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FSL-1 a bacterial-derived toll-like receptor 2/6 agonist enhances resistance to experimental HSV-2 infection

机译:FSL-1是细菌衍生的Toll样受体2/6激动剂可增强对实验性HSV-2感染的抵抗力

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摘要

BackgroundHerpes simplex virus type 2 (HSV-2) is a leading cause of genital ulceration that can predispose individuals to an increased risk of acquiring other sexually transmitted infections. There are no approved HSV-2 vaccines and current suppressive therapies require daily compound administration that does not prevent all recurrences. A promising experimental strategy is the use of toll-like receptor (TLR) agonists to induce an innate immune response that provides resistance to HSV-2 infection. Previous studies showed that anti-herpetic activity varied based on origin of the agonists and activation of different TLR indicating that activity likely occurs through elaboration of a specific innate immune response. To test the hypothesis, we evaluated the ability of a bacterial-derived TLR2/6 agonist (FSL-1) to increase resistance to experimental genital HSV-2 infection.
机译:背景2型单纯疱疹病毒(HSV-2)是导致生殖器溃疡的主要原因,它可能使个体更容易患上其他性传播感染。目前尚无批准的HSV-2疫苗,目前的抑制疗法要求每天服用化合物,不能预防所有复发。一种有前途的实验策略是使用Toll样受体(TLR)激动剂来诱导先天免疫应答,从而提供对HSV-2感染的抵抗力。先前的研究表明,抗疱疹活性根据激动剂的来源和不同TLR的激活而变化,这表明该活性可能是通过阐述特定的先天免疫应答而发生的。为了验证该假设,我们评估了细菌来源的TLR2 / 6激动剂(FSL-1)增强对实验生殖器HSV-2感染的抵抗力的能力。

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