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细胞因子网络与急性原发性HIV-1感染

Cytokine network and acute primary HIV-1 infection.

作者信息

Sinicco A, Biglino A, Sciandra M, Forno B, Pollono A M, Raiteri R, Gioannini P

机构信息

Institute of Infectious Disease, University of Turin, Italy.

出版信息

AIDS. 1993 Sep;7(9):1167-72. doi: 10.1097/00002030-199309000-00003.

Abstract

OBJECTIVE

To investigate the relationship between cytokine serum levels, peripheral blood lymphocyte subsets and clinical picture in acute primary HIV-1 infection.

PATIENTS AND METHODS

Absolute number/microliters total lymphocytes, CD4+, CD8+ and natural killer (NK) cells, as well as serum levels of soluble CD8 receptor, interleukin (IL)-1 beta, IL-2, IL-4, IL-6, tumour necrosis factor (TNF)-alpha, interferon (IFN)-gamma, beta 2-microglobulin and 5'-neopterin were determined in 15 patients with acute primary HIV-1 infection, 16 asymptomatic HIV-1-seropositive individuals and 18 HIV-1-seronegative individuals at risk for HIV-1 infection.

RESULTS

Acute primary HIV-1 infection was characterized by significant CD4+ lymphocytopenia with low IL-2 serum concentrations, and by high absolute number of circulating CD8+ and NK cells, with elevated serum levels of soluble CD8 receptor, IL-1 beta, IFN-gamma and 5'-neopterin. Follow-up of acute seroconverters showed a significant decrease in NK cell counts and IL-1 beta levels, with an increase of IL-6.

CONCLUSIONS

In acute primary HIV-1 infection, significant alteration of cytokine release, possibly induced by viral antigens, could be responsible for both clinical picture and activation of cytotoxic cells through abnormal mechanisms.

摘要

目的

研究急性原发性HIV-1感染中细胞因子血清水平、外周血淋巴细胞亚群与临床表现之间的关系。

患者与方法

测定了15例急性原发性HIV-1感染患者、16例无症状HIV-1血清学阳性个体以及18例有HIV-1感染风险的HIV-1血清学阴性个体的每微升总淋巴细胞、CD4⁺、CD8⁺和自然杀伤(NK)细胞的绝对数量,以及可溶性CD8受体、白细胞介素(IL)-1β、IL-2、IL-4、IL-6、肿瘤坏死因子(TNF)-α、干扰素(IFN)-γ、β2-微球蛋白和5'-新蝶呤的血清水平。

结果

急性原发性HIV-1感染的特征为CD4⁺淋巴细胞显著减少,IL-2血清浓度降低,循环CD8⁺和NK细胞绝对数量增加,可溶性CD8受体、IL-1β、IFN-γ和5'-新蝶呤血清水平升高。对急性血清转化者的随访显示NK细胞计数和IL-1β水平显著下降,IL-6升高。

结论

在急性原发性HIV-1感染中,细胞因子释放的显著改变可能由病毒抗原诱导,可能通过异常机制导致临床表现和细胞毒性细胞的激活。

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