Genetic control and dynamics of the cellular immune response to the human T-cell leukaemia virus, HTLV-I.
About 1% of people infected with the human T-cell leukaemia virus, type 1 (HTLV-I) develop a disabling chronic inflammatory disease of the central nervous system known as HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Patients with HAM/TSP have a vigorous immune response to HTLV-I, and it has been widely suggested that this immune response, particularly the HTLV-I-specific cytotoxic T-lymphocyte (CTL) response, causes the tissue damage that is seen in HAM/TSP. In this paper we summarize recent evidence that a strong CTL response to HTLV-I does in fact protect against HAM/TSP by reducing the proviral load of HTLV-I. We conclude that HTLV-I is persistently replicating at a high level, despite the relative constancy of its genome sequence. These results imply that antiretroviral drugs could reduce the risk of HAM/TSP by reducing the viral load, and that an effective anti-HTLV-I vaccine should elicit a strong CTL response to the virus. The dynamic nature of the infection also has implications for the epidemiology and the evolution of HTLV-I.
Bangham
C R
CR
Department of Immunology, Imperial College School of Medicine, London, UK. c.bangham@ic.ac.uk
Hall
S E
SE
Jeffery
K J
KJ
Vine
A M
AM
Witkover
A
A
Nowak
M A
MA
Wodarz
D
D
Usuku
K
K
Osame
M
M
D015368:Human T-lymphotropic virus 1 / Q000235:genetics* / Q000276:immunology* / Q000502:physiology; D006801:Humans; D015493:Paraparesis, Tropical Spastic / Q000453:epidemiology / Q000276:immunology*; D012307:Risk Factors; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*; D019562:Viral Load; D014779:Virus Replication