To identify factors that may modify the heterosexual transmission of human T cell leukemia/lymphoma virus type I (HTLV-I), 534 married couples enrolled in the Miyazaki Cohort Study between November 1984 and April 1989 were studied: 95 husband HTLV-I-seropositive (H+)/wife seropositive (W+), 33 H+/W-, 64 H-/W+, and 342 H-/W-. After 5 years of follow-up, seven seroconversions occurred and clustered significantly among serodiscordant pairs (relative risk [RR] = 41.2); the rate of transmission was 3.9 times higher if the carrier spouse was male (P = .19). Among H+/W- couples, husband's age > or = 60 years strongly predicted seroconversion in the wives (RR = 11.5). All 4 carrier husbands whose wives seroconverted had HTLV-I titers > or = 1:1024 (P = .04) and were anti-tax antibody positive (P = .06). In cross-sectional analysis, total parity also was independently associated with wife's serostatus but only length of marriage with husband's. Overall, sexual transmission of HTLV-I was primarily from older infected husbands to their wives, with husbands' viral status being an important factor.
Although it is thought that infection with human T‐lymphotropic virus type I (HTLV‐I) is immunosuppressive, this has not been clearly demonstrated among healthy carriers, and there are no data concerning delayed‐type hypersensitivity (DTH). To evaluate this hypothesis, DTH to purified protein derivative (PPD) of tuberculin was measured in 126 healthy adults from an endemic area for HTLV‐I infection in southern Japan. Among the 39 HTLV‐I carriers, only 15% had detectable induration following PPD exposure, compared to 46% of the 87 non‐carriers. In addition, the size of erythema among those carriers with a positive reaction was about 70% of that among non‐carriers. Overall, there was a significantly inverse association between the degree of DTH response and prevalence of antibody. In relation to subjects with strong to moderate reaction, those with negative or indefinite reaction were 6 times more likely to be a carrier. This association was much stronger among subjects aged 60 years or older than among younger persons. These findings indicate that there is subclinical immunosuppression among HTLV‐I carriers, which increases with age.
Data on human T-cell lymphotropic-virus-type-I (HTLV-I) status and hematology from 528 individuals were analyzed for associations with low reactivity to the purified protein derivative (PPD) of Mycobacterium tuberculosis recall antigen. Subjects were classified as HTLV-I carriers with abnormal lymphocytes (Ably), carriers without Ably, and seronegatives. All carriers had a significant 2.6-fold risk of being low responders to PPD compared with the seronegatives, carriers with Ably having the highest relative risk. Carriers with HTLV-I-antibody titer > or = 1:256, or with other detectable markers of virus status such as antibody to tax and proviral DNA, had increased risk for low response to PPD similar to the estimate for HTLV-I seropositivity alone, compared with the seronegatives. Subjects with a low lymphocyte count had 3.5 times the risk for being low responders to PPD, compared with subjects with high counts. Similarly, subjects with a low monocyte count had 2.0 times the risk for low reactivity of those with a moderate to high count. Results were not confounded by age, sex, smoking or alcohol drinking. Using multiple logistic regression, only HTLV-I seropositivity and low lymphocyte and monocyte counts were predictive of low reactivity to PPD. Analysis indicates that suppression of delayed-type hypersensitivity is associated with HTLV-I infection per se, and not with viral replication or load. Furthermore, this effect may occur in part via changes in the number and function of lymphocytes and monocytes. Such a mechanism may involve altered cytokine production in carriers and concomitant changes in cell populations involved in delayed-type hypersensitivity.
The presence of circulating “flower cells” and a low prevalence of antibody to Tax regulatory protein of human T-lymphotropic virus type I (HTLV-I) are characteristics of adult T-cell leukemia (ATL). To examine the predictability of levels of HTLV-I antibodies and of flower cell-like abnormal lymphocytes (Ably) for the risk of ATL among asymptomatic HTLV-I carriers, we prospectively evaluated the levels of viral markers of five HTLV-I carriers who developed ATL and 38 age-, sex-, and screen-matched HTLV-I–positive controls in the Miyazaki Cohort Study. After accounting for matching factors, Ably level was slightly, but not significantly, higher among cases than among controls (P = .13). Anti–HTLV-I (odds ratio [OR] = 1.6 per twofold dilution; 95% confidence interval [CI] 0.94, 3.8) was associated with ATL diagnosis, but antibody to Tax regulatory protein (anti-Tax) was not (OR = 0.78; 95% CI 0.26, 1.7). Anti-Tax level was low for all ATL cases for up to 10 years preceding their diagnosis, independent of the level of anti–HTLV-I titer. HTLV-I carriers with a higher anti–HTLV-I titer and a lower anti-Tax reactivity may be at greatest risk of ATL.
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.
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