Innate immunity in acute HIV-1 infectionBorrow, PersephoneCurrent Opinion in HIV & AIDS: September 2011 - Volume 6 - Issue 5 - p 353–363 doi: 10.1097/COH.0b013e3283495996 Innate immunity: Edited by William A. Paxton and Teunis B.H. Geijtenbeek Abstract Author Information Purpose of review: Acute HIV-1 infection (AHI) is composed of the eclipse phase, during which the transmitted virus struggles to avoid eradication and achieve amplification/spread; the expansion phase when virus disseminates and undergoes exponential replication associated with extensive CD4+ T-cell destruction; and the containment phase when set-point levels of viremia and immune activation are established. The importance of interactions between HIV-1 and innate responses in determining events throughout AHI is increasingly recognized, and is reviewed here. Recent findings: During the eclipse phase, HIV-1 subverts dendritic cell functions to promote its replication at mucosal sites and employs multiple strategies to minimize control by type 1 interferons. Systemic virus dissemination is associated with widespread activation of innate responses which fuels HIV-1 replication. To minimize the protective effects of innate responses, HIV-1 resists control by natural killer cells and may impair innate regulation of adaptive responses. Innate responses remain chronically activated after HIV-1 containment which is thought to drive HIV-1 pathogenesis. Summary: Innate responses are pivotal determinants of events at all stages of AHI. Increased understanding of mechanisms involved in innate control of HIV-1 and pathways regulating innate activation during HIV-1 infection could facilitate development of novel approaches to combating this infection. Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK Correspondence to Dr Persephone Borrow, PhD, Nuffield Department of Clinical Medicine, University of Oxford, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DS, UKTel: +44 1865 222528; e-mail: email@example.com © 2011 Lippincott Williams & Wilkins, Inc.