HIV type 1 V3 peptide constructs act differently on HIV type 1 infection of peripheral blood lymphocytes and macrophages

被引:9
作者
Benjouad, A
Seddiki, N
Ylisastigui, L
Gluckman, JC
机构
[1] FAC SCI RABAT,BIOCHIM LAB,RABAT,MOROCCO
[2] FAC MED,ECOLE PRAT HAUTES ETUD,LAB IMMUNOL CELLULAIRE,F-75651 PARIS 13,FRANCE
[3] UNIV PARIS NORD,FAC MED LEONARD DE VINCI,BIOL CELLULAIRE LAB,BOBIGNY,FRANCE
关键词
D O I
10.1089/aid.1997.13.219
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We have previously shown that a multibranched peptide construct derived from the tip of the B clade V3 loop consensus sequence (MPBC1: [GPGRAF]8-[K]4-[K]2-K-beta A-OH), but not V3 monomer peptides, inhibit human immunodeficiency virus type 1 (HIV-1) infection and syncytium formation of CD4(+) T cells from immortalized lines. Here, we show that MBPC1 attaches to normal peripheral blood lymphocytes (PBLS) and monocytes but not to erythrocytes. While treatment with 5 mu M MBPC1 had no significant antiviral effect on HIV-1(Ba-L) infection of monocyte-derived macrophages as assessed by p24 production in culture supernatants, this dose inhibited both HIV-1(Ba-L) and HIV-1(LAI) infection of PBLs. Virus production was inhibited up to 90% when MBPC1 was added to PBLs immediately after the virus, and was inhibited about 50% when it was added after 3 days; no effect was noted when it was added 7 days postinfection, MBPC1 did not affect PBL growth or IL-2 receptor and CD4 surface expression level, These observations suggest a selective antiviral effect of MBPC1 on CD4(+) T lymphocytes and they provide additional circumstantial evidence that HIV-1 enters lymphocytes and monocytes by different mechanisms.
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页码:219 / 226
页数:8
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