title: Residual inflammation and viral reservoirs: alliance against an HIV cure.
abstract: OBJECTIVE
  HIV persists in cellular and anatomical reservoirs during antiretroviral therapy (ART). Viral persistence is ensured by a variety of mechanisms including ongoing viral replication and proliferation of latently infected cells. In this review, we summarize recent findings establishing a link between the unresolved levels of inflammation observed in virally suppressed individuals on ART and the mechanisms responsible for HIV persistence.
  
  
  RESULTS
  Residual levels of viral replication during ART are associated with persistent low levels of immune activation, suggesting that unresolved inflammation can promote the replenishment of the HIV reservoir in tissues. In addition, the recent findings that the latent HIV reservoir is maintained by continuous proliferation of latently infected cells provide another mechanism by which residual inflammation could contribute to HIV persistence.
  
  
  CONCLUSIONS
  Residual inflammation during ART is likely to be a critical parameter contributing to HIV persistence. Therefore, reducing inflammation may be an efficient way to interfere with the maintenance of the HIV reservoir in virally suppressed individuals on ART.
authors.affiliation: aDepartment of Microbiology, Infectiology and Immunology, Faculté de Médecine, Université de Montréal bCentre de Recherche du CHUM, Montréal, Quebec, Canada *Marta Massanella and Rémi Fromentin equally contributed to the writing of this article.
authors.forename: Marta
authors.initials: M
authors.lastname: Massanella
authors.forename: Rémi
authors.initials: R
authors.lastname: Fromentin
authors.forename: Nicolas
authors.initials: N
authors.lastname: Chomont
mesh_terms: D019380:Anti-HIV Agents / Q000494:pharmacology / Q000627:therapeutic use; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology; D015497:HIV-1 / Q000187:drug effects / Q000276:immunology; D054884:Host-Pathogen Interactions / Q000276:immunology*; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000821:virology; D017735:Virus Latency / Q000276:immunology*
chemical_list: D019380:Anti-HIV Agents