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无论疾病进展如何,HIV-1感染血友病患者对HIV-1 p17和p24抗原的细胞毒性T淋巴细胞(CTL)及抗体反应均下降。一项5年随访研究。

Decline in CTL and antibody responses to HIV-1 p17 and p24 antigens in HIV-1-infected hemophiliacs irrespective of disease progression. A 5-year follow-up study.

作者信息

O'Toole C M, Lowdell M W, Chargelegue D, Colvin B T

机构信息

Department of Medical Microbiology, London Hospital Medical College, England.

出版信息

AIDS Res Hum Retroviruses. 1992 Aug;8(8):1361-8. doi: 10.1089/aid.1992.8.1361.

Abstract

CTL and antibody responses to HIV-1 p17 and p24 antigens were monitored from 1986-1991, in 4 hemophiliacs. The patients had been infected with HIV-1 between 1980 and 1984. Two patients have remained asymptomatic while two progressed to AIDS in 1990. CTL were boosted by culturing with peptides from p17 aa 86-115, or p24 aa 265-279; and aa 270-373 or PHA. Lysis was measured on autologous or allogeneic targets pulsed with peptides or infected with recombinant vaccinia virus carrying HIV-1 gag or influenza A matrix genes. Antibodies to p17 and p24 were tested by ELISA using peptides and by Western blotting. High levels of CTL activity to p17 and p24 antigens could be generated only with lymphocytes from the two asymptomatic patients between 1986 and 1989, but these responses were absent in 1990 and 1991. Antibodies to p17 peptides disappeared in parallel with CTL activity. Antibodies to some p24 peptides also declined but most patients retained activity to others. In all patients a > or = 3-fold increase in CD8+ cell numbers occurred over time and accompanied the decline of CTL and antibody responses. The loss of CTL and p17 antibodies occurred irrespective of whether patients remained asymptomatic or progressed to AIDS in the intervening two years.

摘要

1986年至1991年期间,对4名血友病患者的HIV-1 p17和p24抗原的细胞毒性T淋巴细胞(CTL)及抗体反应进行了监测。这些患者在1980年至1984年期间感染了HIV-1。两名患者一直无症状,而另外两名患者在1990年发展为艾滋病。用p17第86 - 115位氨基酸的肽段、p24第265 - 279位氨基酸的肽段、第270 - 373位氨基酸的肽段或PHA进行培养,可增强CTL反应。采用自体或异体靶细胞,这些靶细胞用肽段脉冲处理或感染携带HIV-1 gag或甲型流感病毒基质基因的重组痘苗病毒后,检测细胞裂解情况。通过使用肽段的酶联免疫吸附测定(ELISA)和蛋白质印迹法检测针对p17和p24的抗体。仅在1986年至1989年期间,从两名无症状患者的淋巴细胞中能够产生高水平的针对p17和p24抗原的CTL活性,但在1990年和1991年这些反应消失了。针对p17肽段的抗体与CTL活性同时消失。针对一些p24肽段的抗体也有所下降,但大多数患者对其他p24肽段仍保持活性。随着时间推移,所有患者的CD8 +细胞数量均出现≥3倍的增加,并伴随着CTL和抗体反应的下降。无论患者在这两年间是保持无症状还是发展为艾滋病,CTL和p17抗体都会丧失。

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