Research questions
Questions
We aim to answer three main questions:
1) Why does a minority of HTLV-I-infected people develop a chronic inflammatory disease such as HAM/TSP, whereas the great majority remain asymptomatic carriers of the virus?
2) How does HTLV-I spread and persist in the host in the face of a strong cell-mediated immune response?
3) What is the genetic, functional and molecular basis of the efficiency of the cellular immune response to a virus?
To answer these questions we have studied host and virus genetic variation, lymphocyte phenotype and function, and the dynamics of HTLV-I replication and the cellular immune response. We have used techniques in molecular genetics, cellular immunology, cell biology, gene expression microarrays, proteomics and mathematical biology.
Apart from its intrinsic interest and its importance in tropical and subtropical regions, HTLV-I has become an excellent model system to study the immune control of a persistent virus, for two chief reasons. First, the virus reaches a high and stable concentration ('load') in most infected people, but this concentration can differ by more than 1000-fold between individuals. Second, the virus exists in equilibrium with a highly activated immune response: the virus persistently attempts to replicate, and the immune system restricts the spread of the virus through the body.
