Biological embedding of stress experienced early in life is a mechanism proposed to explain the fitness costs of maternal loss in mammals. This embedding is expected to lead to long-term alterations of the hypothalamic pituitary adrenal (HPA) axis activity. This idea has, however, rarely been tested in wild long-lived animals. We assessed whether, as in humans, maternal loss had short and long-term impacts on orphan wild chimpanzee urinary cortisol levels and diurnal urinary cortisol slopes, both indicative of the HPA axis functioning. Immature orphan chimpanzees who experienced early maternal loss had diurnal cortisol slopes indicative of high activation of the HPA axis and recently orphaned immatures had elevated cortisol levels. However, unlike in humans, the cortisol profiles did not differ between orphan and non-orphan adult male chimpanzees. Our study highlights that long-term alteration of stress physiology related to early life adversity may not be viable in some wild animal populations.