Two studies examining ex vivo HIV infection of macrophages have made some progress addressing mechanisms—Wang et al. observed inhibition of HIV infection of primary macrophages by LPS (TLR4), R848 (TLR7) and polyI:C (TLR3) and found that this inhibition was independent of NF-κB and Jak-Stat signaling, but partially required p38 MAPK and JNK [125]. Here, SOAT1 is linked to HIV infectious disease.