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Host restriction factors represent a defence mechanism of the innate immune system against viral pathogens, such as HIV-1. Many studies focused on the interplay between restriction factors and HIV-1 have greatly improved our knowledge about the biology of the virus and the response of the host, but to date there is no evidence on of a possible interaction between host restriction factors to counteract the virus. Here we show that TRIM22 and CIITA, 2 cellular proteins previously shown by us to inhibit HIV-1 proviral transcription with different mechanisms, interact in vivo and co-localize in nuclear bodies whose formation is hierarchically controlled by TRIM22. Importantly, TRIM19/Promyelocytic Leukemia (PML) protein, another repressor of HIV-1 transcription also acting before proviral integration, co-localized in these nuclear bodies upon TRIM22 expression induced by IFN-γ. Finally, TRIM22 nuclear bodies also contained CyclinTI, a crucial elongation factor of HIV-1 primary transcripts. These findings show that TRIM22 nuclear bodies are a site of recruitment of factors crucial for the regulation of HIV-1 transcription and highlight the potential existence of a concerted action between TRIM22, CIITA and TRIM19/PML to maintain a state of proviral latency at least in myeloid cells.