[Epstein-Barr virus-specific immunity in asymptomatic carriers of human T-cell leukemia virus type 1]

Adult T-cell leukemia (ATL) patients are immunosuppressed as evidenced by anergy to recall antigens and the occurrence of opportunistic infections. The immunosuppression appears to be a critical factor or a predictive sign for the development of ATL in carriers of human T-cell leukemia virus type 1 (HTLV-1). This study was aimed at assessing the immune status of asymptomatic HTLV-1 carriers with the immunity specific to Epstein-Barr virus (EBV), a ubiquitous human herpesvirus with oncogenic potential. Forty-three asymptomatic HTLV-I carriers were examined for their EBV serology and EBV-specific cytotoxic T-cell (EBV-CTL) activity, in comparison with 10 HTLV-I-non-infected normal controls. Both carriers and controls were all positive for EBV capsid antigen (VCA) IgG. Significantly elevated titer of VCAIgG and lower titer of EBV-determined nuclear antigen (EBNA) antibodies were observed in asymptomatic HTLV-I carriers, suggesting reactivation of EBV. Among the HTLV-I carriers, 9 (20.9%) had reduced activity of EBV-CTL as revealed by lower incidence of regression of in vitro EBV-induced B-cell transformation. Accordingly, asymptomatic HTLV-I carriers were divided into three groups: the carriers with reduced EBV-specific cellular immunity (group I), the carriers showing normal cellular immunity but aberrant EBV-specific antibody titers (group II), and the carriers with normal EBV-specific cellular immunity and serology (group III). Higher positive rate of anti-HTLV-I Tax antibody was found in the former two groups (44.4% and 56.5%, respectively) compared with group III (18.2%). An immunosuppressive agent, 4-deoxyphorbol ester induced a remarkable decrease of EBV-CTL activity in the carriers of group II and III at the concentration that affected none of the normal controls. These findings indicate that asymptomatic HTLV-I carriers suffer stepwise impairment of EBV-specific immunities, which may be caused by HTLV-I infection.