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Leukemia inhibitor factor (LIF) is thought to play a substantial role in protecting CD4 T cells in lymphoid tissues (LT) from infection by HIV-1.To investigate whether primary HIV-1 infected subjects with sustained virological control (< 1000 HIV-1 RNA copies/ml plasma) post-cessation antiretroviral therapy (ART) had a higher initial LIF response during primary HIV-1 infection (PHI) as compared with those individuals who did not achieve a similar control (> 9000 HIV-1 RNA copies/ml plasma) of HIV-1 replication.Consecutively obtained HIV plasma samples were collected from primary HIV-1 infected subjects. A group of acutely Epstein–Barr virus-infected subjects and a group of HIV-1-seronegative healthy individuals served as controls. All samples were tested by ELISA for LIF and sgp130, the soluble form of LIF's signalling receptor.LIF and sgp130 plasma levels were significantly increased in primary HIV-1-infected subjects as compared with HIV-1-seronegative controls. Peak plasma levels of LIF occurred during the first week of PHI whereas sgp130 peaked between 2 and 4 weeks after the onset of PHI. Furthermore a positive correlation was found between viral load and plasma levels of LIF during PHI. Both LIF and sgp130 plasma concentrations were significantly lower during the viral rebound phase after treatment interruption as compared with the PHI phase.LIF induction occurred in the initial stages of viral dissemination during PHI. It may be a part of the virally induced generalized pro-inflammatory response. LIF levels at PHI did not predict low levels of HIV viraemia after discontinuation of ART. LIF was not increased following ART interruption in this early treated population.