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CD55 is a key complement regulatory protein that counteracts complement-mediated inactivation of Newcastle Disease Virus
Author(s) -
Udaya S. Rangaswamy,
Christopher R. Cotter,
Xing Cheng,
Hong Jin,
Yuyan Chen
Publication year - 2016
Publication title -
journal of general virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.55
H-Index - 167
eISSN - 1465-2099
pISSN - 0022-1317
DOI - 10.1099/jgv.0.000498
Subject(s) - biology , virology , newcastle disease , embryonated , virus , oncolytic virus , cd46 , decay accelerating factor , cd59 , complement system , recombinant dna , microbiology and biotechnology , immune system , immunology , gene , biochemistry
Newcastle disease virus (NDV) is being developed as an oncolytic virus for virotherapy. In this study we analysed the regulation of complement-mediated inactivation of a recombinant NDV in different host cells. NDV grown in human cells was less sensitive to complement-mediated virus inactivation than NDV grown in embryonated chicken eggs. Additionally, NDV produced from HeLa-S3 cells is more resistant to complement than NDV from 293F cells, which correlated with higher expression and incorporation of complement regulatory proteins (CD46, CD55 and CD59) into virions from HeLa-S3 cells. Further analysis of the recombinant NDVs individually expressing the three CD molecules showed that CD55 is the most potent in counteracting complement-mediated virus inactivation. The results provide important information on selecting NDV manufacture substrate to mitigate complement-mediated virus inactivation.

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