Institute of Molecular Virology, Ulm University Medical Center, 89081, Ulm, Germany.
Departments of Medicine and Microbiology, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Nat Commun. 2018 Apr 10;9(1):1371. doi: 10.1038/s41467-018-03762-3.
HIV-1 causes chronic inflammation and AIDS in humans, whereas related simian immunodeficiency viruses (SIVs) replicate efficiently in their natural hosts without causing disease. It is currently unknown to what extent virus-specific properties are responsible for these different clinical outcomes. Here, we incorporate two putative HIV-1 virulence determinants, i.e., a Vpu protein that antagonizes tetherin and blocks NF-κB activation and a Nef protein that fails to suppress T cell activation via downmodulation of CD3, into a non-pathogenic SIVagm strain and test their impact on viral replication and pathogenicity in African green monkeys. Despite sustained high-level viremia over more than 4 years, moderately increased immune activation and transcriptional signatures of inflammation, the HIV-1-like SIVagm does not cause immunodeficiency or any other disease. These data indicate that species-specific host factors rather than intrinsic viral virulence factors determine the pathogenicity of primate lentiviruses.
HIV-1 会在人类体内引起慢性炎症和艾滋病,而相关的猴免疫缺陷病毒(SIV)在其自然宿主中高效复制,却不会导致疾病。目前尚不清楚病毒的哪些特定特性导致了这些不同的临床结果。在这里,我们将两种假定的 HIV-1 毒力决定因素,即一种拮抗 tetherin 并阻断 NF-κB 激活的 Vpu 蛋白,以及一种不能通过下调 CD3 来抑制 T 细胞激活的 Nef 蛋白,整合到一种非致病性的 SIVagm 株中,并测试它们对病毒复制和致病性的影响。尽管在超过 4 年的时间里持续出现高水平的病毒血症,适度增加免疫激活和炎症的转录特征,但类似 HIV-1 的 SIVagm 不会导致免疫缺陷或任何其他疾病。这些数据表明,是种属特异性的宿主因素而不是内在的病毒毒力因素决定了灵长类慢病毒的致病性。