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Modulation of the virus-receptor interaction by mutations in the V5 loop of feline immunodeficiency virus (FIV) following in vivo escape from neutralising antibody

机译:体内逃避中和抗体后猫免疫缺陷病毒(FIV)V5环中的突变对病毒-受体相互作用的调节

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摘要

BackgroundIn the acute phase of infection with feline immunodeficiency virus (FIV), the virus targets activated CD4+ T cells by utilising CD134 (OX40) as a primary attachment receptor and CXCR4 as a co-receptor. The nature of the virus-receptor interaction varies between isolates; strains such as GL8 and CPGammer recognise a "complex" determinant on CD134 formed by cysteine-rich domains (CRDs) 1 and 2 of the molecule while strains such as PPR and B2542 require a more "simple" determinant comprising CRD1 only for infection. These differences in receptor recognition manifest as variations in sensitivity to receptor antagonists. In this study, we ask whether the nature of the virus-receptor interaction evolves in vivo.
机译:背景在猫免疫缺陷病毒(FIV)感染的急性期,该病毒通过利用CD134(OX40)作为主要附着受体和CXCR4作为共受体来靶向活化的CD4 + T细胞。病毒-受体相互作用的性质在分离株之间有所不同。菌株(例如GL8和CPGammer)识别CD134上由分子的富含半胱氨酸的结构域(CRD)1和2形成的“复杂”决定簇,而菌株(例如PPR和B2542)则需要更简单的包含CRD1的决定簇,仅用于感染。受体识别的这些差异表现为对受体拮抗剂敏感性的变化。在这项研究中,我们询问病毒-受体相互作用的性质是否在体内进化。

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