BackgroundMost HIV-infected persons are cytomegalovirus (CMV) seropositive and retain latent virus that can be reactivated by immune activation. Their T cell populations express markers reflecting a late stage of differentiation, but the contributions of HIV and CMV to this profile are unclear. We investigated the immunological “footprint” of CMV in HIV patients who had a history of extreme immunodeficiency but were now stable on antiretroviral therapy (ART).ResultsTwenty CMV seropositive HIV patients >50 years old with nadir CD4 T-cell counts <200 cells/μl were studied after >12 years on ART. 16 CMV seropositive and 9 CMV seronegative healthy controls were included. CMV antibody titres were higher in HIV patients than controls (P < 0.001-0.003). Levels of soluble B-cell activating factor (sBAFF) were elevated in patients (P = 0.002) and correlated with levels of CMV antibodies (P = 0.03-0.002), with no clear relationship in controls. CD8 T-cell IFNγ responses to the IE1 peptide (VLE) remained elevated in HIV patients (P = 0.005). The CD57+CD45RA+CD27− phenotype of CD8 T-cells correlated with age (r = 0.60, P = 0.006), antibodies against CMV IE1 protein (r = 0.44, P = 0.06) and CD4 T-cell IFNγ response to CMV lysate (r = 0.45, P = 0.05).ConclusionsHumoral and T-cell responses to CMV remained elevated in HIV patients after >12 years on ART. Age and presence of CMV disease influenced CD8 T-cell phenotypes. Elevated levels of sBAFF may be a consequence of HIV disease and contribute to high titres of CMV antibody.Electronic supplementary materialThe online version of this article (doi:10.1186/s12979-015-0041-0) contains supplementary material, which is available to authorized users.

BackgroundWhilst ART corrects many effects of HIV disease, T cell populations retain features of accelerated immunological aging.MethodsHere we analyse phenotypic changes to natural killer (NK) cells in HIV patients who began ART with <200 CD4 T-cells/µl and maintained virological control for 12–17 years, compared with CMV seropositive and seronegative healthy control donors.ResultsHumoral responses to CMV antigens (lysate, gB, IE-1) remain elevated in the patients (P < 0.0001) despite the long duration of ART. Patient’s NK cells responded poorly to K562 cells when assessed by CD107a and IFNγ, but this could not be attributed to CMV as responses were low in CMV-seronegative controls. Moreover HIV (and not CMV) increased expression of CD57 on CD56lo cells.ConclusionsComparisons with published studies suggest that CMV accelerates age-related increases in CD57 expression but levels plateau by 60–70 years of age, so the effect of CMV disappears. In HIV patients the plateau is higher and perhaps reached sooner.Electronic supplementary materialThe online version of this article (doi:10.1186/s12981-015-0080-9) contains supplementary material, which is available to authorized users.

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