Vpr attenuates antiviral immune responses and is critical for full pathogenicity of SIVmac239 in rhesus macaques.
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ABSTRACT: The accessory viral protein R (Vpr) is encoded by all primate lentiviruses. Vpr counteracts DNA repair pathways, modulates viral immune sensing, and induces cell-cycle arrest in cell culture. However, its impact in vivo is controversial. Here, we show that deletion of vpr is associated with delayed viral replication kinetics, rapid innate immune activation, development and maintenance of strong B and T cell responses, and increased neutralizing activity against SIVmac239 in rhesus macaques. All wild-type SIVmac239-infected animals maintained high viral loads, and five of six developed fatal immunodeficiency during ∼80 weeks of follow-up. Lack of Vpr was associated with better preservation of CD4+ T cells, lower viral loads, and an attenuated c
SUBMITTER: Laliberte A
PROVIDER: S-EPMC10679897 | biostudies-literature | 2023 Dec
REPOSITORIES: biostudies-literature
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