Foxall, R. B.Soares, R. S.Albuquerque, A. S.Cortesão, A. C.Victorino, R. M.Sousa, A. E.2015-02-032015-02-032008Clinical Immunology (2008) 127, 158–1671521-6616http://dx.doi.org/10.1016/j.clim.2008.01.008http://hdl.handle.net/10451/15878© 2008 Elsevier Inc. All rights reserved.The ability to maintain the CD4-memory pool is currently considered one of the main determinants of AIDS progression. Like HIV-1, HIV-2 infection is characterized by progressive hyper-immune activation, yet it is associated with slower rates of CD4-loss and reduced viremia irrespective of disease stage. In contrast to HIV-1, we observed an increased proportion of CD4(+) T-cells expressing CD25 in HIV-2 infected individuals, independent of the degree of CD4-depletion and levels of immune activation. This was due to CD4(+) T-cells expressing an intermediate intensity of CD25, characterized by an increased ability to produce IL-2 and a lack of other regulatory markers. This expansion, unique to HIV-2 seropositive individuals, may relate to an improved ability to replenish their CD4-memory pool, and thus to the better prognosis that characterizes HIV-2 infection. Identification of the underlying mechanisms regulating this population in HIV-1 and HIV-2 infections may provide a rational for novel therapeutic strategies.engHIV/AIDSHIV-2CD25T-cell subsetsImmune activationjournal article