InHIV-1-infected patients, plasma levels of HIV-1 RNA are inversely correlated with IFN-α responsiveness of whole-blood cultures to sendai virus

被引:7
作者
Chehadeh, W
Chabou, S
Fontier, C
Alm, G
Lion, G
Bocket, L
Mouton, Y
Wattré, P
Hober, D [1 ]
机构
[1] Ctr Hosp Reg & Univ Lille, Inst Gernez Rieux, Virol Lab, F-59037 Lille, France
[2] Ctr Hosp, Valenciennes, France
[3] Biomed Ctr, Dept Vet Immunol, Uppsala, Sweden
[4] Ctr Hosp, Serv Reg & Univ Malad Infect, Tourcoing, France
关键词
IFN-alpha; HIV-1; RNA; DELFIA; sendai virus; MDBK cells;
D O I
10.1016/S1386-6532(99)00088-8
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Background: A diminished or totally blocked IFN-alpha production in cells from HIV-l-infected patients has been reported. Objective: To investigate the relationship between the decreased in vitro production of IFN-alpha and the plasma level of HIV-1 RNA. Study design: Whole blood samples of 39 healthy subjects and 44 HIV-l-infected patients were incubated in the presence of Sendai virus for 24 h. IFN-alpha contained in supernatants was assayed by using an immunochemical method (DELFIA) and by using an antiviral assay. Plasma HIV-1 RNA was measured by the Amplicor HIV-I monitor test. Results: The levels of IFN-alpha obtained were significantly lower in cultures from HIV-I infected patients than in control subjects (P<0.0001). The antiviral activity in supernatants of Sendai virus-activated whole-blood cultures, assayed by protection of MDBK cells against vesicular stomatitis virus (VSV) was significantly lower in cultures from HIV-I infected patients than in corresponding controls (P < 0.0001). IFN-alpha values determined by DELFIA and those determined by bioassay were significantly correlated. In vitro production of IFN-alpha by whole-blood cultures correlated well with the plasma levels of HIV-1 RNA (P < 0.001). Conclusions: In HIV-infected patients an increased rate of HIV-1 replication is associated with reduced responsiveness to induction of IFN-alpha by indicator virus, suggesting that HIV-1 replication causes impaired production of IFN-alpha by blood cells or vice-versa. (C) 2000 Elsevier Science Ireland Ltd. AU rights reserved.
引用
收藏
页码:123 / 128
页数:6
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