Hua, StéphaneVigano, SelenaTse, SamanthaZhengyu, OuyangHarrington, SeanNegron, JordiGarcia-Broncano, PilarMarchetti, GiuliaGenebat, MiguelLeal, ManuelResino, SalvadorRuiz-Mateos, EzequielLichterfeld, MathiasYu, Xu G2023-01-252023-01-252018http://hdl.handle.net/10668/11943Interferon alpha (IFN-α) can potently reduce human immunodeficiency virus type 1 (HIV-1) replication in tissue culture and animal models, but may also modulate residual viral reservoirs that persist despite suppressive antiretroviral combination therapy. However, mechanisms leading to viral reservoir reduction during IFN-α treatment are unclear. We analyzed HIV-1 gag DNA levels in CD4 T cells by digital droplet polymerase chain reaction and CD8 T-cell and natural killer (NK) cell phenotypes by flow cytometry in a cohort of antiretroviral therapy-treated HIV-1/hepatitis C virus-coinfected patients (n = 67) undergoing treatment for hepatitis C infection with pegylated IFN-α and ribavirin for an average of 11 months. We observed that IFN-α treatment induced a significant decrease in CD4 T-cell counts (P These data suggest that the reduction of viral reservoir cells during treatment with IFN-α is primarily attributable to antiviral activities of NK cells.enAdultAgedAntiretroviral Therapy, Highly ActiveCohort StudiesCoinfectionDNA, ViralDisease ReservoirsFemaleHIV InfectionsHIV-1HepacivirusHepatitis CHumansInterferon-alphaKiller Cells, NaturalLymphocyte ActivationMaleMiddle AgedPolyethylene GlycolsRecombinant ProteinsRibavirinSpainViral Loadgag Gene Products, Human Immunodeficiency Virusresearch article29272392open access10.1093/cid/cix11111537-6591PMC5982807https://academic.oup.com/cid/article-pdf/66/12/1910/25084671/cix1111.pdfhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5982807/pdf