ABSTRACT
Objective To investigate the changes in the percentages of CD4+T lymphocyte subsets and the homeostasis of T lymphocytes among MSM ( men who have sex with men) population with different stages of HIV-1 infection. Methods A total of 166 untreated MSM with HIV infection were enrolled and di-vided into three groups including early HIV infection (EHI, n=38) , HIV (n=94) and AIDS (n=34) groups. Sixty-two MSM negative for anti-HIV antibody were selected as healthy controls. Blood samples were collected into EDTA tubes and detected to analyze the changes in the distribution of CD4+ T cells and CD8+T lymphocyte subsets ( CD4+ CD45RA+, CD8+ CD28+, CD4+ CD25+ CD127-) and the percentages of activated (CD38, HLA-DR) and apoptotic cells (CD95) with disease progression by flow cytometry. Re-sults The expression of CD4+CD45RA+ T lymphocytes gradually decreased with the progression of AIDS. The percentage of CD4+CD45RA+ T lymphocytes in HIV group was lower than that of the control group, but higher than that of the AIDS group (P=0. 015, P=0. 000). No significant difference was found between the EHI and the control groups (P>0. 05). CD8+CD28+T cells were significantly reduced in the EHI group and remained at a low level with disease progression. No significant difference in the proportion of CD4+CD25+CD127- T cells was observed among all groups (P>0. 05). The percentage of CD4+CD38+HLA-DR+T cells increased gradually and the highest level was detected in the AIDS group, followed by those in the HIV, EHI and control groups (P<0. 01). The percentages of CD8+CD38+, CD8+HLA-DR+, CD8+ CD38+HLA-DR+and CD8+CD95+T cells in the EHI, HIV and AIDS groups were significantly higher than those in the control group (P<0. 01), but there was no significant difference among the former three groups (P>0. 05). Con-clusion HIV infection caused the changes in the numbers and functions of T lymphocyte subsets and accel-erated the activation and apoptosis of T lymphocytes, which aggravated the T lymphocyte immune dysfunction even further. A comprehensive analysis of the alterations in different T cell subsets would be conducive to re-flect the immune deficiency and the severity of disease. CD4+ and CD8+ T cells were activated in the early stage of HIV infection, which indicated that studying the immune response during that stage might help to understand their roles in disease progression.
ABSTRACT
Objective To study the alternations of regulatory T cells in early HIV infected patients and its association with disease progression.Methods Fifty-one untreated HIV infected patients were enrolled and divided into 3 groups according to their infection time and CD+4 T cell levels(30 early HIV infected patients,15 typical progressors,6 AIDS patients).Twenty normal controls were enrolled.There were no significant differences between the age and sex among four groups.Blood was drawn by venipuncture from each subject in EDTA tubes and the levels of CD+4 CD+25 Foxp3 + regulatory T cells were detected by FACSAria flow-cytometry.Spearman correlation was used to detect association between CD+4 CD+25 Foxp3 + regulatory T cells and the absolute CD+4 T cells,viral load and activation of T cells.Results The levels of CD+4 CD+25Foxp3+ regulatory T cells showed the tendency of increasing tendency from normal control to early HIV infected patients,asymptomatic HIV infected patients and AIDS patients.Early HIV infected patients was significantly lower than that in AIDS group [3.79(2.11 - 5.43) % vs 8.09(4.90 - 8.90) %,Z = - 2.29,P = 0.022].The levels of CD+4 CD+25 Foxp3 + Treg cells were associated with viral set point(r = 0.479,P =0.038) and inversely associated with CD+4 T cells(r = -0.455,P =0.011) and closely associated with HLA-DR expression on CD+3 T cells(r = 0.533,P = 0.002).Conclusions The ratio of CD+4 CD+25 Foxp3 +regulatory T cells of early HIV infected patients was significantly increased and associated with viral set point and CD+4 T cell counts,which indicate that alternation of regulatory T cell may be an important factor contributing to the disease progression in early HIV infection.