The hepatitis E virus (HEV) is an important pathogen that threatens global public health. One-third of the world’s population lives in the epidemic area of HEV, causing 20 million infections and 70,000 deaths annually. In China, HEV transmission has changed from human-to-human transmission of HEV1 to zoonotic transmission of HEV4, causing hepatitis outbreaks throughout the country. Protecting vulnerable groups, such as practitioners related to animal husbandry and downstream consumers who are immune deficient or pregnant, from HEV infections is an urgent task. At present, the commercial human vaccine, Hecolin® (HEV 239 vaccine), is licensed for use only in China. HEV 239 vaccine is a human vaccine developed for HEV1. Although it has a cross-protective effect on HEV4, the level of immune protection is still different. To address the transformation of domestic HEV transmission modes, there is an urgent need to develop a new vaccine against zoonotic HEV4. P206@PLGA is a vaccine candidate in which nanomaterials are used to encapsulate viral capsid proteins for the immunization of livestock animals. Our experiments show that P206@PLGA has excellent biocompatibility and safety. In addition, P206@PLGA can effectively induce animals to produce a high titer of antibodies against HEV4, and thus has the potential to become a veterinary vaccine for the prevention of HEV. This approach provides a new concept for HE prevention to reduce the transmission of HEV in farms and protect susceptible populations.

Background: As a promising nanomaterial for biomedical applications, zirconia nanoparticles (ZrO2) have aroused concern recently, but the toxicity of ZrO2 in vivo has received little attention. Purpose: The aim of this study is to demonstrate the systematic single dose toxicity, biodistribution and oxidative damage of ZrO2 in vivo after intravenous injection in mice. Materials and methods: Ten ICR mice were used at the high dose of ZrO2 including 600, 500, 400 and 300mg/kg. Maximum tolerated dose (MTD) of 150 nm ZrO2 was determined as 500mg/kg. Hematology analysis and blood biochemical assay were determined for the evaluation of oxidative damage caused by ZrO2. Biodistribution of ZrO2 was investigated by ICP-OES and TEM. Results: Mice treated with higher dose (500mg/kg) showed significant spread in white blood cell counts (p<0.05). Especially, the serum ALT levels of 500mg/kg groups increased significantly (p<0.05) compared with the control group. ZrO2 particles would not induce any changes in appearance and micromorphology of liver at 100 and 350mg/kg. Spleen samples showed no significant changes in micromorphology of the lymphoid follicles and in the size of the red pulp after injection of ZrO2 at all doses. The serum of ZrO2-treated animals (350 and 500mg/kg) has reduced levels of SOD compared to the control group (p<0.05). ZrO2 persists in membrane-enclosed vesicles called lysosomes in the liver and spleen macrophages without abnormal changes of ultrastructure. Conclusion: These findings would contribute to the future development of ZrO2-based drug delivery system and other biomedical applications.

Because of the advantages of excellent light stability, carbon dots (CDs) are considered to be a promising agent in the bio-marker application. Nevertheless, there are many unresolved issues with the toxicity of CDs in vitro and in vivo. In the study, CDs were synthesized by citric acid and ethylenediamine into deionized water, then the inhalation toxicity and bio-distribution of CDs in vivo were systematically assessed. The results showed that CDs caused animals death at higher dosages and induced injury in the lung and liver including inflammation and necrosis after single inhalation exposure at 5, 2 and 1mg/kg dosages of the CDs. We also found that the injury increase with a dose-dependent and time-dependent manner. Fluorescent examination and TEM results showed that CDs mainly located at the lung and liver. And the fluorescent intensity increase with a time-dependent manner. This study provides a theoretical basis of the respiratory toxicity of CDs, and provides a basis for the use of CDs as a bio-marker.

小鼠经滴鼻途径吸入不同剂量纳米金团簇(1 mg/kg·bw、0.2 mg/kg·bw、0.1 mg/kg·bw),观察纳米金团簇急性毒性表现及纳米金团簇在小鼠体内的生物分布.结果显示,小鼠染毒后无明显临床异常,未出现死亡,血常规血生化指标检测结果显示,与对照组相比,暴露后第5天时白细胞略高出对照组,14 d时,白细胞数量显著升高(P＜0.05),谷丙转氨酶(ALT),谷草转氨酶(AST)显著升高,血尿素氮(BUN)、肌酐(CREA)与对照组无明显差异.组织形态学结果发现染毒组小鼠的肺脏、肝脏病变主要表现为炎症、坏死.体内分布结果表明,纳米金团簇经滴鼻暴露后主要分布于肺脏、肝脏,这与组织形态学结果一致,说明纳米金团簇主要靶器官为肺脏和肝脏.