The cytotoxic T-lymphocyte response to HTLV-I: The main determinant of disease?

被引:39
作者
Bangham, CRM
Kermode, AG
Hall, SE
Daenke, S
机构
[1] SIR CHARLES GAIRDNER HOSP,DEPT NEUROL,NEDLANDS,WA 6009,AUSTRALIA
[2] JOHN RADCLIFFE HOSP,NUFFIELD DEPT CLIN MED,OXFORD OX3 9DU,ENGLAND
来源
SEMINARS IN VIROLOGY | 1996年 / 7卷 / 01期
基金
英国惠康基金;
关键词
CTL; HTLV-I; immune escape; selection; virus load;
D O I
10.1006/smvy.1996.0006
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
There is a powerful, chronically activated cytotoxic T-lymphocyte (CTL) response to the Tax protein of human T-cell leukaemia virus type I (HTLV-I) in most people infected with the virus. The CTL select variant sequences of Tax which escape immune recognition and interfere with recognition of the wild-type protein. This positive selection process is more efficient in healthy HTLV-I carriers than in patients with tropical spastic paraparesis, an inflammatory neurological disease associated with HTLV-I. The mean virus load is more than 10-fold greater in patients with this neurological disease than in healthy carriers of HTLV-I. We conclude that anti-Tax CTL play an important part in limiting the rate of replication of HTLV-I. We suggest that the outcome of infection with HTLV-I is primarily determined by the CTL response of the individual: low CTL responders to HTLV-I develop a high virus load, resulting in widespread chronic activation of T cells. The activated T cells then invade the tissues and cause bystander tissue damage, probably by releasing cytokines and other soluble substances. An efficient CTL response to HTLV-I limits the equilibrium virus load, and so reduces the chance of developing inflammatory disease.
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页码:41 / 48
页数:8
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