Macrophages are the major target of the human immunodeficiency virus (HIV) and represent a productive reservoir due to their resistance to the cytopathic effects of the virus. We have contributed to demonstrating that blocking CCR5 co-receptor trafficking inhibits HIV-1 infection of macrophages (Boncompain et al., 2019). We study cellular factors, and in particular a lysosomal amino acid transporter, crucial for the formation of new virions in human macrophages (Herit et al., to be submitted). In addition, we have shown that the infection of macrophages by HIV-1 leads to a severe impairment of the functions of these cells: uptake defects due to the viral factor Nef (Mazzolini et al., 2010), lack of clearance due to the viral factor Vpr (Dumas et al., 2015), which allows the development of opportunistic pathogens. In particular, we study co-infections between HIV-1 and an invasive strain of Salmonella Typhimurium (iNTS) (Le-Bury et al., 2020 and Lê-Bury BIORXIV: 2025.09.29.679141 ) as well as HIV-1 and Chlamydia trachomatis (Alonso-Bivou, Herit et al., BIORXIV: 2025.08.19.671145).

Viral emergence is a threat to global health. It is therefore critical to anticipate these emergences by understanding the mechanisms of the viral pathogenesis towards the development of new treatments to possibly fight off emerging diseases before they reach the pandemic stage. Yellow fever virus (YFV) represents a major health threat due to its transmission course by mosquitoes and has thus been classified as a virus with a high risk of emergence. YFV is known to replicate in liver macrophages, the Kupffer cells, but its replication in other macrophage types is still debated. Since 1968, only 43 studies have been published on the effect of YFV on macrophages phenotypes and functions. Some results have highlighted that YFV induces immune response as well as inhibit specific immune pathways in macrophages. The full extent of these modulations has yet to be discovered, especially given the lack of animal competent model recapitulating the human pathogenesis.  Therefore, it is important to understand in a human macrophage model (i) what are the extent of the effects of YFV on macrophages functions and (ii) what are the mechanisms responsible for the identified modulations.