TRIM69 and infection: Although we did not further define the mechanism of TRIM69 restriction of HIV-1, its ability to influence replication by diverse viruses, including Coxsackievirus B3, Rift Valley fever virus (RVFV), and Zika virus even in the absence of microtubule acetylation (Fig. 5 and 6), suggests that TRIM69 may not directly bind to viral determinants and may rather perturb cellular processes commonly exploited by viruses during infection.