Because the most well-studied TRIM protein, TRIM5α, was historically considered to be unable to bind and restrict the HIV-1 capsid in human target cells, only a few studies have investigated the role of TRIM5α in the modulation of HIV-1 replication in human primary macrophages, although it was initially shown that TRIM proteins could modulate and block HIV-1 infection more strongly in non-dividing cells such as macrophages than in dividing cells [160]. Here, TRAT1 is linked to HIV-1 infection.