Yi-Jia Li1, Huan-Ling Wang, Tai-Sheng Li. 1. Department of Infectious Diseases, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.
Abstract
OBJECTIVE: This review discusses progress in the studies of hepatitis B virus (HBV)/human immunodeficiency virus (HIV) coinfection and focuses on the interaction among HIV infection, chronic HBV infection, and host immunity. DATA SOURCES: Data and studies published mainly from 2008 to 2011 were selected using PubMed. STUDY SELECTION: Original articles and critical reviews concerning HBV/HIV coinfection and HBV and HIV pathogenesis were selected. RESULTS: HIV may accelerate HBV progression by lowering CD4 count, weakening HBV-specific immunity, "enriching" HBV mutants, causing immune activation, etc. On the other hand, HBV may enhance HIV replication by activating HIV long terminal repeat (LTR) with X protein (HBX) and cause immune activation in synergy with HIV. Paradoxically, HBV may also inhibit HIV dissemination via dendritic cells. CONCLUSIONS: The interaction among HIV, HBV, and host immunity remains poorly understood. Further research is warranted to elucidate the detailed molecular mechanisms and to translate these mechanisms into clinical practice.
OBJECTIVE: This review discusses progress in the studies of hepatitis B virus (HBV)/human immunodeficiency virus (HIV) coinfection and focuses on the interaction among HIV infection, chronic HBV infection, and host immunity. DATA SOURCES: Data and studies published mainly from 2008 to 2011 were selected using PubMed. STUDY SELECTION: Original articles and critical reviews concerning HBV/HIV coinfection and HBV and HIV pathogenesis were selected. RESULTS: HIV may accelerate HBV progression by lowering CD4 count, weakening HBV-specific immunity, "enriching" HBV mutants, causing immune activation, etc. On the other hand, HBV may enhance HIV replication by activating HIV long terminal repeat (LTR) with X protein (HBX) and cause immune activation in synergy with HIV. Paradoxically, HBV may also inhibit HIV dissemination via dendritic cells. CONCLUSIONS: The interaction among HIV, HBV, and host immunity remains poorly understood. Further research is warranted to elucidate the detailed molecular mechanisms and to translate these mechanisms into clinical practice.
Authors: Ambreen Khokhar; Samina Noorali; Muhammad Sheraz; Kuha Mahalingham; Donald G Pace; Mohammad R Khanani; Omar Bagasra Journal: Libyan J Med Date: 2012-12-31 Impact factor: 1.657