title: Selenium blocks porcine circovirus type 2 replication promotion induced by oxidative stress by improving GPx1 expression.
abstract: Porcine circovirus type 2 (PCV2) is recognized as a key infectious agent in postweaning multisystemic wasting syndrome (PMWS), but not all pigs infected with PCV2 will develop PMWS. The aim of this work was to explore the relationships among PCV2 infection, oxidative stress, and selenium in a PK-15 cell culture model of PCV2 infection. The results showed that oxidative stress induced by H(2)O(2) treatment increased PCV2 replication as measured by PCV2 DNA copies and the number of infected cells. Furthermore, PCV2 replication was inhibited by selenomethionine (SeMet) at a high concentration (6μM) and the increase in PCV2 replication by oxidative stress was blocked by SeMet at physiological concentrations (2 or 4μM). PCV2 infection caused a decrease in glutathione peroxidase 1 (GPx1) activity but an increase in GPx1 mRNA levels, suggesting that GPx1 may represent an important defense mechanism during PCV2 infection. SeMet did not significantly block the promotion of PCV2 replication in GPx1-knockdown cells. This observation correlates with the observed influence of SeMet on GPx1 mRNA and activity in GPx1-knockdown cells, indicating that GPx1 plays a key role in blocking the promotion of PCV2 replication. We conclude that differences in morbidity and severity of PMWS observed on different pig farms may be related to variations in oxidative stress and that selenium has a potential role in the control of PCV2 infection.
authors.affiliation: Institute of Nutritional and Metabolic Disorders in Domestic Animals and Fowls, Nanjing Agricultural University, Nanjing, China.
authors.forename: Xingxiang
authors.initials: X
authors.lastname: Chen
authors.forename: Fei
authors.initials: F
authors.lastname: Ren
authors.forename: John
authors.initials: J
authors.lastname: Hesketh
authors.forename: Xiuli
authors.initials: X
authors.lastname: Shi
authors.forename: Junxian
authors.initials: J
authors.lastname: Li
authors.forename: Fang
authors.initials: F
authors.lastname: Gan
authors.forename: Kehe
authors.initials: K
authors.lastname: Huang
mesh_terms: D000818:Animals; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D017925:Circovirus / Q000502:physiology*; D015870:Gene Expression / Q000187:drug effects; D055785:Gene Knockdown Techniques; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000235:genetics / Q000378:metabolism*; D006861:Hydrogen Peroxide / Q000494:pharmacology; D016877:Oxidants / Q000494:pharmacology; D018384:Oxidative Stress; D034622:RNA Interference; D012645:Selenomethionine / Q000494:pharmacology*; D018038:Sodium Selenite / Q000494:pharmacology*; D034421:Sus scrofa; D054481:Thioredoxin Reductase 1 / Q000235:genetics / Q000378:metabolism; D013879:Thioredoxins / Q000235:genetics / Q000378:metabolism; D014779:Virus Replication / Q000187:drug effects*; D000094765:Glutathione Peroxidase GPX1
chemical_list: D016877:Oxidants; D013879:Thioredoxins; D012645:Selenomethionine; D006861:Hydrogen Peroxide; D005979:Glutathione Peroxidase; D054481:Thioredoxin Reductase 1; D005978:Glutathione; D018038:Sodium Selenite; D000094765:Glutathione Peroxidase GPX1