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Human immunodeficiency virus (HIV) transcription is closely associated with chromatin remodeling.Retinoblastoma binding protein 4 (RBBP4) is a histone chaperone implicated in chromatin remodeling.However,the role of RBBP4 in HIV-1 infection and the underlying mechanism remain elusive.In the present study,we showed that RBBP4 plays a negative regulatory role during HIV-1 infection.RBBP4 expression was significantly increased in HIV-1-infected T cells.RBBP4 binds to the HIV-1 long terminal repeat (LTR),represses HIV-1 LTR-mediated transcription through recruiting nuclear receptor subfamily 2 group F member 1 (NR2F1) and histone deacetylase 1 and 2 (HDAC1/2) to HIV-1 LTR,and further controls local histone 3 (H3) deacetylation and chromatin compaction.Furthermore,the occupancy of RBBP4,HDAC1/2,and NR2F1 on LTR in HIV-latent J-lat cells was significantly higher than that in HIV-1-activated cells.In conclusion,our results establish RBBP4 as a new potent antiretroviral factor,which may provide theoretical basis for the treatment of HIV in the future.