Discussed posters

In the last decade many advances have been made in understanding how HIV-1 interacts with macrophages (MØ) and dendritic cells (DC). Based on the notion that HIV-2 is a more attenuate model of infection, we proposed to explore the mechanisms of HIV-2 interaction with MØ and DCs. With this aim, we studied the efficiency of cis-infection of MØ and DCs. A cohort of 7 HIV-1 and 7 HIV-2 primary isolates were chosen based on coreceptors usage profile and on the clinical/immunological stage of infection. MØ, immature monocyte-derived DCs (IM-MDDCs) and mature monocyte-derived DCs (M-MDDCs) were obtained from healthy donors and infected with different HIV-2 and HIV-1 primary isolates or left uninfected as controls. Virus production was monitored by reverse transcriptase (RT) activity. We also analyze integrated viral DNA in exposed cells by amplification of LTR region by a nested-PCR technique to evaluate the ability of each viral isolate to enter cells and to perform initial events of replication cycle. In HIV-2, viral replication on MØ was detected in 4 viral isolates. Two of them were also able to replicate both in IM-MDDCs and M-MDDCs. Regarding HIV-1 infection, only one isolate was able to productively infect MØ. This isolate and another one replicate in IM-MDDCs while none of the HIV-1 tested were able to replicate in M-MDDCs. We further assessed the proviral DNA integration in different cell populations. We observed that one HIV-1 isolate did not integrate its proviral DNA into IM-MDDCs and M-MDDCs host-cell DNA. All the other isolates had integrated their genome. Our results suggest that the ability to infect MØ or DCs is independent on virus phenotype and did not correlate with clinical/immunological stage of the patient. Furthermore, HIV-2 infection of MØ and DCs seems to be more frequently observed than in HIV-1. Finally, there is clear evidence that reverse transcription and integration occurs even in those isolates for which there was no RT activity detection. Introduction: Following breaches of the tissue barrier or infection, interleukin-33 (IL-33) is released as an alarmin to induce inflammation. sST2, the soluble isoform of the IL-33 receptor, acts as a decoy receptor to prevent systemic inflammation. We assessed relationship between the IL-33/ST2 axis and gut mucosal damage markers in patients with early HIV infection (EHI). Materials and methods: We measured IL-33 and sST2 plasma levels in patients with EHI (n=48), chronic HIV infection (CHI; n=61) and in elite controllers (n=21); and prospectively …