DECREASED REACTIVITY TO PPD AMONG HTLV-I CARRIERS IN RELATION TO VIRUS AND HEMATOLOGIC STATUS

Citation
Sl. Welles et al., DECREASED REACTIVITY TO PPD AMONG HTLV-I CARRIERS IN RELATION TO VIRUS AND HEMATOLOGIC STATUS, International journal of cancer, 56(3), 1994, pp. 337-340
Citations number
27
Categorie Soggetti
Oncology
ISSN journal
00207136
Volume
56
Issue
3
Year of publication
1994
Pages
337 - 340
Database
ISI
SICI code
0020-7136(1994)56:3<337:DRTPAH>2.0.ZU;2-8
Abstract
Data on human T-cell lymphotropic-virus-type-I (HTLV-I) status and hem atology from 528 individuals were analyzed for associations with low r eactivity to the purified protein derivative (PPD) of Mycobacterium tu berculosis recall antigen. Subjects were classified as HTLV-I carriers with abnormal lymphocytes (Ably), carries without Ably, and seronegat ives. All carriers had a significant 2.6-fold risk of being low respon ders to PPD compared with the seronegatives, carriers with Ably having the highest relative risk. Carriers with HTLV-I-antibody titer greate r than or equal to 1:256, or with other detectable markers of virus st atus 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, compare d with subjects with high counts. Similarly, subjects with a low monoc yte count had 2.0 times the risk for low reactivity of those with a mo derate 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 delay ed-type hypersensitivity is associated with HTLV-I infection per se, a nd not with viral replication or load. Furthermore, this effect may oc cur in part via changes in the number and function of lymphocytes and monocytes. Such as mechanism may involve altered cytokine production i n carriers and concomitant changes in cell populations involved ind de layed-type hypersensitivity. (C) 1994 Wiley-Liss, Inc.