HIV-infected patients on antiretroviral therapy (ART) may present low-level viremia (LLV) above the detection level of current viral load assays. In many cases LLV is persistent but does not result in overt treatment failure or selection of drug resistant viral variants. To elucidate whether LLV reflects active virus replication, we extensively sequenced pol and env genes of the viral populations present before and during LLV in 18 patients and searched for indications of genetic evolution. Maximum likelihood phylogenetic trees were inspected for temporal structure both visually and by linear regression analysis of root-to-tip and pairwise distances. Viral coreceptor tropism was assessed at different time points before and during LLV. In none of the patients consistent indications for genetic evolution were found over a median period of 4.8 years of LLV. As such these findings could not provide evidence that active virus replication is the main driver of LLV.

接受抗逆转录病毒疗法（ART）感染HIV的患者，其低水平病毒血症（LLV）可能超过当前病毒载量检测的检测水平。在许多情况下，LVL是持久性的，但不会导致明显的治疗失败或选择耐药性病毒变体。为了阐明LLV是否反映了病毒的活跃复制，我们对pol和env进行了广泛的测序在18位患者的LLV之前和期间存在的病毒种群的基因，并寻找遗传进化的迹象。对最大似然系统树的时间结构进行视觉检查，并通过根尖至成对距离的线性回归分析进行检查。在LLV之前和期间的不同时间点评估了病毒共感受器的向性。在LLV的中位时间为4.8年，没有患者发现遗传进化的一致指征。因此，这些发现不能提供证据表明主动病毒复制是LLV的主要驱动力。