Monica VaccariClaudio FeniziaZhong Min MaAnna HryniewiczAdriano BoassoMelvin N. DosterChristopher J. MillerNiklas LindegardhJoel TarningAlan L. LandayGene M. ShearerGenoveffa FranchiniNational Cancer InstituteUC Davis California National Primate Research CenterMahidol UniversityNuffield Department of Clinical MedicineRush University Medical CenterUniwersytet Medyczny w BialymstokuChelsea and Westminster Hospital2018-11-092018-11-092014-04-01AIDS Research and Human Retroviruses. Vol.30, No.4 (2014), 355-36219318405088922292-s2.0-84898752676https://repository.li.mahidol.ac.th/handle/123456789/33978Simian immunodeficiency virus (SIV) infection leads to AIDS in experimentally infected Rhesus macaques similarly to HIV-infected humans. In contrast, SIV infection of natural hosts is characterized by a down-regulation of innate acute responses to the virus within a few weeks of infection and results in limited pathology. Chloroquine (CQ) has been used in the treatment or prevention of malaria and has recently been shown to cause a decrease of immune activation and CD4 cell loss in HIV-infected individuals treated with antiretroviral therapy. Here, we treated Rhesus macaques with CQ during the acute phase of SIVmac251infection with the intent to decrease viral-induced immune activation and possibly limit disease progression. Contrary to what was expected, CQ treatment resulted in a temporary increased expression of interferon (IFN)-stimulating genes and it worsened the recovery of CD4+T cells in the blood. Our findings confirm recent results observed in asymptomatic HIV-infected patients and suggest that CQ does not provide an obvious benefit in the absence of antiretroviral therapy. © 2014 Mary Ann Liebert Inc.Mahidol UniversityImmunology and MicrobiologyMedicineArticleSCOPUS10.1089/aid.2013.0218