Bol, Sebastiaan M.Moerland, Perry D.Limou, Sophievan Remmerden, YvonneCoulonges, Cédricvan Manen, DaniëlleHerbeck, Joshua T.Fellay, JacquesSieberer, MargitSietzema, Jantine G.van 't Slot, RubenMartinson, JeremyZagury, Jean-FrançoisSchuitemaker, Hannekevan 't Wout, Angélique B2011-04-112011-04-112011-04-11201110.1371/journal.pone.0017190https://infoscience.epfl.ch/handle/20.500.14299/66253HIV-1 infected macrophages play an important role in rendering resting T cells permissive for infection, in spreading HIV-1 to T cells, and in the pathogenesis of AIDS dementia. During highly active anti-retroviral treatment (HAART), macrophages keep producing virus because tissue penetration of antiretrovirals is suboptimal and the efficacy of some is reduced. Thus, to cure HIV-1 infection with antiretrovirals we will also need to efficiently inhibit viral replication in macrophages. The majority of the current drugs block the action of viral enzymes, whereas there is an abundance of yet unidentified host factors that could be targeted. We here present results from a genome-wide association study identifying novel genetic polymorphisms that affect in vitro HIV-1 replication in macrophages.text::journal::journal article::research article