1. Conclusions Modulation of Mucosal Transmission Oral Poster Session

2. Session Theme: Focusing on identification of mucosal phenotypes associated with lower risk for HIV transmission (HEPS) & how to intervene?

3. Presentations….. Female genital epithelial cells from HIV-exposed seronegative commercial sex workers express a discrete cytokine/chemokines profile upon toll-like receptor activation Nyla Dil, Canada Inhibitory KIR/HLA incompatibility between sexual partners confers protection against HIV-1 transmission Wim Jennes, Belgium The dual role of genital RANTES in the spread of HIV infections Lenine Liebenberg, South Africa Protein engineering of the lectin BanLec reduces its mitogenic activity and prevents vaginal HIV transmission Michael Swanson, United States Characterization of a new use for acyclovir and tenofovir using human cervico-vaginal tissue ex vivo Christophe Vanpouille, United States

4. Questions… Three of the presentations in this session highlighted the value of HEPS cohorts in understanding important translational targets for prevention research: – HEPS individuals tended to have lower inflammatory markers in genital secretions and lower production of important chemokines by epithelial cells following TLR stimulation Two of the presentations explored microbicide and drug methods to block mucosal HIV transmisison – Lectins derived from plants could be formulated to block HIV tranmission in Humice; and combination drug therapy directed against HIV as well as common STIs (HSV-2)

5. Comments… Genital mucosal HIV transmission is dependent on a number of well described and less well understood co-factors (STIs, BV, hormone contraceptives, to name very few) which modulate the genital inflammatory environment to favour infection HIV transmission risk and spread from the genital mucosa to systemic sites is dependent on an inflammatory environment (Li et al., 2009; Haase et al., 2010) Modulation of mucosal transmission of HIV should include combination approaches aimed at managing common STI and/or associated inflammation/immune activation