Our previous work has shown that Saffold virus(SAFV)induced several rodent and primate cell lines to undergo apoptosis(Xu et al.in Emerg Microb Infect 3:1-8,2014),but the essential viral proteins of SAFV involved in a...Our previous work has shown that Saffold virus(SAFV)induced several rodent and primate cell lines to undergo apoptosis(Xu et al.in Emerg Microb Infect 3:1-8,2014),but the essential viral proteins of SAFV involved in apoptotic activity lack study.In this study,we individually transfected the viral proteins of SAFV into HEp-2 and Vero cells to assess their ability to induce apoptosis,and found that the 2B and 3C proteins are proapoptotic.Further investigation indicated the trans-membrane domain of the 2B protein is essential for the apoptotic activity and tetramer formation of the 2B protein.Our research provides clues for the possible mechanisms of apoptosis induced by SAFV in different cell lines.It also opens up new directions to study viral proteins(the 2B,3C protein),and sets the stage for future exploration of any possible link between SAFV,inclusive of its related uncultivable genotypes,and multiple sclerosis.展开更多
Dear Editor,Previous studies had described the adaptation of enterovirus 71(EV-A71)strains that enabled entry and viral replication in Chinese Hamster Ovary(CHO)cell line(Zaini and McMinn 2012;Zaini et al.2012).These ...Dear Editor,Previous studies had described the adaptation of enterovirus 71(EV-A71)strains that enabled entry and viral replication in Chinese Hamster Ovary(CHO)cell line(Zaini and McMinn 2012;Zaini et al.2012).These adapted strains derived from serial passage of a clinical isolate in CHO cells exhibited an amino acid substitution at VP2149,which enhanced viral replication by 100*1000-fold compared to the clinical isolate.The VP2149 mutation was claimed responsible for adaptation to CHO-K1 cells without performing detailed molecular analyses to support these claims.In this study,we evaluate various VP1 and VP2 mutations in two CHO-adapted EV-A71 strains derived in our lab to assess their contribution to the phenotype of CHO cell adaptation.展开更多
基金funded by Temasek Lifesciences Laboratory, an affiliate of National University of Singapore and Nanyang Technological University, Singapore and did not receive any specific grant from any funding agency in the public, commercial, or not-for-profit sectors
文摘Our previous work has shown that Saffold virus(SAFV)induced several rodent and primate cell lines to undergo apoptosis(Xu et al.in Emerg Microb Infect 3:1-8,2014),but the essential viral proteins of SAFV involved in apoptotic activity lack study.In this study,we individually transfected the viral proteins of SAFV into HEp-2 and Vero cells to assess their ability to induce apoptosis,and found that the 2B and 3C proteins are proapoptotic.Further investigation indicated the trans-membrane domain of the 2B protein is essential for the apoptotic activity and tetramer formation of the 2B protein.Our research provides clues for the possible mechanisms of apoptosis induced by SAFV in different cell lines.It also opens up new directions to study viral proteins(the 2B,3C protein),and sets the stage for future exploration of any possible link between SAFV,inclusive of its related uncultivable genotypes,and multiple sclerosis.
基金fully funded by Temasek Lifesciences Laboratory Ltd.
文摘Dear Editor,Previous studies had described the adaptation of enterovirus 71(EV-A71)strains that enabled entry and viral replication in Chinese Hamster Ovary(CHO)cell line(Zaini and McMinn 2012;Zaini et al.2012).These adapted strains derived from serial passage of a clinical isolate in CHO cells exhibited an amino acid substitution at VP2149,which enhanced viral replication by 100*1000-fold compared to the clinical isolate.The VP2149 mutation was claimed responsible for adaptation to CHO-K1 cells without performing detailed molecular analyses to support these claims.In this study,we evaluate various VP1 and VP2 mutations in two CHO-adapted EV-A71 strains derived in our lab to assess their contribution to the phenotype of CHO cell adaptation.
