TAT and infection: While entry into quiescence is thought to play a dominant role in the induction of proviral latency, additional mechanisms, such as direct infection of resting cells7,9,12, the genomic locus of the provirus7,9,13–15, stochastic fluctuations in the expression of the viral Tat protein and cellular proteins such as KAP1 (refs. 16–18) also help regulate proviral entry into latency.