This may be due to the propensity of these cells to preferentially undergo latent infection, which is supported by our observation that LN Tfh express low levels of TRIM28 (thereby favoring HIV integration) but high levels of BRD4, IFI16, IFIT1, and IFITM1 (thereby blocking HIV gene expression and promoting HIV latency). Here, IFI16 is linked to disease arising from reactivation of latent virus.