Vincent Piguet1, Stephan M Caucheteux, Marco Iannetta, Anne Hosmalin. 1. aDepartment of Dermatology and Academic Wound Healing, Institute of Infection & Immunity, Cardiff University bWelsh Institute of Dermatology, University Hospital of Wales, Cardiff, Wales, UK cInserm U1016, Institut Cochin dCNRS UMR8104 eUniversity Paris Descartes fAssistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Cochin, Paris, France.
Abstract
PURPOSE OF REVIEW: The purpose of this study is to describe the alterations that HIV-1 induces in antigen-presenting cells (APCs), in vitro, ex vivo and in vivo. RECENT FINDINGS: HIV-1 disarms several arms of the immune system including APCs. We summarize here recent findings on the impact of the virus on APC. SUMMARY: HIV-1 can invade APC and overall reduce their capacity to present antigens effectively, mostly by reducing their numbers and inducing permanent hyperactivation. This occurs via a combination of alterations; however, the host can counteract, at least in part, some of these defects via restriction factors, autophagy, the production of type I interferon, antiviral cytokines, among others. However, these specific mechanisms of viral evasion from APCs' control lead to a chronic hyperactivation of the immune system implicated in AIDS-related and non-AIDS related pathogenesis. Unfortunately, the current regimens of antiretroviral therapy are unable to dampen sufficiently APC-driven viral-induced immune hyperactivation. Understanding how HIV alters APC will help to tune appropriately both intrinsic immunity and innate immunity, as well as achieve efficient antigen presentation to the adaptive immune system, without inducing a detrimental pervasive hyperactivation of the immune system.
PURPOSE OF REVIEW: The purpose of this study is to describe the alterations that HIV-1 induces in antigen-presenting cells (APCs), in vitro, ex vivo and in vivo. RECENT FINDINGS:HIV-1 disarms several arms of the immune system including APCs. We summarize here recent findings on the impact of the virus on APC. SUMMARY:HIV-1 can invade APC and overall reduce their capacity to present antigens effectively, mostly by reducing their numbers and inducing permanent hyperactivation. This occurs via a combination of alterations; however, the host can counteract, at least in part, some of these defects via restriction factors, autophagy, the production of type I interferon, antiviral cytokines, among others. However, these specific mechanisms of viral evasion from APCs' control lead to a chronic hyperactivation of the immune system implicated in AIDS-related and non-AIDS related pathogenesis. Unfortunately, the current regimens of antiretroviral therapy are unable to dampen sufficiently APC-driven viral-induced immune hyperactivation. Understanding how HIV alters APC will help to tune appropriately both intrinsic immunity and innate immunity, as well as achieve efficient antigen presentation to the adaptive immune system, without inducing a detrimental pervasive hyperactivation of the immune system.