Session focused on understanding known viral/host factors needed for HIV-1 transcriptional control as an approach to understand latency, host RNA processing and the relationship between viral control and activated CD4 T cell HIV RNA expression in breast milk.  The session started with Dr. Kehn-Hall (George Wash. Univ.) discussing how TAR miRNA may aid in suppressing basal transcription leading to latency while also impacting anti-apoptotic effects on host cell. Data on PBAF was also shown to have a role in transcriptional elongation and BAF expected to slow Pol II and increase splicing.  Finally, a proteomic approach with Tat was done to assess what binds to it among different cell types suggesting that Tat complex differences are present between T-cells, monocytes and glial cells.  The latter raises the possibility that different inhibitor strategies will be needed between specific cell types if targeting this step for inhibition.  Dr. Arts (Case Western Univ.) discussed a new HIV inhibition approach based on the blocking of HIV-1 reverse transcription with minor effects on mRNA transcription via a novel Tat peptidomimetic (Davidson, PNAS, 2009) binding the TAR loop region. In contrast to other inhibitors, cell penetrance was shown and activity in PBMC was comparable to nevirapine. Mechanism of action was pursued to show a predominant effect on reverse transcription activity rather than a predominant blockage of viral transcription or effects on entry. Specificity against other viruses (i.e., HIV-2), toxicity and solubility remains to be determined. Dr. Aguiar (Federal Univ of Rio de Janeiro) next discussed how P bodies (lipid free protein aggregates) are needed for HIV-1 virus production by participating in HIV-1 assembly as mRNA processing bodies.   P bodies are involved in mRNA storage which can lead to degradation or translation.  Investigators showed the role of these bodies by targeting two molecules known to be involved in P bodies (GW182, RCK/p54) via SiRNA knock-down resulting in loss of these RNA rich loci.   Infectivity of viruses that bud from target knock-down producer cells showed a loss of infectivity yet not amount of virus particle release (lower RNA incorporation).  Incorporation of APOBEC into particles was also shown to require P-bodies.  Dr. Saleh (Monah Univ., Australia) discussed latent HIV-1 infection in the presence of multiple chemokines may facilitate resting CD4 T cell reservoir formation (Saleh, Blood, 2007). New data now shows that among chemokines tested, CCL19 following CCR7 binding may leads to activation of cofilin and modest changes in actin polymerization that may facilitate HIV entry into nuclei of resting cells. Session ended with Dr. Valea (Univ. Montpellier, France) pursuing the relationship between viremia in the mother and cell-associated viral production between breast milk and blood.  Results showed the presence of activated CD38+HLADR+ cells in breast milk with the number of viral producing cells as comparable to breast milk between aviremic and viremic women.  Results suggest that control of viral replication in the mother does not decrease the probability for cell viral transmission from mother to child.