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To assess the relationship of anti-Tax antibody to human T-cell lymphotropic virus type-I (HTLV-I) transmission, the sero-prevalence of HTLV-I was analyzed among married couples and among mother/child (both adults) pairs. HTLV-I seroprevalence was significantly higher among wives with anti-Tax+ than those with anti-Tax- HTLV-I carrier husbands (82.4% vs. 59.5%). However, in the group of wives aged 60 years or older, there was no statistical difference in HTLV-I seropositivity based on the husbands' anti-Tax sero-status. In the group whose wives were less than 60 years old, more anti-Tax sero-positive than sero-negative husbands had high DNA levels (57.1% and 20.0%), whereas in the group of husbands whose wives were aged 60 years or older, the number of anti-Tax sero-positive and sero-negative individuals with high DNA levels was similar. HTLV-I sero-prevalence was significantly higher among the adult men with anti-Tax+ carrier mothers than those with anti-Tax- carrier mothers (52.0% vs. 14.3%). For women, HTLV-I sero-prevalence did not differ significantly according to their mothers' anti-Tax sero-status. Our results suggest that the presence of anti-Tax antibody in HTLV-I carriers is an age-dependent risk factor for male-to-female HTLV-I transmission. Furthermore, the effect of the mother's anti-Tax antibody as a risk factor for vertical HTLV-I transmission could be observed in men even after becoming adults.

Sera from 1197 adult residents in Miyazaki district, an area in Japan endemic for human T-cell leukemia virus type I (HTLV-I), were tested for anti-Tax antibody by the recombinant Tax (r-Tax) Western blot assay. Among HTLV-I-seropositive individuals, including 21.5% of 484 males and 28.6% of 713 females, the prevalence of anti-Tax antibody were 59.6% and 58.3% respectively, with no apparent difference in age. There was a significant 6-fold difference in the prevalence of anti-Tax among seropositive subjects with titer > or = 1:8192 (84.6%) compared with those with the lowest titer of 1:16 (14.3%), suggesting the increased production of antibodies to viral structural proteins in anti-Tax-positive individuals. Furthermore, among those anti-Tax-positive subjects, the intensity of serum reactivity to r-Tax protein in the high antibody titer (1:1024 or higher) group was significantly stronger than that in the lower antibody titer (1:512 or lower) group. We also found that 1.6% (14/889) of individuals without detectable levels of HTLV-I antibody had anti-Tax antibody. HTLV-I pro-viral DNA signals could not be detected in DNA sample from the lymphocytes of these individuals by the nested polymerase chain reaction method. Further evaluation is needed to clarify the significance of an anti-Tax-only status population in which HTLV-I is endemic.

The level of proviral DNA in peripheral blood mononuclear cells from a representative group of asymptomatic HTLV-I carriers in Miyazaki district, an HTLV-I endemic area in Japan, was determined by a single-cycle polymerase chain reaction method (PCR). Of 217 subjects, 26% had a high level of proviral DNA, 43% a medium level, 18% a low level, and 13% an undetectable level. In the high-DNA group, 60% had at least 0.6% abnormal lymphocytes on peripheral blood smears, significantly higher than in those with low DNA levels (19%). This association was present for men of all ages and for women under 55. Men were more than twice as likely to have abnormal lymphocytes as well as high levels of proviral DNA. These differences may reflect different host responses to the virus by sex or by the time or route of infection. This study supports the utility of PCR for molecular screening in epidemiologic studies of the natural history of HTLV-I, and may lead to the identification of those carriers who are at greatest risk of developing HTLV-I-induced malignancy.

A gene product (p42) of the long open reading frame, now termed tax, of the viral genome of human T-cell leukemia virus type I (HTLV-I) may be related to the transformation of T cells in adult T-cell leukemia-lymphoma (ATLL). To evaluate its association with the disease, we compared the prevalence of antibody to p42 in sera obtained from 105 HTLV-I carriers and 64 ATLL patients from southwest Japan. The prevalence of the anti-p42 antibody reactivity was 63% among carriers and 31% among cases. The cases were more than 3 times as likely to lack antibody to p42 than carriers, the relative odds (OR) = 3.4, p = 0.001. When the samples were tested for antibody against p24, the most immunogenic core protein, the prevalence was somewhat higher among carriers (65%) than in cases (52%), but not significantly so (p = 0.15). Among the healthy carriers, the correlation between the prevalence of both antibodies was high (p = 0.001), and only 25% of those who had antibody to p24 lacked antibody to p42. However, among the cases, reactivity to both antigens was independent (p = 0.52), and 65% of those with antibody to p24 lacked antibody to p42, OR = 6.3, p = 0.0004. Thus the strongest serologic marker of ATLL following diagnosis was lack of reactivity to p42, particularly among those subjects with anti-p24. Whether this altered response is present prior to disease remains to be determined.

Secretory antibodies protect mucosal surfaces against transmission of many viruses. Human T-lymphotropic Virus, Type I (HTLV-I) is transmitted via blood products and via sexual contact across mucosal surfaces. We investigated the presence of HTLV-I-specific antibodies in whole saliva samples from 10 seronegative and 28 seropositive volunteers from a hospital in southern Japan. Antibodies directed to HTLV-I antigens were found in the salivas from 22 of 28 (79%) of the seropositive subjects. None of the seronegative individuals showed evidence of salivary antibodies. Antibodies directed to the envelope antigens of the virus were found in 21 of 22 positive saliva samples. Secretory antibodies may be important in preventing mucosal transmission.