Early and persistent human immunodeficiency virus type 1 (HIV-1)-specific T helper dysfunction in blood and lymph nodes following acute HIV-1 infection.

Early and persistent human immunodeficiency virus type 1 (HIV-1)-specific T helper dysfunction in blood and lymph nodes following acute HIV-1 infection.
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急性 HIV-1 感染后,血液和淋巴结中出现早期和持续的人类免疫缺陷病毒 1 型 (HIV-1) 特异性 T 辅助细胞功能障碍。

DOI:
10.1086/314868
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发表时间:
1999
期刊:
The Journal of infectious diseases.
影响因子:
--
通讯作者:
McElrath,MJ
McElrath,MJ
中科院分区:
--
文献类型:
--
作者:
Musey,LK;Krieger,JN;Hughes,JP;Schacker,TW;Corey,L;McElrath,MJ

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没有有效的抗逆转录病毒治疗,大多数人类免疫缺陷病毒1型(HIV-1)感染者经历CD4+T细胞进行性下降和T辅助功能损伤。目前尚不清楚感染后多久发生T细胞功能障碍。在39例未经治疗的急性HIV-1感染患者的血液和淋巴组织中检测T辅助反应。在前3个月内,淋巴细胞对有丝分裂原、召回抗原和HIV-1抗原的增殖反应受损。6-9个月后,对植物血凝素和召回抗原的反应有所改善。然而,在2年的感染过程中,hiv -1特异性淋巴细胞增殖在很大程度上无法检测到,在评估淋巴样细胞时结果相似。罕见的HIV-1特异性反应患者的血浆HIV-1 RNA水平明显低于无反应患者。这些结果表明,辅助性T细胞功能障碍发生在HIV-1获得后早期,未经治疗的个体很少能恢复hiv特异性辅助性反应;这些发现为早期治疗干预提供了支持,以防止T辅助细胞的破坏和进一步损害。
Without potent antiretroviral therapy, most human immunodeficiency virus type 1 (HIV-1)—infected persons experience a progressive decline in CD4+T cells and impairment in T helper function. It is unclear how soon after infection T cell dysfunction occurs. T helper responses were examined in blood and lymphoid tissue of 39 untreated patients with acute HIV-1 infection. Within the first 3 months, lymphoproliferative responses to mitogen, recall antigens, and HIV-1 antigens were impaired. After 6–9 months, responses to phytohemagglutinin and recall antigens improved. However, HIV-1—specific lymphoproliferation remained largely undetectable throughout 2 years of infection, and results were similar upon evaluation of lymphoid cells. Rare patients with HIV-1—specific responses had significantly lower plasma HIV-1 RNA levels than did nonresponders. These results indicate that T helper dysfunction occurs early after HIV-1 acquisition and that untreated individuals rarely recover HIV-specific helper responses; these findings lend support for early therapeutic intervention to prevent the destruction and further impairment of the T helper cells.