Decreased T cell apoptosis and T cell recovery during highly active antiretroviral therapy (HAART).
Decreased T cell apoptosis and T cell recovery during highly active antiretroviral therapy (HAART).
复制标题
高活性抗逆转录病毒治疗 (HAART) 期间 T 细胞凋亡和 T 细胞恢复减少。
作者：
F. Ensoli;V. Fiorelli;C. Alario;M. De Cristofaro;D. Santini Muratori;A. Novi;M. Cunsolo;F. Mazzetta;A. Giovannetti;B. Mollicone;E. Pinter;F. Aiuti
T cell apoptosis represents a common mechanism of T cell depletion in HIV-1-infected individuals reflecting maturational and functional T cell abnormalities either directly or indirectly induced by the virus. In the present study, the effects of highly active antiretroviral therapy (HAART) on the spontaneous apoptosis of distinct T cell subsets were investigated during a 6-month follow-up in a cohort of HIV-1-infected individuals with CD4(+) cell counts between 100 and 500 cells/microliter and plasma HIV-1 RNA levels >/=10, 000 copies/ml. We determined that the rapid and sustained increase of both naive (CD45RA(+)CD62L(+)) and memory (CD45R0(+) and CD45RA(+)/CD62L(-)) CD4(+) and, to as lesser extent, CD8(+) T cells in peripheral blood was associated with a significant decrease of apoptotic CD4(+) and CD8(+) as well as CD3(+)CD4(-)CD8(-) T cells. Among CD4(+) lymphocytes, at enrollment, the highest frequency of apoptotic cells was observed within the memory compartment, as defined by CD45R0 expression. During HAART, however, the frequency of CD4(+)CD45R0(+) apoptotic T cells progressively decreased in association with a significant downregulation of surface activation markers that indicated decreased levels of systemic immune stimulation. These results indicate that effective viral suppression can contribute to progressive normalization of maturational and functional T cell abnormalities responsible for the high levels of T cell apoptosis in HIV-1-infected individuals. This, in turn, may contribute to a reduced rate of T cell loss and immune reconstitution during HAART.
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影响因子：
158.5
作者：
Gulick, RM;Mellors, JW;Chodakewitz, JA
通讯作者：
Chodakewitz, JA
影响因子：
4.4
作者：
S. Patel;M. Wacholtz;A. Duby;D. Thiele;P. Lipsky
通讯作者：
S. Patel;M. Wacholtz;A. Duby;D. Thiele;P. Lipsky
影响因子：
6.4
作者：
Karavellas, MP;Plummer, DJ;Freeman, WR
通讯作者：
Freeman, WR
影响因子：
4.4
作者：
T. McCloskey;M. Ott;Eugene Tribble;Shabbir A. Khan;S. Teichberg;M. Paul;S. Pahwa;E. Verdin;N. Chirmule;N. Chirmule;N. Chirmule
通讯作者：
T. McCloskey;M. Ott;Eugene Tribble;Shabbir A. Khan;S. Teichberg;M. Paul;S. Pahwa;E. Verdin;N. Chirmule;N. Chirmule;N. Chirmule
HIV 1 型 CD4 T 细胞的感染关键取决于包膜糖蛋白 120 V3 结构域中的碱性氨基酸残基。
影响因子：
1.5
作者：
Okada,T;Patterson,BK;Otto,PA;Gurney,ME
通讯作者：
Gurney,ME