth
er serum sample collected in 1989. Seven children had detectable antib
odies against hepatitis C virus before vaccination, and all were posit
ive in 1989. With specific solid-phase enzyme immunoassays, all childr
en had antibodies against hepatitis B virus, X and polymerase antigens
in 1981, and six had one or both antibodies in 1989. Hepatitis B viru
s infection was confirmed by means of polymerase chain reaction, which
demonstrated virus DNA in 13 of the 14 children. The amplification pr
oducts spanning the X/precore region were smaller than expected, sugge
sting mutations in this region. Cloning and sequencing of these produc
ts revealed deletions spanning part or all of the X gene. The results
show that these children were infected with hepatitis B virus even wit
hout other markers in serum, that hepatitis B persists years after vac
cination and that such infections are associated with the presence of
X deletion mutants. Coinfection with hepatitis B and C viruses, the fo
rmer containing a new class of variants, is common in children with be
ta-thalassemia.