Replication-incompetent Sendai virus can suppress the antiviral action of type I interferon

Replication-incompetent Sendai virus can suppress the antiviral action of type I interferon Altered baby hamster kidney (BHK-R) cells, which were established by serial passage of BHK cells in the presence of Sendai virus (SeV), allowed vesicular stomatitis virus (VSV) to replicate despite treatment with type I interferon (IFN). We have analyzed here mechanisms of the unresponsiveness to IFN. BHK-R cells cultured in the absence of SeV for 10 days under the conditions of no cell division (BHK-R10D) became sensitive to IFN. Studies on induction of unresponsiveness to IFN in BHK-R10D cells revealed that entry of SeV nucleocapsids into a cell was essential. Interestingly, even UV-inactivated SeV but not Newcastle disease virus was found to be able to confer resistance to IFN on HeLa or BHK cells as well as on BHK-R10D cells, suggesting that the IFN-resistance resulted from functions of SeV independent of replication of the viral genome but not from mutations of the cellular genome. Furthermore immunofluorescent experiments demonstrated that UV-inactivated SeV could rescue VSV replication from the antiviral action of IFN without expression of SeV antigens, confirming that the secondary transcription resulting in synthesis of large amounts of viral proteins was dispensable for the IFN-resistance. Thus we have revealed a unique strategy of SeV against the antiviral action of IFN. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Replication-incompetent Sendai virus can suppress the antiviral action of type I interferon

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Publisher
Springer Journals
Copyright
Copyright © Wien by 1999 Springer-Verlag/
Subject
Legacy
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s007050050568
Publisher site
See Article on Publisher Site

Abstract

Altered baby hamster kidney (BHK-R) cells, which were established by serial passage of BHK cells in the presence of Sendai virus (SeV), allowed vesicular stomatitis virus (VSV) to replicate despite treatment with type I interferon (IFN). We have analyzed here mechanisms of the unresponsiveness to IFN. BHK-R cells cultured in the absence of SeV for 10 days under the conditions of no cell division (BHK-R10D) became sensitive to IFN. Studies on induction of unresponsiveness to IFN in BHK-R10D cells revealed that entry of SeV nucleocapsids into a cell was essential. Interestingly, even UV-inactivated SeV but not Newcastle disease virus was found to be able to confer resistance to IFN on HeLa or BHK cells as well as on BHK-R10D cells, suggesting that the IFN-resistance resulted from functions of SeV independent of replication of the viral genome but not from mutations of the cellular genome. Furthermore immunofluorescent experiments demonstrated that UV-inactivated SeV could rescue VSV replication from the antiviral action of IFN without expression of SeV antigens, confirming that the secondary transcription resulting in synthesis of large amounts of viral proteins was dispensable for the IFN-resistance. Thus we have revealed a unique strategy of SeV against the antiviral action of IFN.

Journal

Archives of VirologySpringer Journals

Published: Jun 1, 1999

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