We estimated the contribution of asymptomatic and clinical infections to *R*_{0} (the basic reproductive number) under equilibrium prevalence by adapting a previously published trypanosomiasis transmission model [11]. Consistent with empirical data showing no domestic or wildlife reservoir, we removed the nonhuman-animal contribution to *R*_{0} and instead allowed for a polymorphic human population in which a fraction (*f*) of the population develop clinical infections when infected (population I), with the remainder (1–*f*) developing asymptomatic infections (population II). This leads to , where *i**_{v} is the infected tsetse prevalence, *I*_{I}* is the number of clinical infections present at equilibrium, *I*_{II}* is the number of asymptomatic infections at equilibrium, and *N* is the total human population size. We simulated this equation with epidemiologic and demographic surveys from the Forécariah focus in Guinea. Specifically, there were 13 clinical infections and 16 suspected asymptomatic infections identified during the survey. Of the suspected asymptomatic individuals, one-third tested negative on follow-up using the TL test and one-third developed symptoms [10]. Therefore, we set the number of asymptomatic infections as *I*_{II}* = 16*X* (where *X*~Uniform(1/3,1)) and the number of clinical infections as *I*_{I}* = 29–*I*_{II}*. The total population size was set as *N* = 10,837, based on 7,586 surveyed individuals and a survey completeness of 70%. These results suggest that transmission is not sustainable (*R*_{0} < 1) when nearly all infections are either clinical (*f* > 0.98) or asymptomatic infections (*f* < 0.02). The shaded areas represent 95% predictive intervals when the number of asymptomatic and clinical infections were sampled 1,000 times. HAT, human African trypanosomiasis; TL, trypanolysis.