Infectivity of Trypanosoma brucei rhodesiense to humans is due to its resis
tance to a lytic factor present in human serum. In the ETat 1 strain this c
haracter was associated with antigenic variation, since expression of the E
Tat 1.10 variant surface glycoprotein was required to generate resistant (R
) clones. In addition, in this strain transcription of a gene termed SRA wa
s detected in R clones only. We show that the ETat 1.10 expression site is
the one selectively transcribed in R variants. This expression site contain
s SRA as an expression site-associated gene (ESAG) and is characterized by
the deletion of several ESAGs. Transfection of SRA into T.b. brucei was suf
ficient to confer resistance to human serum, identifying this gene as one o
f those responsible for T.b. rhodesiense adaptation to humans.