During infection of a mammalian host, African trypanosomes are in cons
tant contact with the host's immune system. These protozoan parasites
are infamous for their ability to evade the immune responses by period
ically switching their major variant surface glycoprotein (VSG), a phe
nomenon called antigenic variation. Antigenic variation, however, is l
ikely to be only one of several mechanisms enabling these organisms to
thrive in the face of the immune defenses. The ability to grow in hig
h levels of interferon-gamma (IFN-gamma) and to avoid complement-media
ted destruction may also facilitate the parasite's survival. In this r
eview we summarize (i) the activation of trypanosome genes for three d
ifferent VSGs during antigenic variation, (ii) the secretion of a tryp
anosome protein that induces host CD8(+) T cells to produce IFN-gamma,
and (iii) the evidence for trypansome protein similar to a surface pr
otease of Leishmania that plays a role in resistance to complement-med
iated lysis. (C) 1998 Francqui Foundation. Published by Elsevier Scien
ce B.V. All rights reserved.