Murdoch University Research Repository

Welcome to the Murdoch University Research Repository

The Murdoch University Research Repository is an open access digital collection of research
created by Murdoch University staff, researchers and postgraduate students.

Learn more

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

Bangham, C.R.M., Kermode, A.G., Hall, S.E. and Daenke, S. (1996) The cytotoxic T-lymphocyte response to HTLV-I: the main determinant of disease? Seminars in Virology, 7 (1). pp. 41-48.

Link to Published Version: http://dx.doi.org/10.1006/smvy.1996.0006
*Subscription may be required

Abstract

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.

Item Type: Journal Article
Publisher: Elsevier Inc
Copyright: © 1996 Elsevier Inc
URI: http://researchrepository.murdoch.edu.au/id/eprint/29317
Item Control Page Item Control Page