Sponsored by Chinese Society for Microbiology
ISSN 1000-8721 CN 11-1865/R
6 issues per year
Current Issue: Issue 06, 2019
Chinese Journal of Virology, an academic periodical established in 1985, publishes Original Articles, Brief Reports, Reviews, and so on, covering the advances and achievements of fundamental and applied research concerning human, animal, plant, and insect viruses as well as bacteriophages and prions. The subscribers of Chinese Journal of Virology are mainly workers in research institutes, universities, and other institutions of virological and biological studies in China, as well as world-known databases and libraries. Chinese Journal of Virology is supervised by the China Association for Science and Technology, sponsored by the Chinese Society for Microbiology, run by the National Institute for Viral Disease Control and Prevention, China CDC, and published by its Editorial Office. The International Standard Serial Number is ISSN 1000-8721; the Domestic Journal Number is CN 11-1865/R; the Domestic Postal Distribution Code is 82-227 (domestically distributed by all local post offices in China); the Overseas Distribution Code is BM6448 (distributed by China International Book Trading Corporation). Chinese Journal of Virology has been published bimonthly since 2005 and is now distributed worldwide. Chinese Journal of Virology is included in the Outstanding S&T Journals of China, Chinese Core Journals of Science and Technology, A Guide to the Core Journals of China (published by Peking University), Research Center for Chinese Science Evaluation, Wuhan University, and Chinese Science Citation Database source journals. In addition, it is indexed in CA, BA, CBST, MEDLINE (PubMed), and WPRIM. Chinese Journal of Virology has been included in the databases of CNKI (Disc Edition) since December 30, 2008. It began to tentatively offer Advance Online Publication in 2009 and has been formally offering Advance Online Publication since 2011. The composite impact factor of Chinese Journal of Virology is 1.355, according to the Annual Report for Chinese Academic Journal Impact Factors (Basic Medical Sciences) (2015, Volume 13), ranking top among the journals of basic medical and biological sciences. The homepage of Chinese Journal of Virology on CNKI is http://bdxb.cbpt.cnki.net. Chinese Journal of Virology started a pilot program of bilingual publication on November 8, 2016 to publish papers in both Chinese and English on CNKI net.
Honorary Editor-in-Chief: HOU Yunde
Editor-in-Chief: SHU Yuelong
LIU Xiufan, FANG Rongxiang, WU Guizhen, JIN Qi, LIANG Mifang, LI Mengfeng, XIA Ningshao, TAN Wenjie, XU Wenbo, WANG Yumei
Vol 35,No. 06
Orf virus (ORFV) can cause a strong immune response after infection. To investigate the maturation of mouse bone marrow-derived dendritic cells (BMDCs) and the polarization of naïve cluster of differentiation (CD) 4 + T cells by ORFV and find immunologically differentially expressed genes (DEGs) after ORFV infection of BMDCs. BMDCs were infected by ORFV with different multiplicity of infection (MOI) values. Whether the cell could mature after infection was tested based on the expression of surface co-stimulatory molecules, secretion of cytokines, and phagocytic activity of BMDCs. The effect of the cells on the stimulatory ability of naïve CD4 + T cells was detected. High-throughput sequencing of BMDCs infected by ORFV of 1 MOI was performed. We found that ORFV of 1 MOI could promote the maturation and differentiation of naïve CD4 + T cells into Th1 cells. A total of 8 241 DEGs (4 205 up-regulated genes and 4 036 down-regulated genes) were detected by RNA-seq. These DEGs contributed to antigen presentation/processing, T-cell receptor signaling pathway, T-cell activation and cytokine secretion pathways, and apoptotic signaling pathways. Some DEGs were verified by fluorescence quantitative reverse transcription-polymerase chain reaction, and the results were consistent with the result of transcriptome sequencing. These data lay a foundation for further elucidating the mechanism of the interaction between ORFV and immune cells.
Vol 35,No. 06
Rana grylio virus (RGV) and Andrias davidianus ranavirus (ADRV) belong to the genus Ranavirus (family Iridoviridae), which are pathogens causing high mortality in aquatic animals. Their homologous early protein RGV-27R and ADRV-85L have identities more than 99% with the 25R protein [frog virus 3 (FV3)-25R, or FV3 early protein P31K] of FV3, the type species of the genus Ranavirus. On the basis of observing and comparing the microscopic pathologies of giant salamander thymus cells (GSTC) infected by RGV and ADRV, we cloned the ADRV-85L and RGV-27R genes into the prokaryotic expression vector plasmids pET-32a and pMAL-p5X which were transformed into the host E. coli BL21 (DE3) and induced for expression. The prokaryotic expression and immunogenicity of the two proteins were analyzed by SDS-PAGE and Western blotting. Results showed that the expression efficiency of the two genes in plasmid pET-32a was significantly higher than that in plasmid pMAL-p5X. The highly expressed pET-32a-RGV-27R product was then selected and purified by Ni-NTA His-Bind affinity chromatography to obtain recombinant fusion protein His-RGV-27R with a concentration of 1.2 mg/mL. The purified recombinant protein was used to immunize animals to generate antibody 27R-Ab, and the titer of the antibody was determined as 1:6.25 × 10 6 by ELISA. The GSTC suspension infected with RGV or ADRV was frozen and thawed repeatedly, and then examined by Western blotting with the antibody that was adsorbed by normal E. coli and normal GSTC suspensions as the primary antibody. Meanwhile, the fusion proteins His-RGV-27R and His-ADRV-85L expressed and purified above were used as the positive controls and the normal GSTC suspension was used as negative control. The results of Western blotting showed that the specific protein bands with the size of 31 kD were detected in GSTC suspensions infected by RGV or ADRV respectively. Our results revealed that the two ranavirus homologous early proteins RGV-27R and ADRV-85L not only express in amphibian cells, but also share the same antigenic characters. Our study also provides useful materials for in-depth study of the effect of these viral proteins on ranavirus replication and the molecular mechanism of their interaction with host.