Recent developments in parasite immune evasion and exploitation
are
reviewed with special reference to the papers
presented in this volume. Parasites, broadly defined, of animals with good
immune responses have evolved many strategies
that adapt them to survive and reproduce. These strategies may be passive,
or may involve active intervention with host
immune regulation, and can be categorized as immune evasion, immune exploitation
and molecular piracy. The concept
of immune evasion began with Paul Ehrlich's demonstration of antigenic
variation in African trypanosomes and was
reinforced by later ideas on molecular mimicry. Molecular mimicry is updated
in the light of recent discoveries about
degeneracy and plasticity of TCR/MHC-peptide recognition. Possible
connections between two of its postulated consequences, evasion and autoimmunity,
are discussed. Another putative consequence of molecular mimicry, host
antigenic
polymorphism, is also updated. The concept of exploitation of host immune
responses by parasites has been reinforced
by new data on its first known examples, especially the immune dependence
of
schistosome egg excretion. Newer examples
include use of host cytokines as parasite growth factors, virokines,
viroreceptors and helminth pseudocytokines. Finally,
questions of host gene capture by viruses and possible horizontal gene
transfer
between host and parasite mediated by
retroviruses are examined. The latter is compared with molecular conservation
as a source of molecular mimicry and other aspects of host–parasite
coevolution.