The life-cycle analysis (LCA) is conducted with a combination of real-time fuel consumption rate data for diesel/liquefied natural gas (LNG) heavy-duty vehicles (HDVs) in China, actual provincial diesel/LNG HDV population data, and a life-cycle inventory database for the Tsinghua-LCA Model (TLCAM) specified for the context of China. The results indicate that direct energy consumption and the life-cycle energy use (MJ) of an LNG HDV are approximately 7.4% and 6.2% higher than that of a comparable diesel HDV, whereas an approximate 8.0% reduction in the life cycle of GHG emissions is estimated if diesel HDVs are replaced with LNG HDVs in China. Due to the increasing use of LNG as an HDV fuel in China (i.e., approximately 4.6 billion cubic metres of natural gas in 2015), the accumulated diesel fuel substituted with LNG was approximately 16 million tons, which generated a GHG emission reduction of 6 million tons of CO2 equivalent in the HDV fleet from 2006 to 2015. Given that the HDV fleet contributed approximately 6.1% of all GHG emissions in China in 2015, growing the LNG HDV population can increase GHG emission reduction by an approximate range of 6.5-9.1 million tons of CO2 equivalent by 2020. (C) 2017 Elsevier Ltd. All rights reserved.

Background & Aims: Studying hepatitis delta virus (HDV) and developing new treatments is hampered by the limited availability of small animal models. Herein, a description of a robust mouse model of HDV infection that mimics several important characteristics of the human disease is presented. Methods: HDV and hepatitis B virus (HBV) replication competent genomes were delivered to the mouse liver using adenoassociated viruses (AAV; AAV-HDV and AAV-HBV). Viral load, antigen expression and genomes were quantified at different time points after AAV injection. Furthermore, liver pathology, genome editing, and the activation of the innate immune response were evaluated. Results: AAV-HDV infection initiated HDV replication in mouse hepatocytes. Genome editing was confirmed by the presence of small and large HDV antigens and sequencing. Viral replication was detected for 45 days, even after the AAV-HDV vector had almost disappeared. In the presence of HBV, HDV infectious particles were detected in serum. Furthermore, as observed in patients, co-infection was associated with the reduction of HBV antigen expression and the onset of liver damage that included the alteration of genes involved in the development of liver pathologies. HDV replication induced a sustained type I interferon response, which was significantly reduced in immunodeficient mice and almost absent in mitochondrial antiviral signaling protein (MAVS)-deficient mice. Conclusion: The animal model described here reproduces important characteristics of human HDV infection and provides a valuable tool for characterizing the viral infection and for developing new treatments. Furthermore, MAVS was identified as a main player in HDV detection and adaptive immunity was found to be involved in the amplification of the innate immune response. Lay summary: Co-infection with hepatitis B and D virus (HBV and HDV, respectively) often causes a more severe disease condition than HBV alone. Gaining more insight into HDV and developing new treatments is hampered by limited availability of adequate immune competent small animal models and new ones are needed. Here, a mouse model of HDV infection is described, which mimics several important characteristics of the human disease, such as the initiation and maintenance of replication in murine hepatocytes, genome editing and, in the presence of HBV, generation of infectious particles. Lastly, the involvement of an adaptive immunity and the intracellular signaling molecule MAVS in mounting a strong and lasting innate response was shown. Thus, our model serves as a useful tool for the investigation of HDV biology and new treatments. (C) 2017 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.