Ebola hemorrhagic fever is an acute infectious disease caused by Ebola virus,the mor-tality rate of which is up to 90% . Due to its high infection rate,high mortality rate as well as being a serious threat to public health and safety,Ebola virus is listed as a World Health Organization Risk Group 4 Patho-gen(requiring Biosafety Level 4-equivalent containment). However,there is no effective control method and treatment for Ebola virus infection. Different approaches have been used to develop vaccines and therapeutic drugs against Ebola virus infection and clinical trials of some products have been initiated,such as ZMapp, BCX-4430,GS-5734,DNA vaccines,and adenovirus vector vaccines. National Institutes of Health(NIH) announced a successful development of vaccine for Ebola virus which had passed the clinical trial by the end of 2014. At the meantime,the first anti-Ebola virus medicine had also been approved in China for emergency use only. Recent advances in the research and development of therapeutic drugs and vaccines against Ebola virus will be described in this review.

Vaccinia virus ( VACV) has been widely used in humans for the eradication of small-pox. Since its natural ability of selective infection and replication in tumor cells without harming the normal tissue, VACV becomes a promising candidate in cancer therapy. In recent years, a variety of strategies have been successfully applied to further enhance the tumor selectivity and anti-tumor efficacy of VACV. These engineered VACVs, such as JX-594, have shown promising results in cancer treatment and have made re-markable progress in clinical trials. This review first briefly introduces the oncolytic VACV, and then focuses on the strategies applied in VACV engineering. We also discuss the main challenges and the future directions in the development of oncolytic VACV.

Objective To clone the fragment of hepatitis C virus(HCV) core gene and express it in E.coli.Methods The fragment of HCV core gene(approximate 366bp) was amplified by PCR and inserted into the pMD18-T vector.The cloned HCV core gene,which was confirmed by the digestion with EcoRⅠ/BamHⅠ,was subcloned into the expression vector pBV220 to construct recombinant plasmid pBV220/HCV-C.The expressed gene product was identified by SDS-PAGE and Western blotting.Results The fragment of HCV core gene was expressed successfully after temperature induction and a protein of 14 000 u was resulted.Conclusion Expression of the HCV-C gene in E.coli was achieved,which may be helpful for further studies on characterizations of HCV-C gene.

Innate lymphoid cells (ILCs) are a recently characterized family of immune cells that have critical roles in innate immunity, immune regulation, maintenance of tissue homeostasis, and tissue repair and remodeling. Besides the conventional innate lymphocytes including NK cells and lymphoid tissue-inducer cells, the ILC family can be categorized into three groups, ILC1s, ILC2s and ILC3s. These non-cytotoxic ILC subsets have been identified to confer a diverse array of functions in oncogenesis and metastasis, immune surveillance, and antitumor immunity. In this review, we summarized the emerging findings in recent years regarding the roles of ILCs in immuno-oncology, and highlighted their potentials in immunotherapeutic approaches to tumors.

Objective To evaluate the regulatory effects of Astragalus polysaccharide (APS) on macrophage polarization and NK cell-mediated anti-tumor responses in mice. Methods C57BL/ 6 mice were injected intraperitoneally with APS once a day for seven consecutive days. Activation of immune cells was then induced by intraperitoneal injection of polyinosinic-polycytidylic acid (Poly I : C) 24 h after the APS intervention. Peritoneal macrophages were collected 24 h after induction to analyze the status of polari-zation and the production of nitric oxide (NO). Cytotoxicity and exocytosis of activated NK cells were meas-ured to assess the effector functions of these cells. NK cell activities induced by NKG2D were studied in the absence of the whole JNK or JNK2 signaling pathway. Results Intraperitoneal injection of APS promoted the polarization of macrophages induced by tumor cells in mice, and enhanced the cytotoxicity of NK cells to tumor cells. However, APS was in need of the involvement of appropriate stimulatory factors to have regula-tory effects. Complete inhibition of JNK signaling pathway dramatically reduced the effector functions of NK cells, which could not be recovered by APS administration. Conclusions APS was involved in the regula-tion of anti-tumor innate immunity through enhancing the M1-polarization of macrophages and improving the effector functions of NK cells. This study might to some extent elucidate the mechanism of APS in immune regulation and anti-tumor immunity.