Human pegivirus (HPgV) protects HIV+ people from HIV-associated disease, but the mechanism of this protective effect remains poorly understood. We sequentially infected cynomolgus macaques with simian pegivirus (SPgV) and simian immunodeficiency virus (SIV) to model HIV+HPgV co-infection. SPgV had no effect on acute-phase SIV pathogenesis–as measured by SIV viral load, CD4+ T cell destruction, immune activation, or adaptive immune responses–suggesting that HPgV’s protective effect is exerted primarily during the chronic phase of HIV infection. We also examined the immune response to SPgV in unprecedented detail, and found that this virus elicits virtually no activation of the immune system despite persistently high titers in the blood over long periods of time. Overall, this study expands our understanding of the pegiviruses–an understudied group of viruses with a high prevalence in the global human population–and suggests that the protective effect observed in HIV+HPgV co-infected people occurs primarily during the chronic phase of HIV infection.

人类佩吉病毒（HPgV）保护HIV +人群免受HIV相关疾病的侵害，但这种保护作用的机制仍知之甚少。我们依次用猿猴pegivirus（SPgV）和猿猴免疫缺陷病毒（SIV）感染食蟹猕猴，以模拟HIV + HPgV共同感染。SPgV对急性期SIV发病机制没有影响-通过SIV病毒载量，CD4 + T细胞破坏，免疫激活或适应性免疫应答来衡量-提示HPgV的保护作用主要在HIV感染的慢性期发挥。我们还以前所未有的细节检查了对SPgV的免疫反应，发现尽管长时间以来血液中的滴度一直很高，但这种病毒实际上并未引起免疫系统的激活。全面的，