Relative Contribution Of Cellular Complement Inhibitors Cd59, Cd46, And Cd55 To Parainfluenza Virus 5 Inhibition Of Complement-Mediated Neutralization
Keywords
Cell surface inhibitors; Complement; Virus neutralization
Abstract
The complement system is a part of the innate immune system that viruses need to face during infections. Many viruses incorporate cellular regulators of complement activation (RCA) to block complement pathways and our prior work has shown that Parainfluenza virus 5 (PIV5) incorporates CD55 and CD46 to delay complement-mediated neutralization. In this paper, we tested the role of a third individual RCA inhibitor CD59 in PIV5 interactions with complement pathways. Using a cell line engineered to express CD59, we show that small levels of functional CD59 are associated with progeny PIV5, which is capable of blocking assembly of the C5b-C9 membrane attack complex (MAC). PIV5 containing CD59 (PIV5-CD59) showed increased resistance to complement-mediated neutralization in vitro comparing to PIV5 lacking regulators. Infection of A549 cells with PIV5 and RSV upregulated CD59 expression. TGF-beta treatment of PIV5-infected cells also increased cell surface CD59 expression and progeny virions were more resistant to complement-mediated neutralization. A comparison of individual viruses containing only CD55, CD46, or CD59 showed a potency of inhibiting complement-mediated neutralization, which followed a pattern of CD55 > CD46 > CD59.
Publication Date
5-1-2018
Publication Title
Viruses
Volume
10
Issue
5
Document Type
Article
Personal Identifier
scopus
DOI Link
https://doi.org/10.3390/v10050219
Copyright Status
Unknown
Socpus ID
85046151055 (Scopus)
Source API URL
https://api.elsevier.com/content/abstract/scopus_id/85046151055
STARS Citation
Li, Yujia and Parks, Griffith D., "Relative Contribution Of Cellular Complement Inhibitors Cd59, Cd46, And Cd55 To Parainfluenza Virus 5 Inhibition Of Complement-Mediated Neutralization" (2018). Scopus Export 2015-2019. 8279.
https://stars.library.ucf.edu/scopus2015/8279