We conclude that the ability of DMOG to protect cells from IR is mediated through the transcriptional activity of Hif1a rather than through a general inhibition of endogenous KDMs in the cell. In addition to CHD4 and MTA3, we also identified the Suv39h1 methyltransferase as a target of the Hif1a. Suv39h1 is a key player in the di- and trimethylation of H3 on lysine 9.However, activation of the mucosal responses at the vaginal and intestinal levels by the intramuscular route, using non-replicative vectors like virosomes might be more an exception than the rule. In an upcoming clinical trial, additional mucosal samples will be collected to clarify the respective contribution of the intramuscular and intranasal route for the induction of mucosal immunity. At the end of the study, the mean total P1-specific antibody concentration in vaginal samples is at least 100-fold lower than serum samples. These low mucosal antibody concentrations preclude their successful TH-302 distributor testing in current in vitro neutralization assays, which were initially developed for serum samples and generally require at least 200 ng/well of neutralizing specific antibodies. Currently, we cannot exclude the presence of low levels of neutralizing antibodies in vaginal or rectal fluids and antibody purification might be necessary for detecting them. Meanwhile, adding purification steps for specific IgGs and IgAs could introduce risks of losing or affecting the quality of samples and this approach might not be easily applicable to clinical trials evaluating thousands of samples. It might be more realistic to improve the in vitro neutralization assay sensitivity by at least 100-fold, ideally requiring less than 1 ng/well of specific antibodies for reliable testing of low amount of unpurified mucosal samples. Although few ng/mL of specific mucosal antibodies might be perceived as a very low antibody concentration in the vaccine field, respective to serums that generally contain mg/mL of specific antibodies, it still represents billions of antibodies per mL of vaginal secretion. Furthermore, it is likely an underestimation, considering the contribution of the mucosal antibodies also trapped in the mucus or located in the lamina propria underneath the mucosal tissue that could not be estimated from the collected secretion samples of this study. Tubacin Transcytosis inhibition was investigated only for vaginal samples, as our previous studies had shown that circulatory antibodies could not inhibit HIV-1 transcytosis and rectal samples were too limited. Although the transcytosis assay has been standardized to some extent in various laboratories, variations are inherent to in vitro cell-based assays and very often, experiments are conducted at least twice for confirming the in vitro observations. Transcytosis assay was developed to obtain robust data but was not formally qualified, as it is done for bioanalysis of the active pharmaceutical ingredient.