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Title: [T-lymphocyte immune in HIV-infected people and AIDS patients in China].
Author: Li T, Qiu Z, Wang A, Sheng R.
Journal: Zhonghua Yi Xue Za Zhi; 2002 Oct 25; 82(20):1391-5. PubMed ID: 12509921.
Abstract:
OBJECTIVE: To study the T-lymphocyte immune alterations and its clinical significance in HIV-infected persons and AIDS patients in China. METHODS: Peripheral blood samples were collected from 13 HIV-infected persons, 27 AIDS patients, and 51 healthy blood donors (controls) and then labeled with monoclonal antibodies. Flow cytometry was used to detect the count of CD4(+) T-lymphocytes, CD8(+) T-lymphocytes, and its different subsets including the naive cell subset (CD4(+) CD45RA(+) CD62L(+)), activated cell subsets (CD4(+) HLA-DR(+), CD8(+) HLA-DR(+), CD8(+) CD38(+)), functional cell subsets (CD4(+) CD28(+)), and apoptotic cell subsets (CD4(+) CD95(+), CD8(+) CD95(+)). The plasma HIV loading was also detected. RESULTS: The CD4(+) cell count was (849 +/- 288) x 10(6)/L in the control group, significantly higher than that in HIV-infected person group [(437 +/- 184) x 10(6)/L, P < 0.01], and that in AIDS patient group [(50 +/- 51) x 10(6)/L, P < 0.01]. The CD8(+) cell count was (579 +/- 175) x 10(6)/L in the control group, significantly lower than that in HIV-infected person group [(1 031 +/- 345) x 10(6)/L, P < 0.05], and not significantly different from that in AIDS patient group (535 +/- 338) x 10(6)/L, with a significant difference between the HIV-infected person group and AIDS patient group (P < 0.05). The percentage of CD4(+) CD45RA(+) CD62L(+) were 43.0% +/- 11.4% in the control group, not significantly different from that in HIV-infected person group (44.2% +/- 12.8%), but significantly higher than that in AIDS patient group (24.8% +/- 15.5%, P < 0.05). The CD4(+) CD45RA(+) CD62L(+) cell count was (368 +/- 162) x 10(6)/L in the control group, significantly higher than those in HIV-infected person group [(185 +/- 134) x 10(6)/L] and in AIDS patient group [(18 +/- 20) x 10(6)/L, both P < 0.01] with a significant difference between the HIV-infected person group and AIDS patient group (P < 0.01). The percentage of CD4(+) CD28(+) was 93.1% +/- 8.1% in the control group, significantly higher than those in HIV-infected person group (62.6% +/- 28.2%) and in AIDS patient group (56.9% +/- 26.4%) with a significant difference between any two groups (all P < 0.01). The percentages of CD4(+) HLA-DR(+), CD8(+) HLA-DR(+), and CD8(+) CD38(+) in the AIDS patient group were higher than those in the HIV-infected person group and control group with significant difference between any two groups (all P < 0.01). The percentages of CD4(+) CD95(+) and CD8(+) CD95(+) in the AIDS patient group were not significantly different from that in control group, but significantly higher than that in HIV-infected person group (P < 0.05). The plasma HIV loading was 3.74 +/- 0.78 lg copies/ml in the HIV-infected person group and was 4.94 +/- 0.68 lg copies/ml in AIDS patient group (P < 0.05), and the count of CD4(+) cells and CD4(+) CD45RA(+) CD62L(+) cells were obviously negatively correlated with the plasma HIV loading (r = -0.796, r = -0.750, P < 0.01). CONCLUSION: The T-lymphocyte immune dysfunction occurring in HIV-infected persons and AIDS patients in China involves not only the number, but also the function and activation of T-lymphocytes. Synthetical analysis of the alterations of different T cell subsets reflects the immune deficiency and severity of disease more comprehensively than pure examination of the amounts of CD4(+) and CD8(+) cells.

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