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Current trends in management of hepatitis B virus reactivation in the biologic therapy era

World Journal of Gastroenterology 2011年第34期17卷 3881-3887页

作者： Claudio M Mastroianni Miriam Lichtner Rita Citton Cosmo Del Borgo Angela Rago Helene Martini Giuseppe Cimino vincenzo vullo Infectious Diseases Unit Fondazione Eleonora Lorillard Spencer Cenci Sapienza University SM Goretti Hospital Hematology Unit Sapienza University SM Goretti Hospital Department of Public Health and Infectious Diseases Sapienza University Policlinico Umberto I

Hepatitis B virus (HBV) reactivation represents an emerging cause of liver disease in patients undergoing treatment with biologic agents. In particular, the risk ofHBV reactivation is heightened by the use monoclonalantibodies, such as rituximab (anti-CD20) and alemtuzumab (anti-CD52) that cause profound and longlasting immunosuppression. Emerging data indicatethat HBV reactivation could also develop following theuse of other biologic agents, such as tumor necrosis factor (TNF)-α inhibitors. When HBV reactivation is di-agnosed, it is mandatory to suspend biologic treatmentand start antiviral agents immediately. However, preemptive antiviral therapy prior to monoclonal antibodyadministration is crucial in preventing HBV reactivationand its clinical consequences. Several lines of evidencehave shown that risk of HBV reactivation is greatlyreduced by the identifi cation of high-risk patients andthe use of prophylactic antiviral therapy. In this article, we discuss current trends in the management of HBV reactivation in immunosuppressed patients receiving biologic therapy, such as rituximab, alemtuzumab and TNF-α antagonists.

关键词：生物治疗乙肝病毒激活管理抗病毒治疗乙型肝炎病毒肿瘤坏死因子生物制剂

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Microbial translocation, residual viremia and immune senescence in the pathogenesis of HIV-1 infection

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World Journal of Clinical Infectious Diseases 2013年第4期3卷 47-57页

作者： Alessandra Fantauzzi Francesca Falasca Gabriella d’Ettorre Eugenio Nelson Cavallari Ombretta Turriziani vincenzo vullo Ivano Mezzaroma Department of Clinical Medicine University of Rome Department of Molecular Medicine University of Rome Department of Public Health and Infectious Diseases University of Rome

The pathophysiological mechanisms that underlie the progression of human immunodeficiency virus-1(HIV-1) disease to full-blown AIDS are not well understood. Findings suggest that, during HIV-1 infection, plasma lipopolysaccharide(LPS) levels, which are used as an indicator of microbial translocation(MT), are elevated throughout the acute and chronic phases of HIV-1 disease. The translocation of bacterial products through the damaged gastrointestinal barrier into the systemic circulation has been described as a driver of immune activation. In contrast, comorbidities that are associated with HIV-1 infection have been attributed to chronic inflammation and immune system dysfunction secondary to MT or low-level HIV-1 replication in plasma and cell reservoirs. Moreover, accelerated aging is significantly associated with chronic inflammation, immune activation, and immune senescence. In this review, we aimed to investigate the role of inflammation as a pivotal marker in the pathogenesis of HIV-1 disease. We will discuss the key features of chronic inflammation and immune activation that are observed during the natural course of the disease and those features that are detected in c ART-modified infection. The review will focus on the following aspects of HIV-1 infection:(1) MT;(2) the role of residual viremia; and(3) "immune senescence" or "inflammaging." Many questions remain unanswered about the potential mechanisms that are involved in HIV-1 pathogenesis. Further studies are needed to better investigate the mechanisms that underlie immune activation and their correlation with HIV-1 disease progression.

关键词： Human immunodeficiency virus-1 Combined antiretroviral therapy Immune activation Microbial translocation Residual viremia Immune senescence

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