TY - JOUR
T1 - A universal mammalian vaccine cell line substrate
AU - Murray, Jackelyn
AU - Todd, Kyle V.
AU - Bakre, Abhijeet
AU - Orr-Burks, Nichole
AU - Jones, Les
AU - Wu, Weilin
AU - Tripp, Ralph A.
N1 - Funding Information:
The funders had no role in study design, data collection and analysis decision to publish, or preparation of this manuscript. This work was in part supported by the Center of Excellence for influenza Research and Surveillance (HHSN272201500004C), the Bill and Melinda Gates foundation, and the Georgia Research Alliance (GRA). The GRA is an independent nonprofit organization that works in partnership with the University System of Georgia and Georgia’s Department of Economic Development.
Publisher Copyright:
© 2017 Murray et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2017/11
Y1 - 2017/11
N2 - Using genome-wide small interfering RNA (siRNA) screens for poliovirus, influenza A virus and rotavirus, we validated the top 6 gene hits PV, RV or IAV to search for host genes that when knocked-down (KD) enhanced virus permissiveness and replication over wild type Vero cells or HEp-2 cells. The enhanced virus replication was tested for 12 viruses and ranged from 2-fold to >1000-fold. There were variations in virus-specific replication (strain differences) across the cell lines examined. Some host genes (CNTD2, COQ9, GCGR, NDUFA9, NEU2, PYCR1, SEC16G, SVOPL, ZFYVE9, and ZNF205) showed that KD resulted in enhanced virus replication. These findings advance platform-enabling vaccine technology, the creation of diagnostic cells substrates, and are informative about the host mechanisms that affect virus replication in mammalian cells.
AB - Using genome-wide small interfering RNA (siRNA) screens for poliovirus, influenza A virus and rotavirus, we validated the top 6 gene hits PV, RV or IAV to search for host genes that when knocked-down (KD) enhanced virus permissiveness and replication over wild type Vero cells or HEp-2 cells. The enhanced virus replication was tested for 12 viruses and ranged from 2-fold to >1000-fold. There were variations in virus-specific replication (strain differences) across the cell lines examined. Some host genes (CNTD2, COQ9, GCGR, NDUFA9, NEU2, PYCR1, SEC16G, SVOPL, ZFYVE9, and ZNF205) showed that KD resulted in enhanced virus replication. These findings advance platform-enabling vaccine technology, the creation of diagnostic cells substrates, and are informative about the host mechanisms that affect virus replication in mammalian cells.
UR - http://www.scopus.com/inward/record.url?scp=85035199461&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0188333
DO - 10.1371/journal.pone.0188333
M3 - Article
C2 - 29176782
AN - SCOPUS:85035199461
SN - 1932-6203
VL - 12
SP - 1
EP - 17
JO - PLoS One
JF - PLoS One
IS - 11
M1 - e0188333
ER -
