1,25-二羟维生素D3上调U937阴性克隆中功能性CXCR4人免疫缺陷病毒1型共受体：病毒复制的非核因子κB依赖性增强。
1,25-Dihydroxyvitamin D3 upregulates functional CXCR4 human immunodeficiency virus type 1 coreceptors in U937 minus clones: NF-kappaB-independent enhancement of viral replication.
作者信息
Biswas P, Mengozzi M, Mantelli B, Delfanti F, Brambilla A, Vicenzi E, Poli G
机构信息
AIDS Immunopathogenesis Unit, DIBIT, Milan, Italy.
出版信息
J Virol. 1998 Oct;72(10):8380-3. doi: 10.1128/JVI.72.10.8380-8383.1998.
Abstract
U937 cell clones which sustain efficient or poor replication of human immunodeficiency virus type 1 (HIV-1) (referred to herein as plus clones and minus clones, respectively) have been previously described. 1,25-Dihydroxyvitamin D3 (vitamin D3) potently induced HIV-1 replication and proviral DNA accumulation in minus clones but not in plus clones. Vitamin D3 did not induce NF-kappaB activation but selectively upregulated CXCR4 expression in minus clones. The CXCR4 ligand stromal-cell derived factor-1 induced Ca2+ fluxes and inhibited both constitutive and vitamin D3-enhanced HIV replication in minus clones.
摘要
先前已描述了支持1型人类免疫缺陷病毒（HIV-1）高效或低效复制的U937细胞克隆（本文分别称为正克隆和负克隆）。1,25-二羟基维生素D3（维生素D3）在负克隆中强力诱导HIV-1复制和前病毒DNA积累，但在正克隆中则不然。维生素D3不诱导核因子κB激活，但在负克隆中选择性上调CXCR4表达。CXCR4配体基质细胞衍生因子-1在负克隆中诱导钙离子通量并抑制组成型和维生素D3增强的HIV复制。
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