Autographa californica Nuclear Polyhedrosis Virus Structural Proteins Compared from in vivo and in vitro Sources

Intervirology ◽  
1979 ◽  
Vol 11 (2) ◽  
pp. 82-88 ◽  
Author(s):  
James E. Maruniak ◽  
Max D. Summers ◽  
Louis A. Falcon ◽  
Gale E. Smith
Keyword(s):  
Nuclear Polyhedrosis Virus ◽  
Autographa Californica ◽  
Structural Proteins ◽  
Polyhedrosis Virus ◽  
Nuclear Polyhedrosis

scholarly journals The Effect of a Small Conotoxin-Like ctx Gene from Autographa californica Nuclear Polyhedrosis Virus (AcMNPV) on Insect Hemolymph Melanization

2012 ◽  
Vol 61 (3) ◽  
pp. 183-189 ◽  
Author(s):  
QING CAO ◽  
SHAN$YING ZHU ◽  
YAN WU ◽  
YONG LIU ◽  
JIANG ZHU ◽  
...  
Keyword(s):  
Nuclear Polyhedrosis Virus ◽  
Fusion Gene ◽  
Autographa Californica ◽  
Insect Larvae ◽  
Cysteine Motif ◽  
Bmnpv Bacmid ◽  
Polyhedrosis Virus ◽  
Nuclear Polyhedrosis

The conotoxin-like (ctx) gene encodes a small cysteine-rich polypeptide in various baculoviruses. Previous research has demonstrated that the product of the ctx gene could be purified from insect cells infected by Autographa californica nuclear polyhedrosis virus (AcMNPV), but its function was unknown. In this paper, we compared the conserved cysteine motif structure (CX3GX2CX5CCX3CX6C) of the ctx gene in baculoviruses and generated recombinant Bombyx mori nuclear polyhedrosis virus (BmNPV) with the BmNPV bacmid system. The recombinant BmNPV contained the ctx gene from AcMNPV or a fusion gene of ctx with eGFP, respectively. Fluorescence in CTX-eGFP-positive cells was mainly observed on the cell membrane. To gain insight into CTX function, two methods were used to elucidate the affect CTX had on hemolymph melanization in vivo and in vitro in insect larvae and pupae. The results indicated that CTX abrogates hemolymph melanization; however, the mechanisms require further evaluation.

scholarly journals Physical Factors That Affect In Vitro Autographa californica Nuclear Polyhedrosis Virus Infection

1981 ◽  
Vol 41 (5) ◽  
pp. 1166-1172 ◽  
Author(s):  
Edward M. Dougherty ◽  
Ronald M. Weiner ◽  
James L. Vaughn ◽  
Charles F. Reichelderfer
Keyword(s):  
Virus Infection ◽  
Nuclear Polyhedrosis Virus ◽  
Autographa Californica ◽  
Physical Factors ◽  
Polyhedrosis Virus ◽  
Nuclear Polyhedrosis

scholarly journals Differential Activity of Two Non-hrOrigins during Replication of the Baculovirus Autographa californica Nuclear Polyhedrosis Virus Genome

2000 ◽  
Vol 74 (11) ◽  
pp. 5182-5189 ◽  
Author(s):  
Saman Habib ◽  
Seyed E. Hasnain
Keyword(s):  
Viral Infection ◽  
Nuclear Polyhedrosis Virus ◽  
Late Phase ◽  
Promoter Sequence ◽  
Autographa Californica ◽  
Defective Interfering Particles ◽  
Genomic Deletions ◽  
Polyhedrosis Virus ◽  
Nuclear Polyhedrosis

ABSTRACT The identification of potential baculovirus origins of replication (ori) has involved the generation and characterization of defective interfering particles that contain major genomic deletions yet retain their capability to replicate by testing the replication ability of transiently transfected plasmids carrying viral sequences in infected cells. So far, there has not been any evidence to demonstrate the actual utilization of these putative origins in Autographa californica multinucleocapsid nuclear polyhedrosis virus (AcMNPV) replication. By using the method of origin mapping by competitive PCR, we have obtained quantitative data for theori activity of the HindIII-K region and theie-1 promoter sequence in AcMNPV. We also provide evidence for differential activity of the two oriin the context of the viral genome through the replication phase of viral infection. Comparison of the number of molecules representing theHindIII-K and ie-1 origins vis-à-vis the non-ori polH region in a size-selected nascent DNA preparation revealed that the HindIII-K ori is utilized ∼14 times more efficiently than the ie-1 region during the late phase of infection. HindIII-K also remains the more active ori through the early and middle replication phases. Our results provide in vivo evidence in support of the view that AcMNPV replication involves multipleori that are activated with vastly different efficiencies during the viral infection cycle.

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