Document Detail

High resistance of human parainfluenza type 2 virus protein-expressing cells to the antiviral and anti-cell proliferative activities of alpha/beta interferons: cysteine-rich V-specific domain is required for high resistance to the interferons.
MedLine Citation:
PMID:  11533180     Owner:  NLM     Status:  MEDLINE    
Human parainfluenza type 2 virus (hPIV-2)-infected HeLa (HeLa-CA) cells and hPIV-2 V-expressing HeLa (HeLa-V) cells show high resistance to alpha/beta interferons (IFN-alpha/beta) irrespective of whether vesicular stomatitis virus or Sindbis virus is used as a challenge virus. When Sindbis virus is used, these cells show high susceptibility to human IFN-gamma. Furthermore, the multiplication of HeLa-V cells is not inhibited by IFN-alpha/beta. HeLa cells expressing the N-terminally truncated V protein show resistance to IFN-alpha/beta, showing that the IFN resistance determinant maps to the cysteine-rich V-specific domain. A complete defect of Stat2 is found in HeLa-CA and HeLa-V cells, whereas the levels of Stat1 expression are not significantly different among HeLa, HeLa-CA, HeLa-P, and HeLa-V cells, indicating that IFN-alpha/beta resistance of HeLa-CA and HeLa-V cells is due to a defect of Stat2. HeLa-SV41V cells show high resistance to all IFNs, and no expression of Stat1 can be detected. Stat2 mRNA is fully detected in HeLa-V cells. Stat2 was scarcely pulse-labeled in the HeLa-V cells, indicating that synthesis of Stat2 is suppressed or Stat2 is very rapidly degraded in HeLa-V cells. The V protein suppresses the in vitro translation of Stat2 mRNA more extensively than that of Stat1 mRNA. An extremely small amount of Stat2 can be detected in HeLa-V cells treated with proteasome inhibitors. The half-life of Stat2 is approximately 3.5 and 2 h in uninfected and hPIV-2-infected HeLa cells, respectively. This study shows that synthesis of Stat2 may be suppressed and Stat2 degradation is also enhanced in hPIV-2-infected HeLa and HeLa-V cells.
M Nishio; M Tsurudome; M Ito; M Kawano; H Komada; Y Ito
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of virology     Volume:  75     ISSN:  0022-538X     ISO Abbreviation:  J. Virol.     Publication Date:  2001 Oct 
Date Detail:
Created Date:  2001-09-04     Completed Date:  2001-10-11     Revised Date:  2013-04-18    
Medline Journal Info:
Nlm Unique ID:  0113724     Medline TA:  J Virol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  9165-76     Citation Subset:  IM    
Department of Microbiology, Mie University School of Medicine, Tsu-Shi, Mie-Ken 514-8507, Japan.
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MeSH Terms
Antiviral Agents / pharmacology*,  therapeutic use
Cell Division / drug effects
DNA-Binding Proteins / physiology
Drug Resistance, Microbial*
HeLa Cells
Interferons / pharmacology*,  therapeutic use
Parainfluenza Virus 2, Human / chemistry,  drug effects*,  genetics
Rubulavirus Infections / drug therapy*,  pathology,  virology
STAT1 Transcription Factor
STAT2 Transcription Factor
Trans-Activators / physiology
Virus Replication / drug effects
Reg. No./Substance:
0/Antiviral Agents; 0/DNA-Binding Proteins; 0/STAT1 Transcription Factor; 0/STAT1 protein, human; 0/STAT2 Transcription Factor; 0/STAT2 protein, human; 0/Trans-Activators; 52-90-4/Cysteine; 9008-11-1/Interferons

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