生物
延迟(音频)
病毒潜伏期
病毒学
病毒复制
人类免疫缺陷病毒(HIV)
病毒
免疫系统
细胞生物学
免疫学
电气工程
工程类
作者
Mie Kobayashi-Ishihara,Katarína Frazão Smutná,Florencia E. Alonso,Jordi Argilaguet,Anna Esteve‐Codina,Kerstin Geiger,Meritxell Genescà,Judith Grau-Expósito,Clara Duran-Castells,Selina Rogenmoser,René Böttcher,Jennifer Jungfleisch,Baldomero Oliva,Javier P Martínez,Manqing Li,Michael David,Makoto Yamagishi,Marta Ruiz-Riol,Christian Berthou,Yasuko Tsunetsugu-Yokota,María J. Buzón,Juana Díez,Andreas Meyerhans
标识
DOI:10.1038/s42003-023-04841-y
摘要
Latency is a major barrier towards virus elimination in HIV-1-infected individuals. Yet, the mechanisms that contribute to the maintenance of HIV-1 latency are incompletely understood. Here we describe the Schlafen 12 protein (SLFN12) as an HIV-1 restriction factor that establishes a post-transcriptional block in HIV-1-infected cells and thereby inhibits HIV-1 replication and virus reactivation from latently infected cells. The inhibitory activity is dependent on the HIV-1 codon usage and on the SLFN12 RNase active sites. Within HIV-1-infected individuals, SLFN12 expression in PBMCs correlated with HIV-1 plasma viral loads and proviral loads suggesting a link with the general activation of the immune system. Using an RNA FISH-Flow HIV-1 reactivation assay, we demonstrate that SLFN12 expression is enriched in infected cells positive for HIV-1 transcripts but negative for HIV-1 proteins. Thus, codon-usage dependent translation inhibition of HIV-1 proteins participates in HIV-1 latency and can restrict the amount of virus release after latency reversal.
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