The effect of anti-HIV-1 antibodies on complement activation at the surface of infected cells remains partly understood. Here, we show that a subset of anti-Envelope (Env) broadly neutralizing antibodies (bNAbs), targeting the CD4 binding site and the V3 loop, triggers C3 deposition and complement-dependent cytotoxicity (CDC) on Raji cells engineered to express high surface levels of HIV-1 Env. Primary CD4 T cells infected with laboratory-adapted or primary HIV-1 strains and treated with bNAbs are susceptible to C3 deposition but not to rapid CDC. The cellular protein CD59 and viral proteins Vpu and Nef protect infected cells from CDC mediated by bNAbs or by polyclonal IgGs from HIV-positive individuals. However, complement deposition accelerates the disappearance of infected cells within a few days of culture. Altogether, our results uncover the contribution of complement to the antiviral activity of anti-HIV-1 bNAbs.

中文翻译：

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抗 HIV-1 抗体会触发受感染细胞上的非裂解性补体沉积。

抗 HIV-1 抗体对受感染细胞表面补体激活的影响仍处于部分了解状态。在这里，我们展示了针对 CD4 结合位点和 V3 环的抗包膜 (Env) 广泛中和抗体 (bNAb) 的一个子集，在设计用于表达高表面活性的 Raji 细胞上触发 C3 沉积和补体依赖性细胞毒性 (CDC) HIV-1 环境水平。感染实验室适应型或原代 HIV-1 毒株并用 bNAb 处理的原代 CD4 T 细胞容易受到 C3 沉积的影响，但不会受到快速 CDC 的影响。细胞蛋白 CD59 和病毒蛋白 Vpu 和 Nef 保护受感染的细胞免受 bNAb 或多克隆 IgG 介导的 CDC 介导，这些疾病来自 HIV 阳性个体。然而，补体沉积会加速受感染细胞在培养几天内的消失。总而言之，我们的结果揭示了补体对抗 HIV-1 bNAb 的抗病毒活性的贡献。