Lambda Interferon Inhibits Human Immunodeficiency Virus Type 1 Infection of Macrophages
Lambda Interferon Inhibits Human Immunodeficiency Virus Type 1 Infection of Macrophages
复制标题
λ干扰素抑制人类免疫缺陷病毒1型巨噬细胞感染
DOI：
10.1128/jvi.01773-08
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发表时间：
2009-04-15
影响因子：
5.4
通讯作者：
Ho, Wen-Zhe
中科院分区：
文献类型：
--
作者：
Hou, Wei;Wang, Xu;Ho, Wen-Zhe
新发现的 III 型干扰素 (IFN-lambda) 对多种病毒具有抗病毒活性。 We thus examined whether IFN-lambda has the ability to inhibit human immunodeficiency virus type 1 (HIV-1) infection of blood monocyte-derived macrophages that expressed IFN-lambda receptors.当将 IFN-lambda 1 和 IFN-lambda 2 添加到巨噬细胞培养物中时，均可抑制 HIV-1 感染和复制。 This IFN-lambda-mediated antiHIV-1 activity is broad, as IFN-lambda could inhibit infection by both laboratory-adapted and clinical strains of HIV-1. Investigations of the mechanism(s) responsible for the IFN-lambda action showed that although IFN-lambda had little effect on HIV-1 entry coreceptor CCR5 expression, IFN-lambda induced the expression of CC chemokines, the ligands for CCR5.此外，IFN-lambda 上调 I 型 IFN 和 APOBEC3G/3F（新发现的抗 HIV-1 细胞因子）的细胞内表达。 These data provide direct and compelling evidence that IFN-lambda, through both extracellular and intracellular antiviral mechanisms, inhibits HIV-1 replication in macrophages.这些发现表明IFN-lambda可能在治疗HIV-1感染中具有治疗价值。
The newly identified type III interferon (IFN-lambda) has antiviral activity against a broad spectrum of viruses. We thus examined whether IFN-lambda has the ability to inhibit human immunodeficiency virus type 1 (HIV-1) infection of blood monocyte-derived macrophages that expressed IFN-lambda receptors. Both IFN-lambda 1 and IFN-lambda 2, when added to macrophage cultures, inhibited HIV-1 infection and replication. This IFN-lambda-mediated antiHIV-1 activity is broad, as IFN-lambda could inhibit infection by both laboratory-adapted and clinical strains of HIV-1. Investigations of the mechanism(s) responsible for the IFN-lambda action showed that although IFN-lambda had little effect on HIV-1 entry coreceptor CCR5 expression, IFN-lambda induced the expression of CC chemokines, the ligands for CCR5. In addition, IFN-lambda upregulated intracellular expression of type I IFNs and APOBEC3G/3F, the newly identified anti-HIV-1 cellular factors. These data provide direct and compelling evidence that IFN-lambda, through both extracellular and intracellular antiviral mechanisms, inhibits HIV-1 replication in macrophages. These findings indicate that IFN-lambda may have therapeutic value in the treatment of HIV-1 infection.