Angiogenic and HIV-inhibitory functions of KSHV-encoded chemokines
Angiogenic and HIV-inhibitory functions of KSHV-encoded chemokines
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DOI：
10.1126/science.278.5336.290
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发表时间：
1997-10-10
期刊：
影响因子：
56.9
通讯作者：
Weiss, RA
中科院分区：
文献类型：
--
作者：
Boshoff, C;Endo, Y;Weiss, RA
卡波西肉瘤相关疱疹病毒（KSHV或HHV-8）编码趋化因子样蛋白（vMIP-I和VMIP-II），在已知的人类疱疹病毒中是独特的。VMIP-II显示出阻断人类免疫缺陷病毒1型（HIV-1）对表达CCR 3的CD 4阳性细胞系的感染，并且在较小程度上阻断对表达CCR 5的细胞系的感染，而vMIP-I和VMIP-II均部分抑制外周血单核细胞的HIV感染。与嗜酸性粒细胞趋化因子类似，VMIP-II通过CCR 3激活并化学吸引人嗜酸性粒细胞。vMIP-Ⅰ和VMIP-Ⅱ，而不是细胞MIP-1 α或RANTES，在绒毛膜尿囊试验中具有高度的血管生成性，表明在卡波西肉瘤中可能具有致病作用。
Unique among known human herpesviruses, Kaposi's sarcoma-associated herpesvirus (KSHV or HHV-8) encodes chemokine-like proteins (vMIP-I and VMIP-II). VMIP-II was shown to block infection of human immunodeficiency virus-type 1 (HIV-1) on a CD4-positive cell line expressing CCR3 and to a lesser extent on one expressing CCR5, whereas both vMIP-I and VMIP-II partially inhibited HIV infection of peripheral blood mononuclear cells. Like eotaxin, VMIP-II activated and chemoattracted human eosinophils by way of CCR3. vMIP-I and VMIP-II, but not cellular MIP-1 alpha or RANTES, were highly angiogenic in the chorioallantoic assay, suggesting a possible pathogenic role in Kaposi's sarcoma.