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The levels of apostosis markers in different HIV infected patients groups
Retrovirologyvolume 9, Article number: P20 (2012)
HIV-1 infection is characterized by a progressive loss of CD4+ T cells. The role of apoptotic processes was identified recently, but a limited information is available so far. The aim of this study was to compare levels of apoptosis markers - cytokeratin 18 neoepitope (CK18) and cytochrome C (CC) in different HIV infected patient groups.
There were 69 HIV infected patients enrolled in the study and divided into four groups according to CD4+ T cell count and presence of opportunistic infections (OI): 19 patients with CD4+ T cell count above 200 c/mcl without OI, 15 patients with CD4+ T cell count below 200 c/mcl without OI, 7 patients with CD4+ T cell count above 200 c/mcl with OI, 28 patients with CD4+ T cell count below 200 c/mcl with OI. Opportunistic infections included tuberculosis, cryptococcosis, CMV infection, PCP. The serum levels of cytokeratin 18 neoepitope and cytochrome C were determined. Comparisons between groups were made using paired T- test.
CC levels were not significantly different between groups with CD4+ cell count above and below 200 c/mcl (with opportunistic infections 0,5>p>0,4, without opportunistic infections p=0,5). Levels of CC were not significantly influenced by presence of opportunistic infections (with CD4+ cell count above 200 c/mcl p=0,6, with CD4+ cell count below 200 c/mcl p=0,7). We found significant diference of CK18 levels between group without opportunistic infections and CD4+ cell count above 200 c/mcl (210,58 ±26,98 u/l) and group without opportunistic infections and CD4+ cell count above 200 c/mcl (132,95±14,09 u/l), p=0,02, as well as between group without opportunistic infections and CD4+ cell count below 200 c/mcl (132,95±14,09 u/l) and group with opportunistic infections and CD4+ cell count below 200 c/mcl (174,56±20,83 u/l), 0.02>p>0.01.
The results obtained from our study demonstrate elevation of levels of apoptosis serum markers early in HIV infection which anticipate further decrease of CD4 cell count.
Ilze Eksteina, Valentina Sondore contributed equally to this work.