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首页> 外文期刊>AIDS Research and Human Retroviruses >Transient increase of interferon-stimulated genes and no clinical benefit by chloroquine treatment during acute simian immunodeficiency virus infection of macaques
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Transient increase of interferon-stimulated genes and no clinical benefit by chloroquine treatment during acute simian immunodeficiency virus infection of macaques

机译：猕猴急性猿猴免疫缺陷病毒感染过程中干扰素刺激基因的瞬时增加，氯喹治疗无临床益处

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Simian immunodeficiency virus (SIV) infection leads to AIDS in experimentally infected Rhesus macaques similarly to HIV-infected humans. In contrast, SIV infection of natural hosts is characterized by a down-regulation of innate acute responses to the virus within a few weeks of infection and results in limited pathology. Chloroquine (CQ) has been used in the treatment or prevention of malaria and has recently been shown to cause a decrease of immune activation and CD4 cell loss in HIV-infected individuals treated with antiretroviral therapy. Here, we treated Rhesus macaques with CQ during the acute phase of SIVmac251 infection with the intent to decrease viral-induced immune activation and possibly limit disease progression. Contrary to what was expected, CQ treatment resulted in a temporary increased expression of interferon (IFN)-stimulating genes and it worsened the recovery of CD4 + T cells in the blood. Our findings confirm recent results observed in asymptomatic HIV-infected patients and suggest that CQ does not provide an obvious benefit in the absence of antiretroviral therapy.
机译：猿猴免疫缺陷病毒（SIV）感染在实验感染的恒河猴中与HIV感染的人类相似，导致AIDS。相反，自然宿主的SIV感染的特征是在感染后几周内对病毒的先天急性反应的下调，导致病理状况有限。氯喹（CQ）已用于治疗或预防疟疾，最近已证明可导致接受抗逆转录病毒治疗的HIV感染者体内免疫活化和CD4细胞损失减少。在这里，我们在SIVmac251感染的急性期用CQ治疗猕猴，目的是减少病毒诱导的免疫激活并可能限制疾病进展。与预期相反，CQ处理导致干扰素（IFN）刺激基因的表达暂时增加，并且使血液中CD4 + T细胞的恢复恶化。我们的发现证实了最近在无症状的HIV感染患者中观察到的结果，并表明在没有抗逆转录病毒疗法的情况下CQ不能提供明显的益处。

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