title: Photochemically inactivated hepatitis B virus promotes upregulation of Th1-type cytokines.
abstract: Photochemical virus inactivation technology is widely used to improve the safety of blood products. However, the process by which this inactivation occurs and the resulting immunogenicity of treated viruses remain to be elucidated. This study aimed to explore the effects of two photochemical inactivation methods (methylene and riboflavin, MP and RP) on hepatitis B virus (HBV) immunogenicity. Inactivated HBV were incubated with PBMC from six healthy donors. Culture supernatants were collected at 0, 24 and 72 h for the analysis of HBsAg and HBeAg expression using ELISA. Cytokine expression was analyzed at 72 h using ELISA. Costimulatory and cell adhesion molecule mRNA expression was analyzed at 24 h by RT-PCR. No significant changes in HBsAg and HBeAg were detected following MP. However, the secretion of TNF-α and IFN-γ was upregulated. Expression of CD80, CD86, ICAM2 and LFA3 mRNA was also upregulated. In contrast, although RP did not significantly alter HBsAg expression, a reduction in HBeAg expression was observed. Furthermore, no upregulation of cytokines and intracellular molecule expression was observed following RP. These data indicate that the immunogenicity of HBV is retained following MP, and the inactivation of HBV could upregulate the Th1-type cellular immune responses, which may play significant roles in the antiviral process.
authors.affiliation: Shanghai Blood Centre, Shanghai, China Shanghai Blood Centre Graduate Student Training Base, East China Normal University, Shanghai, China. xiaoyingliu1@163.com
authors.forename: Xiaoying
authors.initials: X
authors.lastname: Liu
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Zhao
authors.forename: Xun
authors.initials: X
authors.lastname: Wang
authors.forename: Jingjing
authors.initials: J
authors.lastname: Zhang
authors.forename: Yuwen
authors.initials: Y
authors.lastname: Huang
authors.forename: Qin
authors.initials: Q
authors.lastname: Mo
authors.forename: Kaicheng
authors.initials: K
authors.lastname: Qian
authors.forename: Yongming
authors.initials: Y
authors.lastname: Zhu
mesh_terms: D015703:Antigens, CD / Q000235:genetics / Q000276:immunology; D018122:B7-1 Antigen / Q000235:genetics / Q000276:immunology; D051940:B7-2 Antigen / Q000235:genetics / Q000276:immunology; D018968:CD58 Antigens / Q000235:genetics / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000276:immunology; D002478:Cells, Cultured; D005786:Gene Expression Regulation; D006514:Hepatitis B Surface Antigens / Q000096:biosynthesis / Q000276:immunology; D006513:Hepatitis B e Antigens / Q000096:biosynthesis / Q000276:immunology; D006515:Hepatitis B virus / Q000187:drug effects* / Q000528:radiation effects; D006801:Humans; D007371:Interferon-gamma / Q000276:immunology* / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000276:immunology* / Q000378:metabolism / Q000821:virology; D008027:Light; D008751:Methylene Blue / Q000494:pharmacology; D017319:Photosensitizing Agents / Q000494:pharmacology*; D012333:RNA, Messenger / Q000096:biosynthesis*; D012256:Riboflavin / Q000494:pharmacology; D058408:Th1-Th2 Balance; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology* / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D018122:B7-1 Antigen; D051940:B7-2 Antigen; D018968:CD58 Antigens; D015815:Cell Adhesion Molecules; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; C065289:ICAM2 protein, human; D017319:Photosensitizing Agents; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D008751:Methylene Blue; D012256:Riboflavin