J Gen Virol Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lee, J. C.
Right arrow Articles by Chao, Y. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lee, J. C.
Right arrow Articles by Chao, Y. C.
Agricola
Right arrow Articles by Lee, J. C.
Right arrow Articles by Chao, Y. C.

Journal of General Virology, Vol 79, 2293-2300, Copyright © 1998 by Society for General Microbiology


ARTICLES

Apoptosis resulting from superinfection of Heliothis zea virus 1 is inhibited by p35 and is not required for virus interference

JC Lee and YC Chao
Graduate Institute of Life Sciences, National Defence Medical Center, Taipei, Taiwan, Republic of China.

Superinfection of Spodoptera frugiperda insect cells that are persistently infected with Heliothis zea 1 (Hz-1) virus induces general cellular apoptosis and subsequently results in homologous virus interference. Since apoptosis correlates closely with both a significant decrease in yield of virus progeny and expansion of virus infection among cells, further experiments were designed to verify the direct association of apoptosis with homologous interference. It was found that superinfection-induced apoptosis can be efficiently blocked by the stable transfection of p35 into cells before or after the establishment of persistent virus infection. However, persistently infected cells are still strongly resistant to the challenge of Hz-1 virus, indicating that the induction of apoptosis is not essential for the resulting homologous Hz-1 virus interference. Replication and transcription of viral genomes are greatly retarded upon Hz-1 virus superinfection of persistently infected cells, whether stably transfected with p35 or not, suggesting that upon superinfection, the decreasing yield of virus progeny in these persistently infected cells is caused by a blockage early after virus infection.


This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
H.-R. Lo, C.-C. Chou, T.-Y. Wu, J. P.-Y. Yuen, and Y.-C. Chao
Novel Baculovirus DNA Elements Strongly Stimulate Activities of Exogenous and Endogenous Promoters
J. Biol. Chem., February 8, 2002; 277(7): 5256 - 5264.
[Abstract] [Full Text] [PDF]


Home page
J. Virol.Home page
C.-L. Lin, J.-C. Lee, S.-S. Chen, H. Alan Wood, M.-L. Li, C.-F. Li, and Y.-C. Chao
Persistent Hz-1 Virus Infection in Insect Cells: Evidence for Insertion of Viral DNA into Host Chromosomes and Viral Infection in a Latent Status
J. Virol., January 1, 1999; 73(1): 128 - 139.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 1998 by the Society for General Microbiology.