scholarly journals Replication of nucleopolyhedroviruses of Autographa californica (Lepidoptera : Noctuidae), Bombyx mori (Lepidoptera : Bombycidae), Hyphantria cunea (Lepidoptera : Arctiidae), and Spodoptera exigua (Lepidoptera : Noctuidae) in four lepidopteran cell lines

1999 ◽  
Vol 34 (4) ◽  
pp. 507-516 ◽  
Author(s):  
Noriko Shirata ◽  
Motoko Ikeda ◽  
Katsumi Kamiya ◽  
Satoshi Kawamura ◽  
Yasuhisa Kunimi ◽  
...  
2013 ◽  
Vol 94 (9) ◽  
pp. 2102-2111 ◽  
Author(s):  
Rina Hamajima ◽  
Yuya Ito ◽  
Haruka Ichikawa ◽  
Hiroshi Mitsutake ◽  
Jun Kobayashi ◽  
...  

Cell lines derived from the silkworm, Bombyx mori, are only permissive for B. mori nucleopolyhedrovirus (NPV), with other NPVs generally resulting in abortive infection. Here, we demonstrate that rRNA of B. mori BM-N cells undergoes rapid degradation through site-specific cleavage upon infection with NPVs from Autographa californica (AcMNPV), Hyphantria cunea (HycuMNPV), Spodoptera exigua (SeMNPV) and Spodoptera litura (SpltMNPV). No significant decreases in cellular RNA were observed in Ld652Y, Se301, Sf9, SpIm and S2 cells infected with AcMNPV or HycuMNPV, indicating the response is unique to BM-N cells. A transient expression assay using a cosmid library of the HycuMNPV genome demonstrated that HycuMNPV P143 is responsible for rRNA degradation, which was also detected in BM-N cells transfected with plasmids expressing the P143 proteins from AcMNPV, SeMNPV and SpltMNPV. These results indicate that B. mori evolved to acquire a unique antiviral immune mechanism that is activated by P143 proteins from heterologous NPVs.


2003 ◽  
Vol 84 (3) ◽  
pp. 705-714 ◽  
Author(s):  
Hiroki Ishikawa ◽  
Motoko Ikeda ◽  
Kenichi Yanagimoto ◽  
Cristiano A. Felipe Alves ◽  
Yasuhiro Katou ◽  
...  

Ld652Y cells derived from the gypsy moth, Lymantria dispar, were infected with seven different nucleopolyhedroviruses (NPVs) including those from Autographa californica, Bombyx mori (BmNPV), Hyphantria cunea (HycuNPV), Spodoptera exigua (SeMNPV), L. dispar, Orgyia pseudotsugata (OpMNPV) and Spodoptera litura (SpltMNPV). The results showed that Ld652Y cells infected with BmNPV, HycuNPV, SeMNPV, OpMNPV and SpltMNPV underwent apoptosis, displaying apoptotic bodies, characteristic DNA fragmentation and increased caspase-3-like protease activity; HycuNPV induced the most severe apoptosis. In HycuNPV-infected Ld652Y cells, a considerable amount of viral DNA was synthesized although there was no detectable yield of budded virions and polyhedrin. Northern blot and immunoblot analyses revealed that HycuNPV inhibitor of apoptosis 3 (IAP3), which has been shown to function in Sf9 cells, was expressed in HycuNPV-infected Ld652Y cells at a level higher than or comparable with that in HycuNPV-infected SpIm cells, which produced a high titre of progeny virions without any apoptotic response. These results imply that the relative ease of apoptosis induction in NPV-infected Ld652Y cells is largely dependent on inherent cellular properties rather than functions of the respective NPVs, and indicate that the defect in progeny virion production is not merely due to the virus-induced apoptosis in HycuNPV-infected Ld652Y cells.


1993 ◽  
Vol 62 (3) ◽  
pp. 216-219 ◽  
Author(s):  
Q. Chen ◽  
A.H. McIntosh ◽  
Z. Yu ◽  
H. Hong ◽  
C.L. Goodman ◽  
...  

2004 ◽  
Vol 78 (22) ◽  
pp. 12703-12708 ◽  
Author(s):  
Hiroki Ishikawa ◽  
Motoko Ikeda ◽  
Cristiano A. Felipe Alves ◽  
Suzanne M. Thiem ◽  
Michihiro Kobayashi

ABSTRACT Host range factor 1 (HRF-1) of Lymantria dispar multinucleocapsid nucleopolyhedrovirus promotes Autographa californica MNPV replication in nonpermissive Ld652Y cells derived from L. dispar. Here we demonstrate that restricted Hyphantria cunea NPV replication in Ld652Y cells was not due to apoptosis but was likely due to global protein synthesis arrest that could be restored by HRF-1. Our data also showed that HRF-1 promoted the production of progeny virions for two other baculoviruses, Bombyx mori NPV and Spodoptera exigua MNPV, whose replication in Ld652Y cells is limited to replication of viral DNA without successful production of infectious progeny virions. Thus, HRF-1 is an essential viral factor required for productive infection of NPVs in Ld652Y cells.


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