Laboratory of Reference and Research on Viral Hepatitis, National Center of Microbiology, Institute of Health Carlos Iii, Majadahonda, Madrid, Spain.
Departamento de Medicina- Área de Microbiología. Facultad de Medicina. Universidad Complutense, Madrid, Spain.
Virulence. 2021 Dec;12(1):2919-2931. doi: 10.1080/21505594.2021.2004743.
Antiretroviral therapy (ART) allows suppressed viremia to reach less than 50 copies/mL in most treated persons living with HIV (PLWH). However, the existence of PLWH that show events of persistent low-level viremia (pLLV) between 50 and 1000 copies/mL and with different virological consequences have been observed. PLLV has been associated with higher virological failure (VF), viral genotype resistance, adherence difficulties and AIDS events. Moreover, some reports show that pLLV status can lead to residual immune activation and inflammation, with an increased risk of immunovirological failure and a pro-inflammatory cytokine level which can lead to a higher occurrence of non-AIDS defining events (NADEs) and other adverse clinical outcomes. Until now, however, published data have shown controversial results that hinder understanding of the true cause(s) and origin(s) of this phenomenon. Molecular mechanisms related to viral reservoir size and clonal expansion have been suggested as the possible origin of pLLV. This review aims to assess recent findings to provide a global view of the role of pLLV in PLWH and the impact this status may cause on the clinical progression of these patients.
抗逆转录病毒疗法(ART)可使大多数接受治疗的艾滋病毒感染者(PLWH)的病毒血症得到抑制,病毒载量降至 50 拷贝/ml 以下。然而,人们已经观察到,一些 PLWH 会出现持续低水平病毒血症(pLLV),病毒载量在 50 至 1000 拷贝/ml 之间,且具有不同的病毒学后果。pLLV 与更高的病毒学失败(VF)、病毒基因型耐药、药物依从性困难和 AIDS 事件相关。此外,一些报告表明,pLLV 状态可导致残留免疫激活和炎症,增加免疫病毒学失败的风险以及促炎细胞因子水平,从而导致非艾滋病定义事件(NADEs)和其他不良临床结局的发生率增加。然而,到目前为止,已发表的数据显示出相互矛盾的结果,这阻碍了对这一现象的真正原因和起源的理解。与病毒储存库大小和克隆扩增相关的分子机制被认为是 pLLV 的可能起源。本综述旨在评估最新发现,以提供 pLLV 在 PLWH 中的作用以及该状态对这些患者临床进展可能产生的影响的全面观点。