Decreased reactivity to PPD among HTLV-I carriers in relation to virus and hematologic status.

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.