The theme of this session was the study of  mechanisms underlying maintenance of latency in HIV-infected cells. Dr. Lachlan Gray (Burnet Institute) discussed mechanisms controlling HIV latency that are specific to the central nervous system. He found decreased transcriptional activity of HIV within CNS, which was associated with expression of the transcriptional repressor Sp3, in contrast to Sp1 which is a more canonical binder to the HIV LTR. Dr. Fabio Romerio (University of Maryland) performed transcriptional analysis using an in vitro model of latent HIV infection of peripheral blood CD4 T cells. Several transcriptional differences were found between uninfected cells and cells latently HIV infected. These differences suggested that HIV may exploit cellular suppression functions to maintain latency. Dr. Mudit Tyagi (George Mason University) discussed induction and maintenance of latency in HIV-infected primary CD4 T cells and transformed cell lines by recruitment of PcG repressor to the locus of HIV integration. Dr. Tyagi found that CBF-1 can induce repressive chromatin structure by recruiting Polycomb Group corepressors to the HIV LTR. Dr.Stefanie Weber (Erlangen University) discussed epigenetic modifications which occur to the HIV LTR and unexpectedly found LTR-located CpG dinucleotides being mutated. These specific LTR mutations were speculated to be targets of therapeutic interventions. Dr. Suha Saleh (Monash University) discussed unique integration site patterns in peripheral blood CD4 T cells experimentally infected with HIV.  Dr. Saleh found that integration sites of HIV were influenced by the mechanisms by which the CD4 T cells were stimulated, but HIV tended to integrate in transcriptionally active genes. Following the presentations discussion noted that further studies might focus on understanding HIV latency in vivo, but the difficulty in retrieving sufficient latently-infected cells from in vivo reservoirs was mentioned.